Although direct human evidence that TRM cells produce TGF-β in SSc remains limited, the multifaceted secretory capacity of TRM cells in other autoimmune settings, together with the highly inflamed SSc lesions, supports the hypothesis that aberrant TRM cell activation may constitute an important local source of TGF-β that accelerates fibrosis [79]. Here, TGFB1 is linked to systemic sclerosis.