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J Am Soc Nephrol. Feb 2012; 23(2): 194–203.
PMCID: PMC3269181

The Renal Mononuclear Phagocytic System


The renal mononuclear phagocytic system, conventionally composed of macrophages (Mø) and dendritic cells (DCs), plays a central role in health and disease of the kidney. Overlapping definitions of renal DCs and Mø, stemming from historically separate research tracks and the lack of experimental tools to specifically study the roles of these cells in vivo, have generated confusion and controversy, however, regarding their immunologic function in the kidney. This brief review provides an appraisal of the current state of knowledge of the renal mononuclear phagocytic system interpreted from the perspective of immunologic function. Physical characteristics, ontogeny, and known functions of the main subsets of renal mononuclear phagocytes as they relate to homeostasis, surveillance against injury and infection, and immune-mediated inflammatory injury and repair within the kidney are described. Gaps and inconsistencies in current knowledge are used to create a roadmap of key questions to be answered in future research.

The mononuclear phagocytic system in nonlymphoid organs such as the kidney is composed of diverse subsets of bone marrow–derived macrophages (Mø) and dendritic cells (DCs).1 Mø are defined as tissue-resident phagocytic cells that contribute to steady-state tissue homeostasis by clearing apoptotic material and producing growth factors. During infection, they perform antimicrobial effector functions such as phagocytosis and production of toxic metabolites and proinflammatory cytokines.1,2 DCs, however, are defined primarily by the specialized functions of antigen presentation and regulation of immune effector cells. Classically, DCs collect antigenic material in tissues and then migrate to lymph nodes for the purpose of presenting antigen to naïve T cells.1,3 As summarized in Table 1, however, Mø and DCs within the kidney exhibit additional and at times, overlapping functional properties that extend beyond these classic paradigms. Furthermore, similar to mononuclear phagocytes in skin, lung, and gut, the predominant, resident renal mononuclear phagocytes (rMoPh) simultaneously express markers traditionally associated with either Mø or DCs.47 Indeed, as discussed below, many research groups have characterized these rMoPh for over three decades as either Mø or DCs, despite growing evidence of phenotypic and functional overlap, creating a barrier to cohesive progress in the field.

Table 1.
Distinct and shared functions of macrophages and dendritic cells in the kidney

Knowledge of rMoPh began with groundbreaking studies in normal kidneys of mice and rats that identified abundant dendritiform cells within the renal interstitium. These cells were designated antigen-presenting DCs on the basis of MHC class II expression8,9 or resident Mø because of F4/80 expression.810 In addition, rare MHC class II+ globular Mø were identified in the glomerulus11,12 and subcapsular and periarterial connective tissue.13,14 Subsequently, however, multicolor flow cytometry revealed substantial overlap and heterogeneity in expression of historically defined Mø (CD11b, F4/80, and CD68) and DC (CD11c, MHC II, and CD80/86) markers by interstitial rMoPh.1519 Along with similar descriptions in normal human kidney,2022 these studies established the predominant rMoPh at steady state as networked, dendritiform, interstitial cells that coexpress multiple markers previously thought to segregate Mø from DCs. Hence, many investigators, whether originating from Mø or DC disciplines, were unknowingly studying the same predominant rMoPh, while often neglecting knowledge from the other discipline. As a result, the use of markers as surrogates for Mø or DC functions within the renal mononuclear phagocytic system (Table 1) is increasingly questioned.22 This debate has also been heightened by lack of specificity of reagents commonly used to induce loss of function of DCs or Mø (Table 2).

Table 2.
Features and pitfalls of commonly used strategies to induce loss of function of rMoPh

This ambiguity resulting from conventional nomenclature, now recognized and intensely debated for the mononuclear phagocytic system in general,5 dictates that functional properties are required to properly characterize the renal mononuclear phagocytic system.1 Studies on whether the predominant interstitial rMoPh isolated from kidneys perform like splenic DCs by presenting antigen and activating naïve T lymphocytes or like peritoneal Mø by killing phagocytosed microbes showed the former function.15 This finding supports other reports suggesting migratory and phagocytic properties more typical of DCs.16,23 However, these early studies could not anticipate the multitude of additional Mø and DC functions now assigned to the renal mononuclear phagocytic system2430 or the fact that functional plasticity—rather than dichotomy—might exist depending on cues provided to rMoPh from the environment.22,29,30 Moreover, the renal mononuclear phagocytic system at steady state changes dramatically during inflammation, in which resident and recruited rMoPh exhibit great heterogeneity and dynamic phenotypes.3032 In light of these shifting paradigms, we reappraise here the current knowledge of the renal mononuclear phagocytic system. We focus on identifying gaps and inconsistencies in our understanding of the ontogeny and function of rMoPh in surveillance, tolerance, and tissue cytoprotection during steady state, as well as immunity, tissue injury, and repair associated with inflammation. The emerging role for plasticity within the renal mononuclear phagocytic system is also discussed. Notably, knowledge of these topics has come primarily by studying the mouse as a model organism, and translation to humans, which has been limited,20,21 remains an important goal.


During the past 10 years, studies of specific transgene reporter mice and multicolor flow cytometry of mouse kidney cell preparations reveal many characteristics of resident rMoPh during normal health. Transgene reporters of cx3cr1 (CX3CR1) and csf1r (CD115) fate map over 90% of rMoPh within the kidney at steady state.17,18,33 The large majority of CX3CR1+ cells is dendritiform rMoPh, which form a contiguous network throughout the entire renal interstitium of mice, lining the microvascular, peritubular, and periglomerular spaces.17,33,34 These predominant rMoPh are definable by a marker profile: CD11b+MHCII+CX3CR1+CD11c+/–F4/80+/–CD103 (Figure 1, CD11b+ rMoPh), which is similar to that of interstitial CD11b-like DC and tissue macrophages described in other nonlymphoid tissues.6,7,1618 Among this CD11b+ rMoPh subset, the reported frequency of expression of CD11c (either with or without F4/80 coexpression) has varied between 40% and 90%,1517,35 indicating that additional phenotypic characterization of these cells is yet required. In addition, F4/80 is reportedly expressed preferentially by medullary rMoPh at steady state.10,17

Figure 1.
Ontogeny of the renal mononuclear phagocytic system of the mouse at steady state and during inflammation. At steady state, bone marrow–resident MDPs give rise to common dendritic cell precursors (CDPs) and pre-DCs. Pre-DCs circulate to the healthy ...

