Abstract
Abstract Cyclic GMP-AMP synthase (cGAS) is a cytosolic DNA sensor that activates type 1 IFN response via cGAS/cGAMP/STING-dependent pathway to defend against viral and bacterial infections. The role of c-GAS in adaptive immunity is completely unknown. In this study, we attempted to determine whether cGAS also regulates T cell responses using mice deficient for cGAS. We found that cGas−/− mice develop ameliorated experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, which correlates with defective Th1/Th17 responses. This reduced disease activity in cGas−/− mice is unlikely due to the expression cGAS in T cells because Rag1−/− recipients receiving Wild-type and cGas−/− CD4+ T cells develop a comparable degree of EAE. Therefore, our data suggest that cGAS expression in innate immune cells may indirectly regulate pathogenic Th1/Th17 responses during EAE induction.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
