| 초록 |
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by B lymphocyte hyper- reactivity and the production of autoantibodies. It is thought that these autoantibodies form immune complexes, which deposit in tissues and trigger inflammation, thereby contributing to disease pathology. Insight into the pathogenesis of the disease has deepened in recent years. In particular, studies on apoptosis and clearance of apoptotic cells in lupus have shed a new and intriguing light on the development and course of the disease. The disturbances in the elimination of apoptotic cells might result in the presentation of nucleic acid-protein complexes, such as chromatin and small nuclear ribonucleoprotein, to the immune system in such a way that tolerance can be broken and autoimmunity occurs. In addition, growing evidences suggest that recognition of nucleic acid motifs by Toll-like receptors (TLRs) may play a role in both the activation of antinuclear B cells and in the subsequent disease progression after immune complex formation. Recent work that suggests a role for the B-cell receptor and Fca receptors in delivering nuclear antigens to intracellular compartments allowing TLR activation by endogenous nucleic acids. Further understanding of the role of apoptosis and TLRs in pathological autoreactivity will lead to important insights into the pathogenesis of SLE. |