The second definable rMoPh subset, representing ≤5% of steady-state interstitial rMoPh, exhibits the surface phenotype CD11bMHCII+CX3CR1CD11c+F4/80CD103+ (Figure 1, CD103+ rMoPh) and is, therefore, not visible in CX3CR1-GFP reporter mice.18 The function of this second subset in the kidney is unknown at present, but similar cells exist in skin, lung, and intestine where they perform specialized functions, including cross-presentation and induction of regulatory T cells.1,4,6,18,36 Plasmacytoid DCs, which differ ontogenically, functionally, and phenotypically from CD11b+ rMoPh and CD103+ rMoPh, are difficult to detect in normal mouse and human kidneys and may be absent.20,21 CD11b+ rMoPh within normal glomeruli are scarce, more globular-shaped, and seem to lack CD11c and F4/80.15,19,37 The rMoPh of normal human kidneys show generally similar anatomic distribution and population heterogeneity,20,21 but not all murine markers (F4/80 and CX3CR1) can be used to classify human rMoPh. To the extent that it has been characterized to date, the phenotype of the predominant human rMoPh displays the following marker profile: CD11b+CD68+BDCA-1+CD14+DC-SIGN+CD11c+MHC II+CD207.6,20,21

Studies of the ontogeny of resident rMoPh in mice show that both major subsets derive from a common hematopoietic monocyte/Mø/DC precursor (MDP), either through a common DC precursor, which gives rise only to pre-DCs and DCs, or through circulating monocytes (Figure 1).1,18,38 Two bone marrow–derived monocyte subsets, distinguished by high or low expression of the surface protein Ly6C in mouse and expression patterns of CD14 and CD16 in humans,1 may each contribute to the resident rMoPh pool at steady state (Figure 1).18,39 However, circulating monocytes play a larger precursor role for the additional rMoPh populations that arise during inflammatory infiltration of the kidney (discussed below).35,40 Whether all rMoPh represent the progeny of MDP remains unclear, and recent studies of mouse and human hematopoeisis raise the possibility that some rMoPh originate from lymphoid progenitors.41 The development of the renal mononuclear phagocytic system commences before nephrogenesis,42 but whether vestigial, intrarenal progenitor cell niches contribute to renewal of rMoPh populations in postnatal life is unknown.1,18

The renal-derived poietins and other renal-specific factors that induce MDP lineages to rMoPh are relatively unclear. With the exception of CD103+ rMoPh, activation of both the Fms-like tyrosine kinase 3 receptor (CD135) and CD115 are required for the development and maintenance of the vast majority of rMoPh (Figure 1).18,43 Colony-stimulating factor 1 (CSF-1), the ligand for CD115, is expressed by the renal parenchyma44 and when injected, expands circulating monocytes.45 Whether the density of rMoPh in normal kidneys also increases with CSF-1 injection is unclear, but in vivo blockade of CSF-1/CD115 interactions results in depletion of most resident rMoPh.43 Systemic administration of Flt3L, the ligand for CD135, increases the density of rMoPh,46,47 but whether Flt3L is expressed within the kidney is unknown. Nevertheless, isolated kidney stromal cells secrete other trophic factors for MDPs,48 exemplifying the probable role of the renal parenchyma to differentiate the renal mononuclear phagocytic system.49

Few studies have addressed cellular turnover within the renal mononuclear phagocytic system.50 Bromodeoxyuridine (BrdU) labeling and parabiosis experiments in mice show that 10% of the predominant CD11b+ rMoPh in recipient mice becomes BrdU-positive within 12 hours. However, it requires 30 days for rMoPh from parabiotic donors to completely disappear after mice are separated. Of interest, turnover rates for CD103+ rMoPh are approximately two times as fast.18 In contrast to these experimental approaches, bone marrow transplant studies in mice suggest that repopulation of rMoPh by MDP lineages requires at least 8 weeks and possibly several months—variability that may be caused by irradiation techniques and strain of mice.19,35,51,52 In any respect, these studies together suggest that complete turnover of the renal mononuclear phagocytic system is slow at steady state.


Surveillance, the anatomic and functional readiness to respond to environmental cues, is well described for the renal mononuclear phagocytic system, and rMoPh are often considered sentinels of the renal immune system, responding to diverse environmental cues that inform their subsequent functions. In the normal kidney, rMoPh are responsive to a range of stimuli associated with tissue perturbations such as pathogen-associated molecular patterns, damage-associated molecular patterns (DAMPs), other cell and matrix debris, immunoglobulin, complement components, oxygen tension, adenosine, cytokines, chemokines, and cell–cell contact.2429 Nonetheless, the specific protective roles of each surveillance mechanism and the possibilities that surveillance mechanisms differ by anatomic location or rMoPh subpopulation have not been extensively investigated to date. Additional studies are needed to increase understanding of how rMoPh respond to cues with varying characteristics and within different renal compartments.

Peripheral tolerance to self-antigens within the kidney that may escape central tolerance is also likely to be orchestrated by rMoPh. It is known that CD11c+ rMoPh at steady state sample self-antigens derived from tubular filtrate, renal cells, or renal matrix.16,53,54 These cells transport and present antigens to cognate T lymphocytes in renal lymph nodes, supplementing additional rMoPh-independent lymphatic transport and presentation of small filtered antigen, and promote tolerance to such antigens through mechanisms such as cross-tolerance.53,55 The intrarenal sampling, transport, and presentation of antigen occur through interstitial rMoPh, and no studies to date have shown the ability of intraglomerular rMoPh to educate T lymphocytes through antigen presentation, whether to tolerance or immunity. Interestingly, rMoPh isolated from normal kidneys on the basis of CD11c expression induce the expansion of regulatory T lymphocytes in allogeneic mixed leukocyte reactions,46 suggesting the possibility that rMoPh propagate regulatory T lymphocytes in the periphery at steady state in vivo. Aside from hypoxemia,5658 however, the cues within the kidney that may influence rMoPh to enhance or break peripheral tolerance are not well understood.54,55,59

