receptor cross-linking: role of IL-1ß
Department of Internal Medicine and the Heart Lung Research Institute, The Ohio State University School of Medicine and Public Health
Correspondence: Brad H. Rovin, M.D., Nephrology Division, Ohio State University, N210 Means Hall, 1654 Upham Dr., Columbus, OH 43210. E-mail: rovin.1{at}osu.edu
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 Fc
R 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 FcR
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)-1ß in the supernatant. Removing IL-1ß
from the supernatants, antagonizing its activity, or preventing
conversion to mature IL-1ß abrogated renal cell MCP-1 expression by
the lymphocyte supernatants. These data demonstrate that in response to
cross-linking FcR, lymphocytes induce renal cell MCP-1 expression by
secreting IL-1ß. Renal chemokine expression in immune complex disease
may thus be triggered as lymphocytes traffic through the kidney and
encounter deposited immune complexes.
Key Words: chemokine • mesangial • immune complex
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