Page 1196 - Veterinary Immunology, 10th Edition
P. 1196

more frequently than normal in the intestine of patients with active
  VetBooks.ir  ankylosing spondylitis and uveitis, and patients with active disease

               have elevated levels of IgA against Klebsiella in their sera. Cloning
               of B27 into mice and subsequent infection of these animals with K.

               pneumoniae causes an acute spondylitis. HLA-B27–associated
               ankylosing spondylitis has been described in gorillas. Up to 20% of
               wild gorillas may have spondylitis, and the disease has also been
               described in a gibbon, in baboons, and in rhesus macaques.

                  In porcine enzootic pneumonia caused by Mycoplasma
               hyopneumoniae, antibodies to the mycoplasma cross-react with pig
               lungs, and in contagious bovine pleuropneumonia, there is cross-
               reactivity between Mycoplasma mycoides antigens and normal bovine

               lung. It is not known to what extent these autoantibodies contribute
               to the pathogenesis of these diseases. There is a clearer causal
               relationship between Leptospira interrogans infection and the
               development of periodic ophthalmia, the leading cause of blindness

               in horses (Chapter 37).
                  Some microbial superantigens may also trigger autoimmunity.
               The superantigen staphylococcal enterotoxin B activates the same T
               cells that react with myelin and induces an autoimmune

               encephalitis. It has been suggested that a bacterial superantigen
               may trigger rheumatoid arthritis since the T cells in affected joints
               are enriched in cells bearing specific TCR V domains. The only
               known agents that can alter V region gene expression in this way

               are superantigens.


               Epitope Spreading

               In some cases, autoimmunity seems to result from a normal
               immune response against a foreign antigen that subsequently

               “spreads” to recognize self-antigens. When an immune response is
               initiated, the immune response is first directed against a single
               epitope on the inciting antigen. However, as the process continues,
               T and B cell receptors diversify, and responses begin to be directed
               against additional epitopes. At first they will react with other

               epitopes on the same protein. Eventually responses may spread to
               epitopes on autoantigens. Epitope spreading has been
               demonstrated in diseases such as thyrotoxicosis and diabetes

               mellitus and may account for some of the difficulties encountered




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