STAT1 deficiency underlies a proinflammatory imprint of naive CD4+ T cells in spondyloarthritis

Altogether, B27-rat Tn harbor a STAT1 deficiency preceding disease onset, which may occur during their thymic differentiation, secondarily associated with a persistent Th17 bias, which is imprinted at the epigenomic level. This early molecular phenomenon might lead to the persistent proinflammatory skew of CD4⁺ T cells in SpA patients, thus offering new clues to better understand and treat SpA.