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 |
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| Authors: | Nomizo Auro Cardillo Fabíola Postól Edilberto de Carvalho Lain Pontes Mengel José |
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| Institution: | 1. Department of Clinical Analysis, Toxicology and Bromatology, FCFRP, University of São Paulo, Av. Café s/n, CEP 14040-903, Ribeirão Preto, SP, Brazil;2. Department of Immunology, Institute for Biomedical Sciences IV, University of São Paulo, Av. Prof. Lineu Prestes, 1730, CEP 05508-900, São Paulo, Brazil;3. Oswaldo Cruz Foundation, Gonçalo Moniz Research Center, R. Waldemar Falcão 121, CEP 40295-001 Salvador, Bahia, Brazil;1. OncoRay – National Center for Radiation Research in Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Helmholtz-Zentrum Dresden – Rossendorf, Germany;2. Department of Radiotherapy and Radiation Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Germany;3. Helmholtz-Zentrum Dresden – Rossendorf, Institute of Radiooncology – OncoRay, Germany;4. German Cancer Consortium (DKTK), partner site Dresden, Germany;5. German Cancer Research Center (DKFZ), Heidelberg, Germany;6. National Center for Tumor Diseases (NCT), partner site Dresden, Germany;7. Institute for Legal Medicine, Faculty of Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, Germany;1. Department of Medicine, Section of Hematology/Oncology, The University of Chicago, Chicago, IL, USA;2. Rheinische Friedrich-Wilhelms University Bonn, Bonn, Germany;3. University of Pennsylvania, Philadelphia, PA, USA;4. Vanderbilt University, Nashville, TN, USA;5. Department of Pathology, The University of Chicago, Chicago, IL, USA;6. Institute for Genomics and Systems Biology, Chicago, IL, USA;7. The University of Chicago Comprehensive Cancer Research Center, Chicago, IL, USA;1. Department of Otorhinolaryngology, Head and Neck Surgery, Heinrich Heine University, 40225 Düsseldorf, Germany;2. Department of Pathology, Heinrich Heine University, 40225 Düsseldorf, Germany;3. Department of Cranio-and-Maxillo Facial Surgery, Heinrich Heine University, 40225 Düsseldorf, Germany;4. Pediatric Hematology/Oncology, Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN 46202, USA;5. Department of Medical & Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA;1. Department of Surgery, University of Minnesota, United States;2. Masonic Cancer Center, University of Minnesota, United States;3. Department of Diagnostic & Biological Sciences, School of Dentistry, University of Minnesota, United States;4. Institute of Molecular Virology, University of Minnesota, United States |
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| 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. |
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