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The role of STING signaling pathway on the differentiation of regulatory T cells induced by herpes simplex virus-1 (HSV-1) infection

Grant number: 23/05358-2
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): July 01, 2023
Effective date (End): June 30, 2024
Field of knowledge:Biological Sciences - Pharmacology
Principal Investigator:José Carlos Farias Alves Filho
Grantee:Gabriel Azevedo Públio
Supervisor: Ari Waisman
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Research place: Johannes Gutenberg University Mainz (JGU), Germany  
Associated to the scholarship:20/04170-1 - The role of DDX41 on the differentiation and function of regulatory T lymphocytes, BP.DR


Regulatory T lymphocytes (Tregs) are critical immunosuppressive cells that are crucial in regulating inflammatory responses and maintaining immune homeostasis. Understanding the mechanisms involved in the differentiation, activation, function and stability of Tregs can provide novel therapeutic strategies to halt autoimmune diseases. Immune cells express pattern recognition receptors (PRRs) that recognize molecules released by damaged cells or invading pathogens, including nucleic acids as DNA. The stimulator of interferon genes (STING) is an intracellular receptor that recognizes processed dsDNA and is widely studied in innate immunity. Activation of STING and its accessory molecules in cultured lymphocytes leads to a higher expression of Foxp3, a transcription factor important for Treg differentiation. Herpes simplex virus 1 (HSV-1) is a cause of vesicular-ulcerative lesions of the oral or genital mucosa that can establish life-long latent infection in sensory neurons, from which periodic reactivation can occur. Interestingly, Tregs are important for controlling the latency and reactivation of HSV-1, helping the virus establish itself in the host and evade the immune system. However, how HSV1 infection regulates Treg cell function remains unknown. Our hypothesis is that HSV1 can directly induce differentiation and modulate the function of Tregs via the STING signaling pathway. Our preliminary data show that HSV-1 can infect and replicate in T cells without causing cell death. When cultured in Treg polarizing conditions, HSV-1 infection leads to a higher expression of Foxp3 and suppressive molecules. This process depends on STING activation, and HSV-1 expresses latency-related genes in Tregs, suggesting that Tregs can also be a viral reservoir. Therefore, we intend to investigate further the mechanism behind HSV-1 induction of Tregs. To this end, we are applying for the BEPE fellowship program to spend 12 months in Prof. Waisman's laboratory in Germany to develop this project. (AU)

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