TITLE

Mesangial cell accessory functions: Mediation by intercellular adhesion molecule-1

AUTHOR(S)
Brennan, Daniel C.; Jevnikar, Anthony M.; Takei, Fumio; Reubin-Kelley, Vicki E.
PUB. DATE
December 1990
SOURCE
Kidney International;Dec1990, Vol. 38 Issue 6, p1039
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Mesangial cell (MC) proliferation is an early pathologic alteration characteristic of many forms of immune mediated glomerulonephritis. The intracapillary position, contractile capacity, and production of cytokines and other inflammatory molecules place MC in a pivotal position to initiate, mediate, and direct glomerular damage. We as well as others have noted increased levels of cytokines including IFNγ, TNF, and IL-1 and the cell surface MHC class II and ICAM-1 molecules in the kidneys of mice with lupus nephritis. MHC class II and ICAM-l molecules are central to the interaction of T cells with antigen presenting cells (APC). Since cytokines can increase both MHC class II and ICAM-I molecules, we investigated whether mesangial cells could function as APC or accessory cells after cytokine stimulation. For these studies we established a permanent MC line through transformation with origin-deficient SV40 DNA. Surface expression of ICAM-l was similar in untransformed MC as well as SV40 transformed MC from normal mice and in untransformed cells from mice with lupus nephritis. Basal expression of ICAM-l was upregulated rapidly by IFN-γ, TNF, and IL-1. MHC class II expression could not be induced with TNF or IL-1 alone but required prolonged stimulation with IFNγ. MC adhered and presented antigen lo an antigen specific laκ restricted T cell hybridoma. Anti-ICAM-1 mAb decreased adhesion and antigen presentation of cytokine stimulated MC. By comparison, MHC class II mAb abrogated antigen presentation by MC bearing MHC class II but did not block adhesion. Thus, MC, by their unique glomerular location, contractile capacity, cytokine production, adherence, and antigen-presenting capability, are in a pivotal position to initiate and direct renal injury.
ACCESSION #
17656771

 

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