AbstractBackgroundCD40 is a costimulatory molecule for B cells, and CD154 is a marker of CD4+ T cells activation. CD40‐CD154 interaction promotes pro‐inflammatory cytokines secretion and autoantibodies production. PTPN22 gene encodes LYP protein, an inhibitor of T‐ and B‐cell activation. PTPN22 1858C>T polymorphism confers rheumatoid arthritis (RA) susceptibility. Hence, we evaluate the relationship between 1858C>T polymorphism with CD40 and CD154 expression and IFN‐γ secretion in RA patients.MethodsPTPN22 1858C>T polymorphism was genotyped in 315 RA patients and 315 control subjects (CS) using PCR‐RFLP method. Later, we selected only ten anti‐CCP‐positive RA patients, naïve to disease‐modifying antirheumatic drugs and ten CS, all with known 1858C>T PTPN22 genotype. The CD40 and CD154 membrane expressions were determined by flow cytometry in peripheral B and T cells, correspondingly.ResultsThe B cells percentage and mCD40 expression were similar between RA and CS (P > 0.05) and we did not find an association between these variables and the 1858C>T polymorphism. The CD4+ T cells percentage was higher in RA patients than CS (P = 0.003), and in the RA group, the CD4+ T cells percentage and mCD154 expression were higher in the 1858 T allele carriers (P = 0.008 and P = 0.032, respectively). The IFN‐γ levels were lower in RA patients carrying the PTPN22 risk allele (P = 0.032).ConclusionThe PTPN22 1858 T risk allele is associated with increased CD4+ T cells percentage and high mCD154 expression in RA patients, which could favor the pro‐inflammatory cytokine release and the establishment of the inflammatory response at the seropositive RA.