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Lymphocytes induce monocyte chemoattractant protein‐1 production by renal cells after Fcγ receptor cross‐linking: role of IL‐1β
Author(s) -
Rovin Brad H.,
Lu Ling,
Marsh Clay B.
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.69.3.435
Subject(s) - chemokine , monocyte , biology , immune system , lymphocyte , immunology , kidney , ccl2 , endocrinology
Leukocyte recruitment to the kidney in immune complex disease like systemic lupus erythematosus (SLE) is mediated in part by local expression of chemokines such as monocyte chemoattractant protein‐1 (MCP‐1). Recent studies from this laboratory demonstrated that cross‐linking FcγR on lymphocytes causes release of a soluble factor that induces monocyte chemokine production. To explain the induction of renal chemokine expression in immune complex disease, we postulated that this lymphocyte factor stimulates renal parenchymal cell MCP‐1 expression. To test this hypothesis, human peripheral blood lymphocytes were incubated on immobilized IgG, a model for immune complex FcγR cross‐linking. Supernatants from these lymphocyte cultures significantly increased MCP‐1 production by human mesangial, glomerular capillary endothelial, and proximal tubular epithelial cells. Mesangial cells incubated on immobilized IgG or with soluble, preformed immune complexes did not secrete MCP‐1 above control levels. Lymphocyte supernatant‐induced MCP‐1 production appeared to be dependent on the presence of interleukin (IL)‐1β in the supernatant. Removing IL‐1β from the supernatants, antagonizing its activity, or preventing conversion to mature IL‐1β abrogated renal cell MCP‐1 expression by the lymphocyte supernatants. These data demonstrate that in response to cross‐linking FcγR, lymphocytes induce renal cell MCP‐1 expression by secreting IL‐1β. Renal chemokine expression in immune complex disease may thus be triggered as lymphocytes traffic through the kidney and encounter deposited immune complexes.