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1.
Figure 3

Figure 3. From: Dendritic cells and regulation of graft-versus-host disease and graft-versus-leukemia activity.

Potential DC-based therapies for GVHD. TolDCs can be used as a negative cellular vaccine after in vitro generation via their pharmacologic manipulation, cell sorting (subsets), or expansion after interaction with other immune regulatory cell populations. In vivo, DCs can be targeted by the inhibition of molecular pathways (HDAC; NF-κB) or the expression of maturation markers or costimulatory molecules (eg, CD80/CD86; CD83). Other cellular therapies, such as MSCs, MDSCs, and Treg, mediate immunosuppressive effects through DCs. VIP indicates vasoactive intestinal peptide. Professional illustration by Alice Y. Chen.

Elizabeth O. Stenger, et al. Blood. 2012 May 31;119(22):5088-5103.
2.
Figure 1

Figure 1. From: Dendritic cells and regulation of graft-versus-host disease and graft-versus-leukemia activity.

DC hematopoiesis and subsets. (A) All identified DC subsets can be generated from either a common myeloid progenitor (CMP) or common lymphoid progenitor (CLP) depending on the cytokines and growth factors present. DCs can be broadly categorized as cDCs or precursor DCs. pDCs are understood to be a subset of precursor DCs that have plasma cell morphology, an immature phenotype, and secrete type I IFN after activation. Monocyte-derived DCs or “inflammatory DCs” are similar to cDCs in form and function and correlate with in vitro GM-CSF-generated DCs. cDCs can be categorized as lymphoid tissue resident and migratory DCs. DCs were categorized previously as lymphoid or myeloid (mDCs) based on the hypothesis that each had separate progenitors, a convention that has persisted in the experimental and clinical evaluation of DC subsets. Professional illustration by Alice Y. Chen. (B) In mice, pDCs are identified as CD11cloCD11b Siglec-H+PDCA-1+, whereas in humans, they are linMHC II+CD11cCD123(IL-3Rα)+BDCA2(CD303)+. Mouse mDCs are identified as CD11c+CD11b+B220 (CD45R) NK1.1, whereas human mDCs are lin MHCII+CD11c+CD123BDCA1(CD1b/c)+. Other phenotypic differences between mouse and human DC precursors are also listed in the table. HSC indicates hematopoietic stem cells; MPP, multipotent progenitor; CMP, common myeloid progenitor; CLP, common lymphoid progenitor; pDC, plasmacytoid DC; mDC, myeloid DC; LN, lymph node; and LP, lamina propria.

Elizabeth O. Stenger, et al. Blood. 2012 May 31;119(22):5088-5103.
3.
Figure 2

Figure 2. From: Dendritic cells and regulation of graft-versus-host disease and graft-versus-leukemia activity.

Role of DCs in the pathogenesis of GVHD. (A) Recipient pretransplant conditioning results in target organ tissue damage, leading to the so-called “cytokine storm,” a progressive amplification of proinflammatory cytokine production and immune activation as inflammatory cytokines feed forward unabated. IL-1β, IL-6, and TNF-α are particularly implicated in this process. In addition to proinflammatory cytokines, conditioning-released damage-associated molecular patterns (DAMPS) and translocation of lipopolysaccharide in the intestine also lead to the activation of host and subsequently donor DCs, including epidermal LCs and dermal DCs in the skin. Mature DCs up-regulate MHC, costimulatory, and intercellular adhesion molecule expression. (B) DCs present host allo-Ag to donor T cells. Host DCs resistant to conditioning present alloAg via the direct pathway, whereas transplanted donor DCs present processed alloAg peptides on MHC syngeneic with donor T cells via the indirect pathway. Donor T-cell activation requires Ag presentation via MHC molecules to the T-cell Ag receptor (TCR), as well as stimulation via various costimulatory molecules. This interaction results in T-cell activation, proliferation, differentiation (Th1, Th2), migration to GVHD target organs, and secretion of various chemokines and cytokines, importantly IFN-γ and IL-2. (C) Cellular and inflammatory effectors lead to target organ tissue damage. CTLs mediate target cell apoptosis via interactions between TNF and TNF receptors, TRAIL (TNF-related apoptosis-inducing ligand)/TRAIL-R and Fas (CD95)/FasL interactions and release of cytotoxic mediators (perforin and granzyme). Recruited macrophages release TNF-α, IL-1, and NO, which also damage target cells. RT indicates radiation therapy; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1; ICOS, inducible costimulator; and NO, nitric oxide. (A-C) Professional illustrations by Alice Y. Chen.

Elizabeth O. Stenger, et al. Blood. 2012 May 31;119(22):5088-5103.

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