| Grant number: | 17/11499-7 |
| Support Opportunities: | Scholarships in Brazil - Master |
| Start date: | November 01, 2017 |
| End date: | August 31, 2019 |
| Field of knowledge: | Biological Sciences - Immunology - Cellular Immunology |
| Principal Investigator: | Jose Ronnie Carvalho de Vasconcelos |
| Grantee: | Leonardo Moro Cariste |
| Host Institution: | Instituto de Saúde e Sociedade (ISS). Universidade Federal de São Paulo (UNIFESP). Campus Baixada Santista. Santos , SP, Brazil |
| Associated research grant: | 12/22514-3 - Migration study of specific T cells generated by vaccination or Trypanosoma cruzi infection, AP.JP |
Abstract CD8 + T lymphocytes play an important role in the control of infections by intracellular pathogens such as Trypanosoma cruzi, the causative agent of Chagas' disease. These lymphocytes control infection through the release of IFN-g and the elimination of infected target cells by direct cytotoxicity. To perform these functions, lymphocytes must migrate to infected tissues, establish stable contact with antigen-presenting cells, and be activated through the interaction of the TCR with the MHC-peptide complex and costimulatory molecules. Chemokine and integrin molecules are essential for the migration of T lymphocytes to the sites of infection. In addition, the role of these molecules in the activation and differentiation of CD8 + T lymphocytes during viral and bacterial infections has now been reported. However, the role of these molecules during T. cruzi infection is unclear. Interestingly, CX3CR1 and CXCR3 chemokine molecules are highly expressed on the surface of CD8 + T lymphocytes during infection by intracellular pathogens, such as T. cruzi, and are important in the activation and differentiation of these cells. Studies indicate that chemokines and integrins are important to facilitate the encounter of these lymphocytes with the antigen-presenting cells in the lymph node, and consequently, in the activation and subsequent differentiation of lymphocytes. LFA-1 integrin also plays a role in the activation and differentiation of lymphocytes, since it is extremely important in establishing contact of lymphocytes with antigen-presenting cells. However, there are still few works in the literature that describe exactly how this molecule interferes in the induction of memory cells. Our preliminary results demonstrated that blockade of CXCR3 and / or LFA-1 render mice of the C57BL / 6 strain susceptible to T. cruzi infection. Furthermore, we observed that the chemokine receptor CX3CR1 is highly expressed in the CD8 + T cells of the infected animals. Therefore, the objective of this project is to evaluate the role of CXCR3 and CX3CR1 chemokines and LFA-1 integrin in the differentiation of memory effector cells and activation of CD8 + T lymphocytes during T. cruzi infection. The knowledge of the mechanisms involved with the induction of effector cells that will give rise to the memory cells is of extreme importance for the generation of vaccine strategies. (AU) | |
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