In summary, it may be proposed that there is a possible involvement of HLA−G in SSc pathogenesis, as the elevated HLA−G membrane expression by PBMC and the increased sHLA−G plasma levels may reflect an attempt to control the immune derangement occurring in this disease and concur, through TGF-β up-regulation, with fibroblast activation and fibrosis development (34). Here, HLA-G is linked to systemic sclerosis.