#FILEMON TAN MD HOUSTON SKIN#

There have been conflicting reports in the literature regarding the role of T cells and the T-helper type 1 (Th1)/T-helper type 2 (Th2) cytokine balance in SSc.

Whole genome gene expression profiling of peripheral blood has demonstrated the presence of a type-I interferon signature in SSc.

#FILEMON TAN MD HOUSTON SKIN#

Skin biopsies of early scleroderma skin demonstrate perivascular infiltrates of mononuclear inflammatory cells, including CD4 + T cells, which produce cytokines and chemokines that induce tissue damage, recruit additional inflammatory cells, and promote extracellular matrix production and fibrosis. Multiple lines of evidence support the importance of immune dysregulation in the pathogenesis of SSc. How the disease process is triggered remains to be established, but current paradigms point towards immune dysregulation as a central process in the pathogenesis of SSc. Pathologically, SSc exhibits three cardinal features: inflammation and autoimmunity, vasculopathy, and excessive extracellular matrix production and deposition.

Systemic sclerosis (SSc) (scleroderma) is a chronic, multisystem autoimmune disease clinically characterized by progressive fibrosis of the skin and internal organs. Authors: Pravitt Gourh Frank C Arnett Shervin Assassi Filemon K Tan Mei Huang Laura Diekman Maureen D Mayes John D Reveille Sandeep K Agarwal (corresponding author)

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