Yet these PD-1+ subsets are not exhausted; CD4+CXCR5+PD-1+ T follicular helper (Tfh) and CD4+CXCR5−PD-1+ T peripheral helper (Tph) cells have been proposed to contribute to the pathogenesis of RA by secreting B cell-promoting factors and promoting B cell differentiation and maturation, thus driving autoantibody production11,13. This evidence concerns the gene CD4 and rheumatoid arthritis.