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The importance of STING signaling pathway on the differentiation and function of T regulatory cells

Grant number: 22/02651-8
Support Opportunities:Scholarships in Brazil - Doctorate (Direct)
Effective date (Start): August 01, 2022
Effective date (End): July 31, 2026
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:José Carlos Farias Alves Filho
Grantee:Caroline Vitória Souza Fernandes de Oliveira
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:13/08216-2 - CRID - Center for Research in Inflammatory Diseases, AP.CEPID

Abstract

Nucleic acids, including DNA and RNA from pathogenic microorganisms and mammals, can activate the immune system. This activation depends on molecular sensors, such as the protein STING (Stimulator of Interferon Genes). This protein is described as an intracellular sensor capable of detecting microbial or own nucleic acids, promoting the activation of a variety of transcription factors, including those involved in the production of type I interferons (IFN-I). Although STING is widely described in innate immunity cells, little is known about its role on lymphocytes. T regulatory cells (Tregs) are a subpopulation of lymphocytes that express FoxP3 protein (Forkhead box P3), a transcription factor that plays a fundamental role in the regulation of the development, maintenance and immunosuppressive function of these cells. It is well established that Tregs have a central role on the immune system's homeostasis, as well as on the prevention of autoimmune diseases' development and of the exacerbation of inflammatory responses during infections. In this context, unexpectedly, preliminary results obtained during the period of my undergraduate research demonstrate that STING activation enhances Treg cells differentiation. Therefore, the present project aims to evaluate the influence of STING signaling pathway on the generations and activation of Tregs and its consequence on autoimmunity. (AU)

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