[CCL2/MCP1: a novel target in systemic lupus erythematosus and lupus nephritis].
Cytokine blockade, a valid therapeutic concept, is not established in lupus nephritis as yet. In lupus nephritis CCL2/MCP-1 and its chemokine receptor CCR2 are of interest because CCL2/CCR2 mediate the recruitment of macrophages and T cells in the nephritic kidney. Lupus nephritis is markedly attenuated in CCL2- or CCR2-deficient autoimmune mice. Epidemiological studies addressing mutations in the CCL2 gene support the hypothesis that CCL2 mediates renal inflammation. Meanwhile experimental studies have shown that several classes of CCL2 antagonists can control established lupus nephritis. Interestingly, therapeutic CCL2 blockade does not affect the autoimmune lymphoproliferative syndrome and the production of lupus autoantibodies. This article briefly summarizes the potential role of therapeutic CCL2 blockade in lupus nephritis.
Kulkarni
O
O
Medizinische Poliklinik, Ludwig-Maximilians-Universität München, Pettenkoferstrasse 8a, 80336 München.
Anders
H-J
HJ
D000818:Animals; D018932:Chemokine CCL2 / Q000037:antagonists & inhibitors* / Q000502:physiology; D004195:Disease Models, Animal; D008180:Lupus Erythematosus, Systemic / Q000188:drug therapy* / Q000276:immunology; D008181:Lupus Nephritis / Q000188:drug therapy* / Q000276:immunology; D008262:Macrophage Activation / Q000187:drug effects / Q000276:immunology; D051379:Mice; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D016896:Treatment Outcome
C111835:CCL2 protein, human; D018932:Chemokine CCL2