| Grant number: | 15/08814-2 |
| Support Opportunities: | Scholarships in Brazil - Doctorate (Direct) |
| Start date: | December 01, 2015 |
| End date: | September 30, 2019 |
| Field of knowledge: | Biological Sciences - Immunology - Cellular Immunology |
| Principal Investigator: | Jose Ronnie Carvalho de Vasconcelos |
| Grantee: | Camila Pontes Ferreira |
| Host Institution: | Centro de Terapia Celular e Molecular. Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil |
| Associated research grant: | 12/22514-3 - Migration study of specific T cells generated by vaccination or Trypanosoma cruzi infection, AP.JP |
| Associated scholarship(s): | 17/21314-4 - Role of the CXCR3 chemokine receptor in the differentiation, migration, activation and functionality of T lymphocytes during Trypanosoma cruzi infection, BE.EP.DD |
Abstract Trypanosoma cruzi is the causative agent of Chagas disease, a neglected disease that is endemic in South and Central America, affecting approximately 10 million. CD8 + T cells play a key role in protective immunity against intracellular pathogens such as T. cruzi. The heterologous prime-boost immunization consists of a booster dose with two different genetic vectors carrying the same gene, one important strategy to generate CD8 + T cells and protection against experimental infection with T. cruzi. This protection is dependent lymphocyte recirculation, since treatment with FTY720 drug that leads to the retention of specific CD8 + T cells in the lymph node, it vaccinated mice susceptible to infection. The recirculation is accomplished by molecules of chemokines and integrins, both of which mediate inflammation through recruitment and activation of CD8 + T cells and other leukocytes in several models of inflammatory diseases. In a recent study demonstrated that treatment with the monoclonal anti-LFA-1 (lymphocyte associated antigen 1 function) in A/Sn mice immunized and infected reversed the protective immune response elicited by the immunization after systemic challenge with the parasite. This treatment did not affect the frequency of CD8 + T cells specific and not the effector function of these lymphocytes in the production of cytokines such as IFNg and TNFa. The same reversal was observed after treatment with anti-CXCR3 monoclonal antibody in A/Sn mice immunized and infected, and also did not observe any reduction in the frequency and the effector function specific CD8 + T cells. The results so far have shown the importance of these molecules in our vaccination and infection model, so the general objective of this Direct PhD proposal (DD) is continuing the studies obtained in the master, but use new experimental approach to elucidate the mechanisms and functions of these molecules. (AU) | |
| News published in Agência FAPESP Newsletter about the scholarship: | |
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