In addition to maintaining tolerance to self-antigens, mounting evidence suggests that rMoPh at steady state also protect or lessen damage to the renal parenchyma after diverse insults through innate, anti-inflammatory responses.19,6062 This finding may reflect the innate phase response by tolerogenic rMoPh utilizing counter-regulators such as single Ig receptor-related protein,63 IFN regulatory factor 4,64 adenosine 2A receptor,65 hemeoxygenase-1,56,62 and Fc γ-receptor.66 Secretion of IL-10 by resident rMoPh is emerging as one of the key effectors of cytoprotection,61,66 raising the possibility of therapeutically augmenting this secretion by rMoPh to enhance cytoprotection.30,67 Additional research is needed to determine whether this function of the renal mononuclear phagocytic system represents an active response by rMoPh to silence insults that should not be perceived as injurious to the kidney, such as periods of brief ischemia or products from normal cellular turnover.68


Unlike rMoPh functioning at steady state, rMoPh during inflammation exhibit highly complex and dynamic responses that can determine renal outcomes after injury.3032 Studies of mouse models of acute kidney injury induced by endotoxemia, ischemia reperfusion, acute urinary obstruction, and pyelonephritis show that resident rMoPh in the interstitium increase in size, upregulate MHC and costimulatory proteins, and secrete inflammatory mediators within hours after initiating injury.15,16,69,70 In some studies, an unknown fraction of resident rMoPh vacate the interstitium within 24–48 hours coincident with the accumulation of rMoPh in draining renal lymph nodes.16,71 During the same interval, large numbers of Ly-6C+ (inflammatory) monocytes as well as some Ly6C monocytes infiltrate the kidney and along with remaining resident rMoPh, undergo activation and differentiation to progeny rMoPh with diverse functional phenotypes (Figure 1).35,40,69 Bone marrow release of Ly-6C+ monocytes and trafficking of these cells to the injured kidney is triggered by CCR2 ligation.40,72 In glomerular inflammation, a similar influx and expansion of rMoPh, functioning primarily as Mø, is well described.73,74 Whether intraglomerular rMoPh present at the initiation of injury also migrate to renal lymph nodes for antigen presentation is unknown, but glomerular infiltration by rMoPhs with the phenotype of conventional and plasmacytoid DCs has been described in human lupus nephritis.21,75 In any respect, the degree to which inflammatory monocyte-derived rMoPh perform the repertoire of Mø and DC functions (Figure 1 and Table 1) within glomerular or tubulointerstitial compartments is not fully understood. In the following sections, we summarize current knowledge of the role of the renal mononuclear phagocytic system in active renal immunity and inflammation and their resolution.


The renal mononuclear phagocytic system plays pivotal roles in proinflammatory innate and adaptive immune responses initiated within the kidney. rMoPh resident at steady state are induced to rapidly produce proinflammatory innate cytokines (TNF, IL-6, and IL-1) and chemokines (CCL2, CCL5, CXCL10, and CXCL2) depending on environmental cues.40,70,74,76 As a result, Ly6C+ monocytes and other leukocytes are recruited into the kidney, providing a secondary and major source of innate mediators.35,40,74 This innate phase, evident during either glomerular or tubulointerstitial inflammation, shapes subsequent adaptive immune responses by rMoPh, although this progression has been more clearly described for interstitial compared with glomerular rMoPh. For example, in models of GN, resident interstitial CD11c+ rMoPh suppress T helper type 1 (Th1) lymphocytes recruited early after injury.60 With prolonged innate inflammation, likely in concert with DAMPs,7779 these CD11c+ rMoPh mature and now stimulate Th1 effectors.80,81 Studies in models of ureteral obstruction suggest that this pattern may also influence intrarenal Th17 responses orchestrated by resident interstitial rMoPh.69 Additional research is clearly needed to define the full spectrum of immune stimulatory properties of the major rMoPh subpopulations as well as any role for intraglomerular rMoPh in adaptive immune responses.

In addition to orchestrating other leukocyte populations that may induce injury, rMoPh may also directly damage the renal parenchyma. As described above, resident rMoPh elaborate damaging innate cytokines.30,40,70 In addition, recruited inflammatory monocytes35,40 that differentiate into inflammatory rMoPh also produce oxygen radicals, hydrogen peroxide, nitric oxide, IL-1, TNF-α, and other effectors of tissue injury.8286 The vast majority of reports on this acute phase of injury, whether focused on glomerular or tubulointerstitial compartments, assign responsibility for tissue damage to resident or recruited rMoPh polarized to a classically activated (M1, proinflammatory) Mø phenotype.27,30 In contrast, later fibrotic phases of injury are orchestrated by resident or recruited rMoPh polarized to an alternatively activated (M2, anti-inflammatory and wound healing) Mø phenotype.29,30,87

In contrast to their role in tissue injury, rMoPh are also associated with repair of damaged renal parenchyma during resolution of renal inflammation. Seminal studies using clodronate-containing liposomes (Table 2) to ablate rMoPh show that recruited glomerular rMoPh are required for the spontaneous repair that occurs after glomerular injury in the Thy1.1 model of mesangioproliferative GN.88 Ablation and adoptive transfer studies conducted later similarly showed that recruited rMoPh actively promote repair of injured renal tubules.67,87,8991 These reparative rMoPh clear DAMPs and other cell and matrix debris, stimulate proliferation of surviving cells through elaboration of wnt ligands, and promote angiogenesis.92 This biphasic response by recruited rMoPh to first injure and then repair renal parenchyma may reflect a process of reprogramming. After injury, resident and recruited rMoPh subpopulations exhibit distinct expression of proinflammatory, anti-inflammatory, profibrotic, and reparative factors35,40 suggestive of the presence of heterogeneous populations of rMoPh fulfilling disparate functions. Although functional heterogeneity is undoubtedly present among rMoPh at any given time after an episode of renal injury, individual rMoPh can switch from inflammatory to reparative phenotypes within the renal interstitium,30,90 a process referred to as plasticity (discussed below). Regardless of their origin, additional studies are needed to determine whether reparative rMoPh are retained after kidneys heal to comprise a long-lasting component of the renal mononuclear phagocyte system at steady state.


