|MadSci Network: Immunology|
The cytotoxic/suppressor component of T cells are characterized by the presence of CD8 antigen on their surface. These cells recognize antigen presented on the surface as antigenic peptide complexed with class I MHC molecules, which are classically known as transplantation antigens because genetic differences in these molecules induce rapid graft rejection. Class I molecules are found on virtually all cells and are specialized to present antigen synthesized endogenously, within host cells, such as cell associated viral or tumor antigens. In this manner, the cytotoxic (killer) T cells bind to cells that express the antigen to which they react (usually virus or tumor) and kill those cells through the release of cytokines (also called lymphokines) T suppressor cells act to inhibit T helper cells from function, thereby preventing the initiation of the response. They can also act directly on B cells or effector T cells to inhibit their activity, but this is probably less important than their inhibition of T helper cell activity. Some autoimmune diseases (immune responses against one's own tissues) are thought result from defects in T suppressor cell function. The suppressor situation has become somewhat complicated, since some suppression can be explained by the reciprocal inhibition of T helper 1 (Th1) and T helper 2 (Th2) cells. For example, addition of Th1 cells to a culture in which antibody synthesis was the measure of T cell help would look like T suppressor cell activity. Indeed, antibody synthesis would be inhibited in a situation where it would be expected without the addition of Th1 cells. However, one would also see an increase in delayed hypersensitivity if it were also measured in the system. Both T and B memory cells are cells that have undergone differentiation and clonal expansion. These cells continue to circulate and upon exposure to antigen will undergo rapid clonal expansion to provide a secondary immune response. This process ensures that the second response is much faster than the primary immune response to a foreign antigen.
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