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Interference With CD28, CD80, CD86 or CD152 in Collagen-Induced Arthritis. Limited Role of IFN-gamma in anti-B7-mediated Suppression of Disease

Interference With CD28, CD80, CD86 or CD152 in Collagen-Induced Arthritis. Limited Role of IFN-gamma in anti-B7-mediated Suppression of Disease

A C Tellander, U Pettersson, A Runström, M Andersson, E Michaëlsson

J Autoimmun. 2001 Aug;17(1):39-50.

PMID: 11488636

Abstract:

We have investigated interference with co-stimulation by administering mAbs towards CD28, CD80, CD86, and CD152 in mice immunized for the development of collagen-induced arthritis (CIA). Anti-CD80 and anti-CD86 treatment inhibited disease score and incidence, whereas anti-CD28 treatment led only to a delayed disease onset. Administration of anti-CD152 had no effect. The CII-specific Ab-response was suppressed by the co-stimulatory blockade, with a stronger effect on IgG1 than on IgG2a. The CII-driven T cell proliferation, on the other hand, was not affected. Furthermore, T cells primed in the presence of either anti-B7 or anti-CD28 produced markedly increased amounts of IFN-gamma in response to CII. To investigate whether this increase in IFN-gamma was related to disease suppression, IFN-gamma-deficient mice were immunized with CII, treated with anti-B7 and followed for the development of arthritis. As in the wild-type mice, administration of anti-B7 to IFN-gamma-deficient mice led to a reduced disease incidence and severity as well as reduced anti-CII IgG titers. Collectively, these data stress the importance of co-stimulation for the delivery of B cell help rather than for production of Th1 cytokines. We also demonstrate that the enhanced production of IFN-gamma observed after B7-blockade is not accountable for the anti-B7 mediated inhibition of CIA.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42414697	Monoclonal Anti-CD152 antibody produced in mouse			Price

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