As the recent study by Lee et al.90 illustrates, the ability of rMoPh to change functions over time may be an important general property of the renal mononuclear phagocytic system (Figure 2). Classic examples of rMoPh plasticity include the maturation of renal DCs to educate T lymphocytes and the polarization of renal Mø to M1 or M2 functional phenotypes in response to environmental cues.30,93 More recent studies show that bone marrow-derived Mø or rMoPh display biphasic expression of proinflammatory factors followed by anti-inflammatory and reparative factors in response to challenge with lipopolysaccharide or ischemic injury, respectively.62,92,94,95 Within the kidney, specific paracrine factors released from renal parenchymal cells, such as IL-10, DAMPs, or apoptotic bodies, initiate or augment this phenotypic reprogramming of rMoPh.90,96,97

Figure 2.
Proposed model for plasticity of rMoPh during inflammation and repair. During inflammation, rMoPh are derived from both resident and infiltrating cells. The release of DAMPs provides a proinflammatory stimulus and activates rMoPh to produce injurious ...

The plasticity of rMoPh may also represent inducible reactivation of developmental programs normally active in differentiating precursors. For example, pre-DCs are the immediate precursors for CD103+ rMoPh; however, pre-DCs can also be induced to repopulate CD11b+ rMoPh.18 The former progeny functions solely as DCs, although this finding has not been formally shown within the kidney, whereas the latter progeny clearly harbors subsets performing functions as Mø.18 The balance of poietins produced within the kidney for rMoPhs, particularly during inflammation or its resolution, may be a key driving force for this altered lineage commitment.44 Intriguingly, although no studies have been done on rMoPh per se, emerging evidence suggests that intrinsic molecular programs of plasticity governed by microRNA (miRNA)98 determine the commitment and transition of rMoPh to function as DCs or Mø. In addition, studies of bone marrow-derived Mø suggest that epigenetic chromatin modification by histone-modifying enzymes,99,100 and gene-silencing polycomb group proteins101 may be key regulators of Mø activation status. Future research on plasticity within the renal mononuclear phagocyte system may help to develop a unifying nomenclature that represents the function of rMoPh.


Significant progress in understanding the renal mononuclear phagocytic system has been achieved over the past three decades. Many typical DC and Mø-associated functions of the major rMoPh subsets have been described, especially in the last 5 years. As this brief review highlights, however, rMoPh may fulfill definitions and functions both of DCs and Mø, hampering definitive classification. Indeed, parallel streams of literature have been created that do not provide a fully integrated body of knowledge to this point. As a roadmap for future research, we highlight in Table 3 some of the specific areas of investigation that may yield valuable new insights. Engaging in this roadmap will require acknowledging that the complexity of the renal mononuclear phagocytic system, as with the mononuclear phagocytic system in general,5 does not fit well with simple, binary naming conventions. Specifically, historic divisions that have separated renal investigators into Mø and DC camps are falling, allowing for some key unifying conclusions to be made (Table 4) and paving the way for novel, joint approaches to better understand the role of the renal mononuclear phagocytic system in health and disease of the kidney.

Table 3.
Roadmap of key topics for future research on the renal mononuclear phagocytic system
Table 4.
Key conclusions




The authors acknowledge that many more excellent original research studies of relevance to the understanding of the renal mononuclear phagocytic system have been published than could be cited in this brief review article.

P.J.N. is supported by US National Institutes of Health (NIH) Grants DK83375, DK83375S1, and DK83912 and a Sponsored Research Agreement with Genzyme. A.J.R. is supported by the European Union (EU) FP7 Marie Curie Program MACRORIEN and TranSVIR, the EU FP7 Health Program INTRICATE, and the Austrian Vienna Science and Technology Fund. M.D.G. is supported by Science Foundation Ireland Grants SFI PI 06/IN.1/B652 and SFI SRC 09/SRC/B1794 and Health Research Board of Ireland Grant HRA HSR/2010/63. J.H. is supported by United Kingdom Medical Research Council Grants G0700330 and G0801235 and the Genzyme Renal Innovation Program. C.K. is supported by Deutsche Forschungsgemeinschaft Grants Ku1063/5, KFO228, and SFBTR57, the EU consortium INTRICATE, and the German National Academic Foundation. J.S.D. is supported by NIH Grants DK73299, DK84077, and DK8739, a Genzyme Research in Progress Award, the Nephcure Foundation, and a Sponsored Research Agreement with Regulus Therapeutics.


Published online ahead of print. Publication date available at www.jasn.org.


