MIF, CD74 and other partners in kidney disease: Tales of a promiscuous couple

被引：61

作者：

Sanchez-Nino, M. D. ^{[1
]}

Sanz, A. B. ^{[1
]}

Ruiz-Andres, O. ^{[2
]}

Poveda, J. ^{[2
]}

Izquierdo, M. C. ^{[2
]}

Selgas, R. ^{[1
]}

Egido, J. ^{[2
,3
,4
]}

Ortiz, A. ^{[2
,3
,4
]}

机构：

[1] IDIPaz, Serv Nefrol, Madrid, Spain

[2] Fdn Jimenez Diaz, IIS, E-28040 Madrid, Spain

[3] Univ Autonoma Madrid, Madrid, Spain

[4] Fdn Renal Inigo Alvarez Toledo IRSIN, Madrid, Spain

来源：

CYTOKINE & GROWTH FACTOR REVIEWS | 2013年 / 24卷 / 01期

关键词：

Kidney; CD74; CXCR2; CXCR4; Macrophage inhibitory factor; MIGRATION-INHIBITORY-FACTOR; RENAL-ALLOGRAFT REJECTION; D-DOPACHROME TAUTOMERASE; INVARIANT CHAIN EXPRESSION; ACTIVATED PROTEIN-KINASE; TUBULAR EPITHELIAL-CELLS; RAT CRESCENTIC GLOMERULONEPHRITIS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; FACTOR INDUCES ANGIOGENESIS; HUMAN MESANGIAL CELLS;

D O I：

10.1016/j.cytogfr.2012.08.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Macrophage migration inhibitory factor (MIF) is increased in kidney and urine during kidney disease. MIF binds to and activates CD74 and chemokine receptors CXCR2 and CXCR4. CD74 is a protein trafficking regulator and a cell membrane receptor for MIF, D-dopachrome tautomerase (D-DT/MIF-2) and bacterial proteins. MIF signaling through CD74 requires CD44. CD74, CD44 and CXCR4 are upregulated in renal cells in diseased kidneys and MIF activation of CD74 in kidney cells promotes an inflammatory response. MIF or CXCR2 targeting protects from experimental kidney injury, CD44 deficiency modulates kidney injury and CXCR4 activation promotes glomerular injury. However, the contribution of MIF or MIF-2 to these actions of MIF receptors has not been explored. The safety and efficacy of strategies targeting MIF, CD74, CD44 and CXCR4 are under study in humans. (C) 2012 Elsevier Ltd. All rights reserved.

引用

页码：23 / 40

页数：18

共 237 条

[1] Endogenous macrophage migration inhibitory factor modulates glucocorticoid sensitivity in macrophages via effects on MAP kinase phosphatase-1 and p38 MAP kinase [J].