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The contribution of different T cells subsets to development of neuropathic pain

Grant number: 23/04332-0
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): August 25, 2023
Effective date (End): February 24, 2024
Field of knowledge:Biological Sciences - Biochemistry
Principal Investigator:Deborah Schechtman
Grantee:Beatriz Caroline de Moraes
Supervisor: Allan I. Basbaum
Host Institution: Instituto de Química (IQ). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Research place: University of California, San Francisco (UCSF), United States  
Associated to the scholarship:22/00594-7 - Role of PLCg in experimental acute and chronic hypersensitivity, BP.DR


Following a nerve damage, T cells infiltrate the lesion site to allow tissue repair and homeostatic balance. Locally, T cells release various pro-inflammatory mediators for tissue repair that can influence local neuron activity. We therefore hypothesize that T cells may contribute to chronic pain development after nerve injury through communication with neurons at specific intersectional sites located at the junction of the nervous and immune system compartments. We thus aim to investigate the temporal involvement of different T cell subsets in promoting mechanical and cold sensitivity following nerve injury using a spared nerve injury (SNI) model in mouse lines lacking specific T cell subsets. We next will identify where the communication between T cells and neurons takes place driving pain hypersensitivity. Different neuroimmune compartments (dorsal root ganglia, lesioned nerve, spinal cord meninges) will be analyzed for subpopulations of T cells using flow cytometry. (AU)

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