1. Geissmann F, Manz MG, Jung S, Sieweke MH, Merad M, Ley K.: Development of monocytes, macrophages, and dendritic cells. Science 327: 656–661, 2010. [PMC free article] [PubMed]
2. Gordon S.: The macrophage. Bioessays 17: 977–986, 1995. [PubMed]
3. Banchereau J, Steinman RM.: Dendritic cells and the control of immunity. Nature 392: 245–252, 1998. [PubMed]
4. Heath WR, Carbone FR.: Dendritic cell subsets in primary and secondary T cell responses at body surfaces. Nat Immunol 10: 1237–1244, 2009. [PubMed]
5. Geissmann F, Gordon S, Hume DA, Mowat AM, Randolph GJ.: Unravelling mononuclear phagocyte heterogeneity. Nat Rev Immunol 10: 453–460, 2010. [PMC free article] [PubMed]
6. Guilliams M, Henri S, Tamoutounour S, Ardouin L, Schwartz-Cornil I, Dalod M, Malissen B.: From skin dendritic cells to a simplified classification of human and mouse dendritic cell subsets. Eur J Immunol 40: 2089–2094, 2010. [PubMed]
7. Hume DA.: Macrophages as APC and the dendritic cell myth. J Immunol 181: 5829–5835, 2008. [PubMed]
8. Hart DN, Fabre JW.: Major histocompatibility complex antigens in rat kidney, ureter, and bladder. Localization with monoclonal antibodies and demonstration of Ia-positive dendritic cells. Transplantation 31: 318–325, 1981. [PubMed]
9. Hart DN, Fuggle SV, Williams KA, Fabre JW, Ting A, Morris PJ.: Localization of HLA-ABC and DR antigens in human kidney. Transplantation 31: 428–433, 1981. [PubMed]
10. Hume DA, Gordon S.: Mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80. Identification of resident macrophages in renal medullary and cortical interstitium and the juxtaglomerular complex. J Exp Med 157: 1704–1709, 1983. [PMC free article] [PubMed]
11. Schreiner GF, Kiely JM, Cotran RS, Unanue ER.: Characterization of resident glomerular cells in the rat expressing Ia determinants and manifesting genetically restricted interactions with lymphocytes. J Clin Invest 68: 920–931, 1981. [PMC free article] [PubMed]
12. Schreiner GF, Cotran RS.: Localization of an Ia-bearing glomerular cell in the mesangium. J Cell Biol 94: 483–488, 1982. [PMC free article] [PubMed]
13. Kaissling B, Le Hir M.: Characterization and distribution of interstitial cell types in the renal cortex of rats. Kidney Int 45: 709–720, 1994. [PubMed]
14. Kaissling B, Hegyi I, Loffing J, Le Hir M.: Morphology of interstitial cells in the healthy kidney. Anat Embryol (Berl) 193: 303–318, 1996. [PubMed]
15. Krüger T, Benke D, Eitner F, Lang A, Wirtz M, Hamilton-Williams EE, Engel D, Giese B, Müller-Newen G, Floege J, Kurts C.: Identification and functional characterization of dendritic cells in the healthy murine kidney and in experimental glomerulonephritis. J Am Soc Nephrol 15: 613–621, 2004. [PubMed]
16. Dong X, Swaminathan S, Bachman LA, Croatt AJ, Nath KA, Griffin MD.: Antigen presentation by dendritic cells in renal lymph nodes is linked to systemic and local injury to the kidney. Kidney Int 68: 1096–1108, 2005. [PubMed]
17. Soos TJ, Sims TN, Barisoni L, Lin K, Littman DR, Dustin ML, Nelson PJ.: CX3CR1+ interstitial dendritic cells form a contiguous network throughout the entire kidney. Kidney Int 70: 591–596, 2006. [PubMed]
18. Ginhoux F, Liu K, Helft J, Bogunovic M, Greter M, Hashimoto D, Price J, Yin N, Bromberg J, Lira SA, Stanley ER, Nussenzweig M, Merad M.: The origin and development of nonlymphoid tissue CD103+ DCs. J Exp Med 206: 3115–3130, 2009. [PMC free article] [PubMed]
19. Tadagavadi RK, Reeves WB.: Renal dendritic cells ameliorate nephrotoxic acute kidney injury. J Am Soc Nephrol 21: 53–63, 2010. [PMC free article] [PubMed]
20. Woltman AM, de Fijter JW, Zuidwijk K, Vlug AG, Bajema IM, van der Kooij SW, van Ham V, van Kooten C.: Quantification of dendritic cell subsets in human renal tissue under normal and pathological conditions. Kidney Int 71: 1001–1008, 2007. [PubMed]
21. Segerer S, Heller F, Lindenmeyer MT, Schmid H, Cohen CD, Draganovici D, Mandelbaum J, Nelson PJ, Gröne HJ, Gröne EF, Figel AM, Nössner E, Schlöndorff D.: Compartment specific expression of dendritic cell markers in human glomerulonephritis. Kidney Int 74: 37–46, 2008. [PubMed]
22. Ferenbach D, Hughes J.: Macrophages and dendritic cells: what is the difference? Kidney Int 74: 5–7, 2008. [PubMed]
23. Austyn JM, Hankins DF, Larsen CP, Morris PJ, Rao AS, Roake JA.: Isolation and characterization of dendritic cells from mouse heart and kidney. J Immunol 152: 2401–2410, 1994. [PubMed]
24. Teteris SA, Engel DR, Kurts C.: Homeostatic and pathogenic role of renal dendritic cells. Kidney Int 80: 139–145, 2011. [PubMed]
25. Panzer U, Kurts C.: T cell cross-talk with kidney dendritic cells in glomerulonephritis. J Mol Med (Berl) 88: 19–26, 2010. [PubMed]
26. John R, Nelson PJ.: Dendritic cells in the kidney. J Am Soc Nephrol 18: 2628–2635, 2007. [PubMed]
27. Duffield JS.: Macrophages and immunologic inflammation of the kidney. Semin Nephrol 30: 234–254, 2010. [PMC free article] [PubMed]
28. Rees AJ.: Monocyte and macrophage biology: an overview. Semin Nephrol 30: 216–233, 2010. [PubMed]
29. Vernon MA, Mylonas KJ, Hughes J.: Macrophages and renal fibrosis. Semin Nephrol 30: 302–317, 2010. [PubMed]
30. Wang Y, Harris DCH.: Macrophages in renal disease. J Am Soc Nephrol 22: 21–27, 2011. [PubMed]
31. Rodríguez-Iturbe B, Pons H, Herrera-Acosta J, Johnson RJ.: Role of immunocompetent cells in nonimmune renal diseases. Kidney Int 59: 1626–1640, 2001. [PubMed]
32. Swaminathan S, Griffin MD.: First responders: understanding monocyte-lineage traffic in the acutely injured kidney. Kidney Int 74: 1509–1511, 2008. [PubMed]
