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TGF-β Mediates CTLA-4 Suppression of Cellular Immunity in Murine Kalaazar
Journal article   Peer reviewed

TGF-β Mediates CTLA-4 Suppression of Cellular Immunity in Murine Kalaazar

Nitza A Gomes, Cerli R Gattass, Victor Barreto-de-Souza, Mary E Wilson and George A DosReis
The Journal of immunology (1950), Vol.164(4), pp.2001-2008
02/15/2000
DOI: 10.4049/jimmunol.164.4.2001
PMID: 10657651

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Abstract

Recent studies indicate important roles for CTLA-4 engagement in T cells, and for TGF-beta production in the immunopathogenesis of murine kalaazar or visceral leishmaniasis, but a functional link between these two pathways in helping intracellular parasite growth is unknown. Here we report that Ag or anti-CD3 activation of splenic CD4+ T cells from visceral leishmaniasis leads to intense CTLA-4-mediated TGF-beta1 production, as assessed either by CTLA-4 blockade or by direct CTLA-4 cross-linkage. Production of TGF-beta1 accounted for the reciprocal regulation of IFN-gamma production by CTLA-4 engagement. Following CD4+ T cell activation, intracellular growth of Leishmania chagasi in cocultured splenic macrophages required both CTLA-4 function and TGF-beta1 secretion. Cross-linkage of CTLA-4 markedly increased L. chagasi replication in cocultures of infected macrophages and activated CD4+ T cells, and parasite growth could be completely blocked with neutralizing anti-TGF-beta1 Ab. Exogenous addition of rTGF-beta1 restored parasite growth in cultures protected from parasitism by CTLA-4 blockade. These results indicate that the negative costimulatory receptor CTLA-4 is critically involved in TGF-beta production and in intracellular parasite replication seen in murine kalaazar.

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