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Items: 1 to 20 of 238

1.

Secreted aspartic protease 2 of Candida albicans inactivates factor H and the macrophage factor H-receptors CR3 (CD11b/CD18) and CR4 (CD11c/CD18).

Svoboda E, Schneider AE, Sándor N, Lermann U, Staib P, Kremlitzka M, Bajtay Z, Barz D, Erdei A, Józsi M.

Immunol Lett. 2015 Nov;168(1):13-21. doi: 10.1016/j.imlet.2015.08.009. Epub 2015 Aug 22.

PMID:
26306739
2.

The role of CR3 (CD11b/CD18) and CR4 (CD11c/CD18) in complement-mediated phagocytosis and podosome formation by human phagocytes.

Lukácsi S, Nagy-Baló Z, Erdei A, Sándor N, Bajtay Z.

Immunol Lett. 2017 Sep;189:64-72. doi: 10.1016/j.imlet.2017.05.014. Epub 2017 May 26.

PMID:
28554712
4.

The yeast Candida albicans evades human complement attack by secretion of aspartic proteases.

Gropp K, Schild L, Schindler S, Hube B, Zipfel PF, Skerka C.

Mol Immunol. 2009 Dec;47(2-3):465-75. doi: 10.1016/j.molimm.2009.08.019. Epub 2009 Oct 31.

PMID:
19880183
5.

Human cytomegalovirus downregulates complement receptors (CR3, CR4) and decreases phagocytosis by macrophages.

Gafa V, Manches O, Pastor A, Drouet E, Ambroise-Thomas P, Grillot R, Aldebert D.

J Med Virol. 2005 Jul;76(3):361-6.

PMID:
15902695
6.

Candida albicans Hgt1p, a multifunctional evasion molecule: complement inhibitor, CR3 analogue, and human immunodeficiency virus-binding molecule.

Lesiak-Markowicz I, Vogl G, Schwarzmüller T, Speth C, Lass-Flörl C, Dierich MP, Kuchler K, Würzner R.

J Infect Dis. 2011 Sep 1;204(5):802-9. doi: 10.1093/infdis/jir455.

7.

CR3 is the dominant phagocytotic complement receptor on human dendritic cells.

Sándor N, Kristóf K, Paréj K, Pap D, Erdei A, Bajtay Z.

Immunobiology. 2013 Apr;218(4):652-63. doi: 10.1016/j.imbio.2012.07.031. Epub 2012 Aug 4.

PMID:
22906751
9.
10.

Participation of CR1 (CD35), CR3 (CD11b/CD18) and CR4 (CD11c/CD18) in membranoproliferative glomerulonephritis type I.

Soma J, Saito T, Seino J, Sato H, Ootaka T, Yusa A, Abe K.

Clin Exp Immunol. 1995 May;100(2):269-76.

12.

An anti-inflammatory property of Candida albicans β-glucan: Induction of high levels of interleukin-1 receptor antagonist via a Dectin-1/CR3 independent mechanism.

Smeekens SP, Gresnigt MS, Becker KL, Cheng SC, Netea SA, Jacobs L, Jansen T, van de Veerdonk FL, Williams DL, Joosten LA, Dinarello CA, Netea MG.

Cytokine. 2015 Feb;71(2):215-22. doi: 10.1016/j.cyto.2014.10.013. Epub 2014 Nov 20.

13.

Extracellular aspartic protease SAP2 of Candida albicans yeast cleaves human kininogens and releases proinflammatory peptides, Met-Lys-bradykinin and des-Arg(9)-Met-Lys-bradykinin.

Bras G, Bochenska O, Rapala-Kozik M, Guevara-Lora I, Faussner A, Kozik A.

Biol Chem. 2012 Aug;393(8):829-39. doi: 10.1515/hsz-2012-0157.

PMID:
22944684
15.

Functional studies of chronic lymphocytic leukemia B cells expressing β2-integrin type complement receptors CR3 and CR4.

Uzonyi B, Mácsik-Valent B, Lukácsi S, Kiss R, Török K, Kremlitzka M, Bajtay Z, Demeter J, Bödör C, Erdei A.

Immunol Lett. 2017 Sep;189:73-81. doi: 10.1016/j.imlet.2017.05.016. Epub 2017 May 31.

PMID:
28577901
16.

The role of beta2 integrins and lipopolysaccharide-binding protein in the phagocytosis of dead Neisseria meningitidis.

Jones HE, Strid J, Osman M, Uronen-Hansson H, Dixon G, Klein N, Wong SY, Callard RE.

Cell Microbiol. 2008 Aug;10(8):1634-45. doi: 10.1111/j.1462-5822.2008.01154.x. Epub 2008 Apr 7.

PMID:
18397383
18.

Serum and saliva antibodies do not inhibit Candida albicans Sap2 proteinase activity using a BSA hydrolysis assay.

Naglik JR, Scott J, Rahman D, Mistry M, Challacombe SJ.

Med Mycol. 2005 Feb;43(1):73-7.

PMID:
15712610
19.

Lymphocyte adhesion to Candida albicans.

Forsyth CB, Mathews HL.

Infect Immun. 2002 Feb;70(2):517-27.

20.

Down-regulation of complement receptors on the surface of host monocyte even as in vitro complement pathway blocking interferes in dengue infection.

Marinho CF, Azeredo EL, Torrentes-Carvalho A, Marins-Dos-Santos A, Kubelka CF, de Souza LJ, Cunha RV, de-Oliveira-Pinto LM.

PLoS One. 2014 Jul 25;9(7):e102014. doi: 10.1371/journal.pone.0102014. eCollection 2014.

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