33. Sasmono RT, Oceandy D, Pollard JW, Tong W, Pavli P, Wainwright BJ, Ostrowski MC, Himes SR, Hume DA.: A macrophage colony-stimulating factor receptor-green fluorescent protein transgene is expressed throughout the mononuclear phagocyte system of the mouse. Blood 101: 1155–1163, 2003. [PubMed]
34. Kaissling B, Le Hir M.: The renal cortical interstitium: morphological and functional aspects. Histochem Cell Biol 130: 247–262, 2008. [PMC free article] [PubMed]
35. Lin SL, Castaño AP, Nowlin BT, Lupher ML, Jr, Duffield JS.: Bone marrow Ly6Chigh monocytes are selectively recruited to injured kidney and differentiate into functionally distinct populations. J Immunol 183: 6733–6743, 2009. [PubMed]
36. Bedoui S, Whitney PG, Waithman J, Eidsmo L, Wakim L, Caminschi I, Allan RS, Wojtasiak M, Shortman K, Carbone FR, Brooks AG, Heath WR.: Cross-presentation of viral and self antigens by skin-derived CD103+ dendritic cells. Nat Immunol 10: 488–495, 2009. [PubMed]
37. Tesch GH, Maifert S, Schwarting A, Rollins BJ, Kelley VR.: Monocyte chemoattractant protein 1-dependent leukocytic infiltrates are responsible for autoimmune disease in MRL-Fas(lpr) mice. J Exp Med 190: 1813–1824, 1999. [PMC free article] [PubMed]
38. Fogg DK, Sibon C, Miled C, Jung S, Aucouturier P, Littman DR, Cumano A, Geissmann F.: A clonogenic bone marrow progenitor specific for macrophages and dendritic cells. Science 311: 83–87, 2006. [PubMed]
39. Geissmann F, Jung S, Littman DR.: Blood monocytes consist of two principal subsets with distinct migratory properties. Immunity 19: 71–82, 2003. [PubMed]
40. Li L, Huang L, Sung SS, Vergis AL, Rosin DL, Rose CE, Jr, Lobo PI, Okusa MD.: The chemokine receptors CCR2 and CX3CR1 mediate monocyte/macrophage trafficking in kidney ischemia-reperfusion injury. Kidney Int 74: 1526–1537, 2008. [PMC free article] [PubMed]
41. Dorshkind K.: Not a split decision for human hematopoiesis. Nat Immunol 11: 569–570, 2010. [PubMed]
42. Rae F, Woods K, Sasmono T, Campanale N, Taylor D, Ovchinnikov DA, Grimmond SM, Hume DA, Ricardo SD, Little MH.: Characterisation and trophic functions of murine embryonic macrophages based upon the use of a Csf1r-EGFP transgene reporter. Dev Biol 308: 232–246, 2007. [PubMed]
43. MacDonald KPA, Palmer JS, Cronau S, Seppanen E, Olver S, Raffelt NC, Kuns R, Pettit AR, Clouston A, Wainwright B, Branstetter D, Smith J, Paxton RJ, Cerretti DP, Bonham L, Hill GR, Hume DA.: An antibody against the colony-stimulating factor 1 receptor depletes the resident subset of monocytes and tissue- and tumor-associated macrophages but does not inhibit inflammation. Blood 116: 3955–3963, 2010. [PubMed]
44. Jang MH, Herber DM, Jiang X, Nandi S, Dai XM, Zeller G, Stanley ER, Kelley VR.: Distinct in vivo roles of colony-stimulating factor-1 isoforms in renal inflammation. J Immunol 177: 4055–4063, 2006. [PubMed]
45. Misawa E, Sakurai T, Yamada M, Tamura Y, Motoyoshi K.: Administration of macrophage colony-stimulating factor mobilized both CD11b+CD11c+ cells and NK1.1+ cells into peripheral blood. Int Immunopharmacol 4: 791–803, 2004. [PubMed]
46. Coates PT, Duncan FJ, Colvin BL, Wang Z, Zahorchak AF, Shufesky WJ, Morelli AE, Thomson AW.: In vivo-mobilized kidney dendritic cells are functionally immature, subvert alloreactive T-cell responses, and prolong organ allograft survival. Transplantation 77: 1080–1089, 2004. [PubMed]
47. Morelli AE, Coates PT, Shufesky WJ, Barratt-Boyes SM, Fung JJ, Demetris AJ, Thomson AW.: Growth factor-induced mobilization of dendritic cells in kidney and liver of rhesus macaques: implications for transplantation. Transplantation 83: 656–662, 2007. [PubMed]
48. Huang Y, Johnston P, Zhang B, Zakari A, Chowdhry T, Smith RR, Marbán E, Rabb H, Womer KL.: Kidney-derived stromal cells modulate dendritic and T cell responses. J Am Soc Nephrol 20: 831–841, 2009. [PMC free article] [PubMed]
49. Svensson M, Kaye PM.: Stromal-cell regulation of dendritic-cell differentiation and function. Trends Immunol 27: 580–587, 2006. [PubMed]
50. Helft J, Ginhoux F, Bogunovic M, Merad M.: Origin and functional heterogeneity of non-lymphoid tissue dendritic cells in mice. Immunol Rev 234: 55–75, 2010. [PubMed]
51. McKenzie JL, Beard ME, Hart DN.: Depletion of donor kidney dendritic cells prolongs graft survival. Transplant Proc 16: 948–951, 1984. [PubMed]
52. Stein-Oakley AN, Jablonski P, Kraft N, Biguzas M, Howard BO, Marshall VC, Thomson NM.: Differential irradiation effects on rat interstitial dendritic cells. Transplant Proc 23: 632–634, 1991. [PubMed]
53. Lukacs-Kornek V, Burgdorf S, Diehl L, Specht S, Kornek M, Kurts C.: The kidney-renal lymph node-system contributes to cross-tolerance against innocuous circulating antigen. J Immunol 180: 706–715, 2008. [PubMed]
54. Macconi D, Chiabrando C, Schiarea S, Aiello S, Cassis L, Gagliardini E, Noris M, Buelli S, Zoja C, Corna D, Mele C, Fanelli R, Remuzzi G, Benigni A.: Proteasomal processing of albumin by renal dendritic cells generates antigenic peptides. J Am Soc Nephrol 20: 123–130, 2009. [PMC free article] [PubMed]
55. Edgtton KL, Kausman JY, Li M, O’Sullivan K, Lo C, Hutchinson P, Yagita H, Holdsworth SR, Kitching AR.: Intrarenal antigens activate CD4+ cells via co-stimulatory signals from dendritic cells. J Am Soc Nephrol 19: 515–526, 2008. [PMC free article] [PubMed]
56. Kotsch K, Martins PN, Klemz R, Janssen U, Gerstmayer B, Dernier A, Reutzel-Selke A, Kuckelkorn U, Tullius SG, Volk HD.: Heme oxygenase-1 ameliorates ischemia/reperfusion injury by targeting dendritic cell maturation and migration. Antioxid Redox Signal 9: 2049–2063, 2007. [PubMed]
