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CXCR3 CHEMOKINE RECEPTOR CONTRIBUTES TO SPECIFIC CD8+ T CELL ACTIVATION BY PDC DURING INFECTION WITH INTRACELLULAR PATHOGENS
CD8+ T cell activation
Infecção
Patógenos intracelulares
Author
Affilliation
Universidade Federal de São Paulo. Departamento de Microbiologia, Imunologia e Parasitologia. São Paulo, SP, Brasil.
Universidade Federal de São Paulo. Departamento de Biociências. Santos, SP, Brasil.
Universidade Federal de São Paulo. Departamento de Microbiologia, Imunologia e Parasitologia. São Paulo, SP, Brasil.
University of Massachusetts Medical School. Department of Medicine. Worcester, Massachusetts,USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia das Interações. Rio de Janeiro, RJ, Brasil.
Universidade Federal de São Paulo. Departamento de Ciências Biológicas. São Paulo, SP, Brasil.
Universidade Federal de São Paulo. Departamento de Biociências. Santos, SP, Brasil.
University of Massachusetts Medical School. Department of Medicine. Worcester, Massachusetts,USA.
University of Massachusetts Medical School. Department of Medicine. Worcester, Massachusetts,USA.
Universidade Federal de São Paulo. Departamento de Microbiologia, Imunologia e Parasitologia. São Paulo, SP, Brasil / Universidade Federal de São Paulo. Departamento de Biociências. Santos, SP, Brasil.
Universidade Federal de São Paulo. Departamento de Biociências. Santos, SP, Brasil.
Universidade Federal de São Paulo. Departamento de Microbiologia, Imunologia e Parasitologia. São Paulo, SP, Brasil.
University of Massachusetts Medical School. Department of Medicine. Worcester, Massachusetts,USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia das Interações. Rio de Janeiro, RJ, Brasil.
Universidade Federal de São Paulo. Departamento de Ciências Biológicas. São Paulo, SP, Brasil.
Universidade Federal de São Paulo. Departamento de Biociências. Santos, SP, Brasil.
University of Massachusetts Medical School. Department of Medicine. Worcester, Massachusetts,USA.
University of Massachusetts Medical School. Department of Medicine. Worcester, Massachusetts,USA.
Universidade Federal de São Paulo. Departamento de Microbiologia, Imunologia e Parasitologia. São Paulo, SP, Brasil / Universidade Federal de São Paulo. Departamento de Biociências. Santos, SP, Brasil.
Abstract
Chemokine receptor type 3 (CXCR3) plays an important role in CD8+ T cells migration during intracellular infections, such as Trypanosoma cruzi. In addition to chemotaxis, CXCR3 receptor has been described as important to the interaction between antigen-presenting cells and effector cells. We hypothesized that CXCR3 is fundamental to T. cruzi-specific CD8+ T cell activation, migration and effector function. Anti-CXCR3 neutralizing antibody administration to acutely T. cruzi-infected mice decreased the number of specific CD8+ T cells in the spleen, and those cells had impaired in activation and cytokine production but unaltered proliferative response. In addition, anti-CXCR3-treated mice showed decreased frequency of CD8+ T cells in the heart and numbers of plasmacytoid dendritic cells in spleen and lymph node. As CD8+ T cells interacted with plasmacytoid dendritic cells during infection by T. cruzi, we suggest that anti-CXCR3 treatment lowers the quantity of plasmacytoid dendritic cells, which may contribute to impair the prime of CD8+ T cells. Understanding which molecules and mechanisms guide CD8+ T cell activation and migration might be a key to vaccine development against Chagas disease as those cells play an important role in T. cruzi infection control.
Keywords in Portuguese
Receptor de quimiocina CXCR3CD8+ T cell activation
Infecção
Patógenos intracelulares
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