Viruses in autoimmune disease

Viruses have been found to be associated with the presence of autoimmune disease in humans and other animals. They may cause autoimmune disease by a number of different mechanisms including polyclonal activation of lymphocytes (e.g. Epstein-Barr virus), release of intracellular organelles due to destruction of

8 cell stimulated by major determinant oil foreign Ag Same epitope is expressed on .self-Ag

8 cell stimulated by major determinant oil foreign Ag Same epitope is expressed on .self-Ag

Foreign Ag Major epitope
Self-Ag Cross-reacting epitope

^P^ Ab binds epitope on foreign Ag

A I) also binds epitope1 on self-Ag

Figure 5.5 The role of antigen mimicry in autoimmune disease

If the major antigenic determinant of an infectious agent is similar antigenically to a self-antigen, then the response elicited by the microorganism can result in an autoimmune response.

^P^ Ab binds epitope on foreign Ag

A I) also binds epitope1 on self-Ag

Figure 5.5 The role of antigen mimicry in autoimmune disease

If the major antigenic determinant of an infectious agent is similar antigenically to a self-antigen, then the response elicited by the microorganism can result in an autoimmune response.

host cells, antigen mimicry (Figure 5.5; Table 5.6), induction of abnormal MHC Class II antigen expression and functional impairment of immunologically regulatory cells, e.g. T suppressor cells.

Role of Epstein-Barr virus in autoimmune disease: Epstein-Barr virus (EBV) infects B cells and directly causes their activation. Although some autoreactive B cells escape elimination in the bone marrow, they are usually prevented from producing autoreactive antibody either by a lack of antigen-stimulated T cell help or by T cell-mediated suppression. However, if a potentially autoreactive B cell is infected by EBV it can proliferate and differentiate into a plasma cell without the help of T cells. Infected cells from both healthy individuals and patients with rheumatoid arthritis secrete polyclonal IgG and IgM anti-immunoglobulin antibodies (rheumatoid factor) but B cells from patients produce more, higher affinity antibody than those from normal persons.

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