title: V gamma 1 gammadelta T cells regulate type-1/type-2 immune responses and participate in the resistance to infection and development of heart inflammation in Trypanosoma cruzi-infected BALB/c mice.
abstract: Many different cell populations or lineages participate in the resistance to Trypanosoma cruzi infection. gammadelta T cells may also take part in a network of interactions that lead to control of T. cruzi infection with minimal tissue damage by controlling alphabeta T cell activation, as was previously suggested. However, the gammadelta T cell population is not homogeneous and its functions might vary, depending on T cell receptor usage or distinct stimulatory conditions. In this study, we show that the in vivo depletion of V gamma 1-bearing gammadelta T cells, prior to the infection of BALB/c mice with the Y strain of T. cruzi, induces an increased susceptibility to the infection with lower amounts of IFN-gamma being produced by conventional CD4+ or CD8+ T cells. In addition, the production of IL-4 by spleen T cells in V gamma 1-depleted mice was increased and the production of IL-10 remained unchanged. Since V gamma 1(+) gammadelta T cell depletion diminished the conversion of naive to memory/activated CD4 T cells and the production of IFN-gamma during the acute infection, these cells appear to function as helper cells for conventional CD4+ Th1 cells. Depletion of V gamma 1(+) cells also reduced the infection-induced inflammatory infiltrate in the heart and skeletal muscle. More importantly, V gamma 1(+) cells were required for up-regulation of CD40L in CD4+ and CD8+ T cells during infection. These results show that a subset of gammadelta T cells (V gamma 1(+)), which is an important component of the innate immune response, up-regulates the type 1 arm of the adaptative immune response, during T. cruzi infection.
authors.affiliation: Department of Clinical Analysis, Toxicology and Bromatology, FCFRP, University of São Paulo, Av. Café s/n, CEP 14040-903, Ribeirão Preto, SP, Brazil.
authors.forename: Auro
authors.initials: A
authors.lastname: Nomizo
authors.forename: Fabíola
authors.initials: F
authors.lastname: Cardillo
authors.forename: Edilberto
authors.initials: E
authors.lastname: Postól
authors.forename: Lain Pontes
authors.initials: LP
authors.lastname: de Carvalho
authors.forename: José
authors.initials: J
authors.lastname: Mengel
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D023201:CD40 Ligand / Q000378:metabolism; D014355:Chagas Disease / Q000276:immunology*; D006331:Heart Diseases / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D007371:Interferon-gamma / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D018482:Muscle, Skeletal / Q000378:metabolism; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000378:metabolism*; D013154:Spleen / Q000166:cytology; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology*; D015854:Up-Regulation
chemical_list: D000911:Antibodies, Monoclonal; D016692:Receptors, Antigen, T-Cell, gamma-delta; D023201:CD40 Ligand; D007371:Interferon-gamma