| Although the cause of scleroderma is unknown, but recent research suggests that many different anti Hugh scleroderma, clinical subtypes associated with immune genetic. In the first generation of scleroderma relatives, MHC¢ò expression enhancement, e.g., HLA-DR1, DR3, DR5 associated with scleroderma, reported resistance to localized isomerase (ScL-70) and HLA-DR5 and anti-centromere antibody HLA- DR1, suggesting HLA- parting with scleroderma-related autoantibodies and clinical subtypes. The DR3 representatives increased incidence of pulmonary fibrosis, DR52 and extensive skin sclerosis, nervous system involvement rate in patients B8 and DR3 is increased, suggesting DR3, DR52 and B8 representatives sicker. |
