The inappropriate response to self-antigens that characterizes all autoimmune diseases can involve either the humoral or cell-mediated branches of the immune system. Identifying the defects underlying human autoimmune diseases has been difficult; more success has been achieved in characterizing the immune defects in the various animal models. Each of the animal models has implicated the CD4+ T cell as the primary mediator of autoimmune disease. For example, the evidence is quite strong that, in mice, EAE is caused by CD4+ TH1 cells specific for the immunizing antigen. The disease can be transferred from one animal into another by T cells from animals immunized with either MBP or PLP or by cloned T-cell lines from such animals. It also has been shown that disease can be prevented by treating animals with anti-CD4 antibodies. These data are compelling evidence for the involvement of CD4 in the establishment of EAE.
T-cell recognition of antigen, of course, involves a trimol-ecular complex of the T-cell receptor, an MHC molecule, and antigenic peptide (see Figure 9-16). Thus, an individual susceptible to autoimmunity must possess MHC molecules and T-cell receptors capable of binding self-antigens.
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.