Approximately 20% of the population is affected by autoimmune or inflammatory diseases mediated by an abnormal immune response. A characteristic feature of autoimmune disease is the selective targeting of a single cell type, organ or tissue by certain populations of autoreactive T-cells. Examples of such diseases include rheumatoid arthritis, insulin-dependent diabetes mellitus, and systemic lupus erythematosus (SLE), all of which are characterized by chronic inflammation, tissue destruction and target organ malfunction. Although strong evidence links most autoimmune diseases to specific genes, considerable controversy prevails regarding the role of regulatory T-cell populations in the disease process. These cells are now also believed to play a key role in mediating transplantation tolerance and inhibiting the induction of tumor immunity. Though the concept of therapeutic immune regulation aimed at treating autoimmune pathology has been validated in many animal models, the development of strategies for the treatment of human autoimmune disorders remains in its infancy. The main obstacles to this include the conflicting findings of different model systems, as well as the contrasting functions of regulatory T-cells and cytokines involved in the development of such disorders. This review examines the role of regulatory T-cells in the pathogenesis of autoimmunity and describes the therapeutic potential of these cells for the prevention of immune-mediated pathologies in the future. Although much remains to be learned about such pathologies, a clearer understanding of the mechanisms by which regulatory T-cells function will undoubtedly lead to exciting new possibilities for immunotherapeutics.
This chapter discusses metabolism and turnover of cell membranes. Alterations of structure of the surface of the cell that are linked to its growth cycle may be of particular importance in malignancy. Fluorescein-labeled wheat germ agglutinin binds at the surface of 3T3 cells only during mitosis and early Gl while virus-transformed cells bind the fluorescent material throughout the cycle. A number of other membrane surface changes have been observed in the mitotic period, such as an increase in blood group H activity in HeLa cells, a decrease of immunoglobulins embedded in the surface of lymphoma cells, and an increased electrophoretic mobility of human osteosarcoma cells, which can be reduced by treatment of these cells with neuraminidase. The H-2 and Moloney leukemia virus-determined cell surface antigens in certain mouse cells are maximal during the Gl phase, drop during S phase, and remain low until the next Gl period. When the cells are synchronized by a double thymidine block method, alterations of B & H activity are observed throughout the cell cycle.
