๐ ็ธฝ็ฎ้ ๏ฝ ๐ ่ฑๆๅๆ๏ผๆฌ็ฏ๏ผ ๏ฝ ๐ ๅฎๆด็ฟป่ญฏ ๏ฝ โญ ็ฒพ่ฏ็ญ่จ
PATHOGENESIS
As in most inflammatory diseases, genetic predisposition contributes to the development of LS, as it may be found in monozygotic and fraternal twins. In addition, association with the MHC class II antigen HLA-DQ7 was observed in a relatively large study. The existence of a relevant susceptibility gene for sclerosis within this region of the MHC is underlined by the finding that the same region is associated with a greater risk of organ-specific autoimmune diseases. Even though inflammation seems essential for initiation and progression of LS, the mechanisms leading to subsequent sclerosis remain speculative. Increased production of IL-6, TNF, and collagen (types I, III, and V) is thought to promote the sclerosis.
Perhaps with the exception of autoantibodies against extracellular matrix protein 1 (ECM-1), no specific immunologic parameters have been identified in patientsโ sera that clearly correlate with either risk of disease or disease activity. IgG autoantibodies against ECM-1 are found in 80% of patients with LS. Moreover, in female patients with LS, there is a higher prevalence of autoimmune diseases (especially autoimmune thyroid disease) and ANA positivity than in male patients with LS.
Oxidative stress may also play a role in the pathogenesis of LS, based upon analysis of lesional skin that showed lipid peroxidation of epidermal basal cell layers, oxidative DNA damage, and oxidative protein damage.