Serum level of sFas in patients with Wegener’s granulomatosis

Excerpt

Apoptosis is considered one of the potential mechanisms responsible for development of autoimmune phenomena. Apoptosis or programmed cell death is a highly regulated biochemical process that precisely orchestrates the orderly breakdown of the cell resulting in its death. It has been suggested that defective apoptosis may contribute to the development of autoimmune phenomena due to expansion of subpopulations of lymphocytes that are eliminated by apoptosis under physiological conditions [1]. Apoptosis is a very complex process that may be initiated by a number of signals. The signals may be internal (the mitochondrial or intrinsic pathway) or external, mediated by so-called death receptors. The death receptors belong to the tumor necrosis/nerve growth factor receptor superfamily and trigger apoptosis after binding with the appropriate ligand. The Fas or APO-1 (CD95) is one of the six currently identified death receptors. It is a cell surface protein with a molecular weight of 42–52 kDa. Triggering of Fas by its ligand results in rapid induction of apoptosis. The ligand (FasL) is expressed on the cell surface of activated T cells and is involved in regulation of T-cell and B-cell interactions, especially killing of harmful cells (e.g., virus infected). The sFas (sAPO-1) is a soluble fragment of the Fas receptors. The sFas can be determined in the serum and may be considered a marker of apoptosis [2]. …