Mitochondrial N-formylmethionine instructs tissue-inflammatory CD4+ T cells by redirecting endolysosomal pathways
Rheumatoid arthritis (RA) is a T-cell dependent autoimmune disease that causes tissue damaging joint inflammation. Mechanisms through which T cells from RA patients mediate tissue injury are poorly understood, but one of their distinguishing features is their poor mitochondrial performance. We performed RNAseq analysis of stimulated CD4+ T cells from 8 RA (ATPlow) and 8 RA (ATPint) patients. CD4+ T cells from RA (ATPlow) (n=4 each) were stimulated and treated with vehicle or the mPTP inhibitor CsA (5uM).CD4+ T cells from RA (ATPint) (n=4 each) were stimulated and treated with vehicle or the fMet (5 ng/ml) for 24 hrs Overall design: We performed RNAseq analysis of stimulated CD4+ T cells from four RA (ATPlow) and four RA (ATPint) patients. CD4+ T cells from RA (ATPlow) (n=4 each) were stimulated and treated with vehicle or the mPTP inhibitor CsA (5uM).CD4+ T cells from RA (ATPint) (n=4 each) were stimulated and treated with vehicle or the fMet (5 ng/ml) for 24 hrs