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VG1 GD 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.
Cardiopatias/imunologia
Inflamação/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
Subpopulações de Linfócitos T/imunologia
Animais
Anticorpos Monoclonais/farmacologia
Ligante de CD40/metabolismo
Interferon gama/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Músculo Esquelético/metabolismo
Baço/citologia
Subpopulações de Linfócitos T/efeitos de drogas
Regulação para Cima
Author
Affilliation
University of São Paulo. Department of Clinical Analysis, Toxicology and Bromatology. FCFRP. Ribeirão Preto, SP, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil
University of São Paulo. Institute for Biomedical Sciences IV. Department of Immunology. São Paulo, SP, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil
University of São Paulo. Institute for Biomedical Sciences IV. Department of Immunology. São Paulo, SP, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil
Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil
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.
DeCS
Doença de Chagas/imunologiaCardiopatias/imunologia
Inflamação/imunologia
Receptores de Antígenos de Linfócitos T gama-delta/metabolismo
Subpopulações de Linfócitos T/imunologia
Animais
Anticorpos Monoclonais/farmacologia
Ligante de CD40/metabolismo
Interferon gama/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Músculo Esquelético/metabolismo
Baço/citologia
Subpopulações de Linfócitos T/efeitos de drogas
Regulação para Cima
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