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Clin Immunol. 2001 Dec;101(3):366-70.

Evidence of a role for C4 in modulating interstitial inflammation in experimental glomerulonephritis.

Author information

1
Division of Nephrology and Hypertension, Children's Hospital Research Foundation, Cincinnati, Ohio 45229, USA.

Abstract

Activation of C4 releases into the fluid phase a fragment of the alpha chain, C4a. Unlike the analogous fragments of C3 and C2, there is no evidence for an anaphylatoxic effect of C4a. There is actually some in vitro evidence that it could have a modulating effect on inflammation by inhibiting monocyte chemotaxis. We induced an immune complex glomerulonephritis in wild-type (WT) and C4 knock out (C4KO) mice. Although the glomerular component of the disease did not differ in the two groups of animals, there were marked differences in the accompanying tubulo-interstitial injury. Compared to WT animals, the C4KO mice had significantly more infiltrating interstitial cells (1910 vs 2720/mm(2)), foci of tubular atrophy (6.3 vs 14.8/section), and interstitial space (22 vs 30% of cortex). C4 is expressed constitutively by renal tubular epithelial cells. These data support a role for such local C4 in modulating interstitial inflammation, consistent with in vitro experiments.

PMID:
11726230
DOI:
10.1006/clim.2001.5125
[Indexed for MEDLINE]

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