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Characterization of the autoimmune response in mice deficient for the DDX41 protein on regulatory T cells.

Grant number: 22/16347-9
Support Opportunities:Scholarships in Brazil - Master
Effective date (Start): May 01, 2023
Effective date (End): January 31, 2025
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal Investigator:José Carlos Farias Alves Filho
Grantee:Gabriella Carolina Scalice Chiari
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


Regulatory T lymphocytes (Tregs) are CD4+ T cells characterized by the expression of the transcription factor Foxp3. Tregs have the role of maintaining peripheral immune self-tolerance, preventing the development of autoimmune diseases, as well as suppressing exacerbated immune responses. The DDX41 protein (Probable ATP-dependent RNA helicase DDX41) is an RNA helicase member of the DEAD box helicase family that recognizes double-stranded DNA and acts in several cellular processes, such as nuclear and mitochondrial splicing, spliceosomes, translation and as a factor precursor of ribosomal RNA processing (pre-rRNA). In addition, DDX41 has other functions that are not yet well defined, such as its participation as an accessory gate in the activation pathway of STING ("STimulator of Interferons Genes"). Furthermore, a study demonstrated that DDX41 is one of the proteins associated with and interacting with the Foxp3 transcription factor. Preliminary results of this project demonstrated that the specific absence of this DDX41 protein in mouse Tregs results in a reduction in the number of Tregs in lymphoid organs, a lymphoproliferative response and the development of systemic inflammation with characteristics of a scurfy-like profile. Our hypothesis is that this protein plays a crucial role in the biology of regulatory T cells. Thus, the present project aims to characterize the autoimmune response in mice deficient for the DDX41 protein in regulatory T lymphocytes.

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