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Autoimmune diseases develop when the immune system starts producing antibodies and T cells that are targeting components of the body. Such state occurs when the ability to recognition of self is disturbed and the immune cells attack healthy cells. The autoimmune diseases are frequently accompanied by self-destruction which is realized via apoptosis. There are two signaling pathways how the immune cells induce apoptosis in the target cells: 1) receptor-mediated; 2) receptor-independent. In the first mechanism, so called “death receptors” that are located on plasma membrane of the target cell are involved, while their “death ligands” are either located on the surface of the immune cell, or released by these cells and acting in free form. The corresponding ligand-receptor interactions cause activation of “death receptors” which use special “death domains” for contacting with specific intracellular signaling proteins and formation of death-inducing signaling complex (DISC). It is considered that this complex is capable of interacting with procaspase 8 and activating this initiator caspase. It is also probable that from this moment (activation of caspase 8), cascade of the apoptotic events gains irreversible character (Ashkenazi & Dixit, 1998). The receptor-independent mechanisms of apoptosis induction in which the immune cells take part, differ significantly (Vermijlen et al., 2001). These mechanisms are based on the ability of cytotoxic T cells to induce formation of special pores in plasma membrane of the target cells. Through these pores, calcium cations and protein granzyme B penetrates the target cells where they directly activate apoptotic enzymes – the caspases. Fas-receptor that belongs to a family of tumor necrosis factor (TNF) receptors (Orlinick & Chao, 1998) is a typical “death receptor”. It is known that TNF is produced by activated macrophages and T cells as a host response to infection (Tartaglia & Goeddel, 1992). Its interaction with specific plasma membrane receptors induces production of transcription factors NF-kB and AP-1 which take part in the activation of specific genes whose products are involved in the inflammation and immunomodulation (Tartaglia & Goeddel, 1992).

Cell Surface Glycans at SLE – Changes During Cells Death, Utilization for Disease Detection and Molecular Mechanism Underlying Their Modification