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Intravenous Immunoglobulin (IVIg) Modulates the Expansion of Vβ3 + and Vβ17 + T Cells Induced by Staphylococcal Enterotoxin B Superantigen In Vitro
Author(s) -
BAUDET V.,
HUREZ V.,
LAPEYRE C.,
KAVERI S. V.,
KAZATCHKINE M. D.
Publication year - 1996
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1996.d01-36.x
Subject(s) - superantigen , enterotoxin , antibody , antigen , t cell , immunology , in vitro , microbiology and biotechnology , cd3 , biology , chemistry , medicine , immune system , cd8 , escherichia coli , biochemistry , gene
The authors investigated the effect of IVIg on T‐cell proliferation induced by the superantigen, staphylococcal enterotoxin B (SEB). The addition of IVIg to normal PBMC stimulated with SEB resulted in a threefold increase in the proportion of CD3 + blast cells expressing Vβ3 and Vβ17, two subsets of T cells that selectively expand in the presence of SEB. There was no increase in the proportion of T‐cell blasts expressing Vβ2, Vβ8 and Vβ13.6 antigens that do not respond to SEB in the absence of IVIg. As described previously, IVIg inhibited T‐cell proliferation independently of Vβ specificity. The effects of IVIg were mediated by variable regions of immunoglobulins since they were reproduced with F(ab′) 2 fragments of IVIg but not with purified Fc fragments of IgG. The observation that SEB‐activated T cells are rescued from inhibition of proliferation by IVIg indicates that IVIg modulates the effects of superantigen on T cells. These results may be of relevance for understanding the mechanisms underlying the effects of IVIg in patients with diseases in which T‐cell superantigens are of pathophysiological significance.