Expression and function of surface antigens on scleroderma fibroblasts

Scleroderma, or systemic sclerosis (SSc), is a disease of connective tissue (skin, bone, cartilage, etc.) which affects multiple body systems. It features an increased deposition of collagen, the major structural protein in connective and other tissues, and this causes formation of fibrous lesions. The process by which SSc arises is still unclear, but inflammation, damage to blood vessels, activation of fibroblasts (cells that give rise to connective tissue), autoimmune mechanisms (involving inappropriate formation of antibodies against the body's own molecules), and interactions between cells and connective tissue components are involved. One known problem is that fibroblasts that are adjacent to blood vessels supplying skin in affected skin areas produce abnormally high levels of collagen. These fibroblasts are often associated with immune cells that contribute to inflammation. To better understand this feature, the reactions between normal or SSc fibroblasts with T cells (T lymphocytes, immune cells important for fighting infection) were studied. About twice as many T cells attached to SSc fibroblasts as to normal fibroblasts. Much of the extra binding was associated with two surface proteins, ICAM-1 (intercellular adhesion molecule type 1) and LFA-1 (lymphocyte function-associated antigen type 1). ICAM-1-mediated adhesion between T cells and normal or SSc fibroblasts was affected similarly by addition of several cytokines, hormone-like proteins that affect functions of lymphocytes and other cells. SSc fibroblasts tended to have higher levels of ICAM-1. The study indicates that in SSc, increased binding of T cells is related to the presence of fibroblasts with higher levels of ICAM-1. (Consumer Summary produced by Reliance Medical Information, Inc.)