57. Cho WY, Choi HM, Lee SY, Kim MG, Kim HK, Jo SK.: The role of Tregs and CD11c(+) macrophages/dendritic cells in ischemic preconditioning of the kidney. Kidney Int 78: 981–992, 2010. [PubMed]
58. George JF, Braun A, Brusko TM, Joseph R, Bolisetty S, Wasserfall CH, Atkinson MA, Agarwal A, Kapturczak MH.: Suppression by CD4+CD25+ regulatory T cells is dependent on expression of heme oxygenase-1 in antigen-presenting cells. Am J Pathol 173: 154–160, 2008. [PMC free article] [PubMed]
59. Rees A.: Cross dendritic cells anger T cells after kidney injury. J Am Soc Nephrol 20: 3–5, 2009. [PubMed]
60. Scholz J, Lukacs-Kornek V, Engel DR, Specht S, Kiss E, Eitner F, Floege J, Groene HJ, Kurts C.: Renal dendritic cells stimulate IL-10 production and attenuate nephrotoxic nephritis. J Am Soc Nephrol 19: 527–537, 2008. [PMC free article] [PubMed]
61. Tadagavadi RK, Reeves WB.: Endogenous IL-10 attenuates cisplatin nephrotoxicity: role of dendritic cells. J Immunol 185: 4904–4911, 2010. [PMC free article] [PubMed]
62. Ferenbach DA, Nkejabega NC, McKay J, Choudhary AK, Vernon MA, Beesley MF, Clay S, Conway BC, Marson LP, Kluth DC, Hughes J.: The induction of macrophage hemeoxygenase-1 is protective during acute kidney injury in aging mice. Kidney Int 79: 966–976, 2011. [PubMed]
63. Lech M, Avila-Ferrufino A, Allam R, Segerer S, Khandoga A, Krombach F, Garlanda C, Mantovani A, Anders HJ.: Resident dendritic cells prevent postischemic acute renal failure by help of single Ig IL-1 receptor-related protein. J Immunol 183: 4109–4118, 2009. [PubMed]
64. Lassen S, Lech M, Römmele C, Mittruecker HW, Mak TW, Anders HJ.: Ischemia reperfusion induces IFN regulatory factor 4 in renal dendritic cells, which suppresses postischemic inflammation and prevents acute renal failure. J Immunol 185: 1976–1983, 2010. [PubMed]
65. Day YJ, Huang L, Ye H, Linden J, Okusa MD.: Renal ischemia-reperfusion injury and adenosine 2A receptor-mediated tissue protection: role of macrophages. Am J Physiol Renal Physiol 288: F722–F731, 2005. [PubMed]
66. Castano AP, Lin SL, Surowy T, Nowlin BT, Turlapati SA, Patel T, Singh A, Li S, Lupher ML, Jr, Duffield JS.: Serum amyloid P inhibits fibrosis through Fc gamma R-dependent monocyte-macrophage regulation in vivo. Sci Transl Med 1: 5ra13, 2009 [PMC free article] [PubMed]
67. Cao Q, Wang Y, Zheng D, Sun Y, Wang Y, Lee VWS, Zheng G, Tan TK, Ince J, Alexander SI, Harris DCH.: IL-10/TGF-beta-modified macrophages induce regulatory T cells and protect against adriamycin nephrosis. J Am Soc Nephrol 21: 933–942, 2010. [PMC free article] [PubMed]
68. Manicassamy S, Pulendran B.: Dendritic cell control of tolerogenic responses. Immunol Rev 241: 206–227, 2011. [PMC free article] [PubMed]
69. Dong X, Bachman LA, Miller MN, Nath KA, Griffin MD.: Dendritic cells facilitate accumulation of IL-17 T cells in the kidney following acute renal obstruction. Kidney Int 74: 1294–1309, 2008. [PMC free article] [PubMed]
70. Dong X, Swaminathan S, Bachman LA, Croatt AJ, Nath KA, Griffin MD.: Resident dendritic cells are the predominant TNF-secreting cell in early renal ischemia-reperfusion injury. Kidney Int 71: 619–628, 2007. [PubMed]
71. Roake JA, Rao AS, Morris PJ, Larsen CP, Hankins DF, Austyn JM.: Dendritic cell loss from nonlymphoid tissues after systemic administration of lipopolysaccharide, tumor necrosis factor, and interleukin 1. J Exp Med 181: 2237–2247, 1995. [PMC free article] [PubMed]
72. Serbina NV, Pamer EG.: Monocyte emigration from bone marrow during bacterial infection requires signals mediated by chemokine receptor CCR2. Nat Immunol 7: 311–317, 2006. [PubMed]
73. Erwig LP, Rees AJ.: Macrophage activation and programming and its role for macrophage function in glomerular inflammation. Kidney Blood Press Res 22: 21–25, 1999. [PubMed]
74. Holdsworth SR, Tipping PG.: Leukocytes in glomerular injury. Semin Immunopathol 29: 355–374, 2007. [PubMed]
75. Bagavant H, Deshmukh US, Wang H, Ly T, Fu SM.: Role for nephritogenic T cells in lupus glomerulonephritis: progression to renal failure is accompanied by T cell activation and expansion in regional lymph nodes. J Immunol 177: 8258–8265, 2006. [PubMed]
76. Tittel AP, Heuser C, Ohliger C, Knolle PA, Engel DR, Kurts C.: Kidney dendritic cells induce innate immunity against bacterial pyelonephritis. J Am Soc Nephrol 22: 1435–1441, 2011. [PMC free article] [PubMed]
77. Schaefer L, Babelova A, Kiss E, Hausser HJ, Baliova M, Krzyzankova M, Marsche G, Young MF, Mihalik D, Götte M, Malle E, Schaefer RM, Gröne HJ.: The matrix component biglycan is proinflammatory and signals through Toll-like receptors 4 and 2 in macrophages. J Clin Invest 115: 2223–2233, 2005. [PMC free article] [PubMed]
78. Lang A, Benke D, Eitner F, Engel D, Ehrlich S, Breloer M, Hamilton-Williams E, Specht S, Hoerauf A, Floege J, von Bonin A, Kurts C.: Heat shock protein 60 is released in immune-mediated glomerulonephritis and aggravates disease: in vivo evidence for an immunologic danger signal. J Am Soc Nephrol 16: 383–391, 2005. [PubMed]
79. Wu H, Ma J, Wang P, Corpuz TM, Panchapakesan U, Wyburn KR, Chadban SJ.: HMGB1 contributes to kidney ischemia reperfusion injury. J Am Soc Nephrol 21: 1878–1890, 2010. [PMC free article] [PubMed]
80. Heymann F, Meyer-Schwesinger C, Hamilton-Williams EE, Hammerich L, Panzer U, Kaden S, Quaggin SE, Floege J, Gröne HJ, Kurts C.: Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury. J Clin Invest 119: 1286–1297, 2009. [PMC free article] [PubMed]
