The role of DNA damage repair protein XPC in TH17 cell pathogenicity of Experimental Autoimmune Encephalomyelitis

Vol. 1 2024 - 347878
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Resumo

TH17 cells are a subpopulation of T CD4+ cells with documented participation in both responses to infections by extracellular pathogens and autoimmune diseases, Experimental Autoimmune Encephalomyelitis (EAE) among them. T CD4+ cells are exposed to multiple sources of DNA damage throughout their effector phase, and as such require DNA damage repair (DDR) pathways to keep their genomic molecules stable and functioning. Recently published work from our group points to TH17 cells being dependent on nucleotide excision repair (NER) DDR component XPC to maintain IL-17A production and RORyt stability in both in vitro and inflammatory bowel disease mice models, but it is unclear if said roles could be observed in other autoimmune diseases. The objective of this work is to analyze the presence of XPC protein in autoimmune TH17 cells in an EAE model and understand the impacts of its deletion for EAE development. We observed TH17 cell infiltration in the Central Nervous System (CNS) after EAE immunization, as well as XPC presence in TH17 cells from spleen, inguinal lymph nodes and CNS in flow cytometry. Through transcriptomic analysis, we noted TH17 cells in EAE demonstrating higher transcriptional activity in genes associated with DDR pathways such as NER and base excision repair (BER). Interestingly, we also observed that XPC deficient (XPCKO) mice are protected from EAE development and show a tendency of XPCKO T CD4+ cells becoming less active and displaying less DNA damage. Overall, these findings point to XPC being a key protein in maintaining autoimmune TH17 cells activity in the CNS, raising the possibility of XPC as a target for autoimmune disease treatment.

 

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Programação
17:00 até 18:45 em 29/10/2026
TV9
Instituições
  • 1 Federal University of Rio de Janeiro
  • 2 ufrj
  • 3 Federal University of Rio de Janeiro (UFRJ)
Eixo Temático
  • Neuroinflammation
Palavras-chave
TH17 cells
EAE
DNA damage