| Grant number: | 11/15832-6 |
| Support Opportunities: | Scholarships in Brazil - Master |
| Start date: | June 01, 2012 |
| End date: | October 31, 2013 |
| Field of knowledge: | Biological Sciences - Immunology - Cellular Immunology |
| Principal Investigator: | João Santana da Silva |
| Grantee: | Marcela Cristina Santiago Françozo |
| Host Institution: | Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil |
Abstract Coxsackieviruses B5 (CVB5) belong to the genus Enterovirus of the family Picornaviridae and they are non-enveloped viruses that have a genome of single-stranded RNA with positive sense. These viruses are highly cytolytic and are considered one of the most common causes of acute infectious myocarditis, and they are able to infect pancreatic acinar cells, which often leads to fulminant pancreatitis resulting in pancreatic insufficiency. Despite the knowledge about the structure and biochemistry of enteroviruses, the pathogenesis of the infection caused by these agents and their control by the immune response are not known in detail. It is known that neutralizing antibodies play a key role in protecting against the virus, while CD4+ and CD8+ T cells, although important in viral clearance, are involved in the pathogenesis of the disease. Regulatory T cells, in contrast, appear to be involved in the suppression of activated T cells by the virus, and thus are able to reduce tissue damage and disease severity. The chemokine receptor CCR4 is present on monocytes, effector and regulatory T cells and the binding to one of its ligands, CCL17 and CCL22, is associated with the recruitment of these cells to sites of infection in several experimental models. Since the balance between Th1, Th2 and regulatory T cells is extremely important in protecting against pancreatitis caused by CVB, and the differential migration of these cells to the site of infection depends on chemokine receptors, especially CCR4, we intend in this study , verify the effect of receptor CCR4 in experimental pancreatitis induced by infection with CVB5. | |
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