81. Hochheiser K, Engel DR, Hammerich L, Heymann F, Knolle PA, Panzer U, Kurts C.: Kidney dendritic cells become pathogenic during crescentic glomerulonephritis with proteinuria. J Am Soc Nephrol 22: 306–316, 2011. [PMC free article] [PubMed]
82. Chavele KM, Martinez-Pomares L, Domin J, Pemberton S, Haslam SM, Dell A, Cook HT, Pusey CD, Gordon S, Salama AD.: Mannose receptor interacts with Fc receptors and is critical for the development of crescentic glomerulonephritis in mice. J Clin Invest 120: 1469–1478, 2010. [PMC free article] [PubMed]
83. Wang Y, Wang Y, Cao Q, Zheng G, Lee VW, Zheng D, Li X, Tan TK, Harris DC.: By homing to the kidney, activated macrophages potently exacerbate renal injury. Am J Pathol 172: 1491–1499, 2008. [PMC free article] [PubMed]
84. Duffield JS, Erwig LP, Wei X, Liew FY, Rees AJ, Savill JS.: Activated macrophages direct apoptosis and suppress mitosis of mesangial cells. J Immunol 164: 2110–2119, 2000. [PubMed]
85. Jansen A, Cook T, Taylor GM, Largen P, Riveros-Moreno V, Moncada S, Cattell V.: Induction of nitric oxide synthase in rat immune complex glomerulonephritis. Kidney Int 45: 1215–1219, 1994. [PubMed]
86. Tipping PG, Leong TW, Holdsworth SR.: Tumor necrosis factor production by glomerular macrophages in anti-glomerular basement membrane glomerulonephritis in rabbits. Lab Invest 65: 272–279, 1991. [PubMed]
87. Cao Q, Wang C, Zheng D, Wang Y, Lee VWS, Wang YM, Zheng G, Tan TK, Yu D, Alexander SI, Harris DCH, Wang Y.: IL-25 induces M2 macrophages and reduces renal injury in proteinuric kidney disease. J Am Soc Nephrol 22: 1229–1239, 2011. [PMC free article] [PubMed]
88. Westerhuis R, van Straaten SC, van Dixhoorn MG, van Rooijen N, Verhagen NA, Dijkstra CD, de Heer E, Daha MR.: Distinctive roles of neutrophils and monocytes in anti-thy-1 nephritis. Am J Pathol 156: 303–310, 2000. [PMC free article] [PubMed]
89. Vinuesa E, Hotter G, Jung M, Herrero-Fresneda I, Torras J, Sola A.: Macrophage involvement in the kidney repair phase after ischaemia/reperfusion injury. J Pathol 214: 104–113, 2008. [PubMed]
90. Lee S, Huen S, Nishio H, Nishio S, Lee HK, Choi BS, Ruhrberg C, Cantley LG.: Distinct macrophage phenotypes contribute to kidney injury and repair. J Am Soc Nephrol 22: 317–326, 2011. [PMC free article] [PubMed]
91. Menke J, Iwata Y, Rabacal WA, Basu R, Yeung YG, Humphreys BD, Wada T, Schwarting A, Stanley ER, Kelley VR.: CSF-1 signals directly to renal tubular epithelial cells to mediate repair in mice. J Clin Invest 119: 2330–2342, 2009. [PMC free article] [PubMed]
92. Lin SL, Li B, Rao S, Yeo EJ, Hudson TE, Nowlin BT, Pei H, Chen L, Zheng JJ, Carroll TJ, Pollard JW, McMahon AP, Lang RA, Duffield JS.: Macrophage Wnt7b is critical for kidney repair and regeneration. Proc Natl Acad Sci USA 107: 4194–4199, 2010. [PMC free article] [PubMed]
93. Williams TM, Little MH, Ricardo SD.: Macrophages in renal development, injury, and repair. Semin Nephrol 30: 255–267, 2010. [PubMed]
94. Lucas M, Stuart LM, Savill J, Lacy-Hulbert A.: Apoptotic cells and innate immune stimuli combine to regulate macrophage cytokine secretion. J Immunol 171: 2610–2615, 2003. [PubMed]
95. Vijayan V, Baumgart-Vogt E, Naidu S, Qian G, Immenschuh S.: Bruton’s tyrosine kinase is required for TLR-dependent heme oxygenase-1 gene activation via Nrf2 in macrophages. J Immunol 187: 817–827, 2011. [PubMed]
96. Wang Y, Tay YC, Harris DC.: Proximal tubule cells stimulated by lipopolysaccharide inhibit macrophage activation. Kidney Int 66: 655–662, 2004. [PubMed]
97. Savill J, Dransfield I, Gregory C, Haslett C.: A blast from the past: clearance of apoptotic cells regulates immune responses. Nat Rev Immunol 2: 965–975, 2002. [PubMed]
98. Bi Y, Liu G, Yang R.: MicroRNAs: novel regulators during the immune response. J Cell Physiol 218: 467–472, 2009. [PubMed]
99. De Santa F, Totaro MG, Prosperini E, Notarbartolo S, Testa G, Natoli G.: The histone H3 lysine-27 demethylase Jmjd3 links inflammation to inhibition of polycomb-mediated gene silencing. Cell 130: 1083–1094, 2007. [PubMed]
100. Satoh T, Takeuchi O, Vandenbon A, Yasuda K, Tanaka Y, Kumagai Y, Miyake T, Matsushita K, Okazaki T, Saitoh T, Honma K, Matsuyama T, Yui K, Tsujimura T, Standley DM, Nakanishi K, Nakai K, Akira S.: The Jmjd3-Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection. Nat Immunol 11: 936–944, 2010. [PubMed]
101. Sienerth AR, Scheuermann C, Galmiche A, Rapp UR, Becker M.: Polycomb group protein Bmi1 negatively regulates IL-10 expression in activated macrophages. Immunol Cell Biol 89: 812–816, 2011. [PubMed]
102. Jung Unutmaz S, Wong D, Sano P, De los Santos G, Sparwasser K, Wu T, Vuthoori S, Ko S, Zavala K, Pamer F, Littman EG. DR, Lang RA: In vivo depletion of CD11c+ dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens. Immunity 17: 211–220, 2002. [PMC free article] [PubMed]
103. Duffield JS, Forbes SJ, Constandinou CM, Clay S, Partolina M, Vuthoori S, Wu S, Lang R, Iredale JP.: Selective depletion of macrophages reveals distinct, opposing roles during liver injury and repair. J Clin Invest 115: 56–65, 2005. [PMC free article] [PubMed]
104. van Rooijen N, van Nieuwmegen R.: Elimination of phagocytic cells in the spleen after intravenous injection of liposome-encapsulated dichloromethylene diphosphonate. An enzyme-histochemical study. Cell Tissue Res 238: 355–358, 1984. [PubMed]

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