Page 1195 - Veterinary Immunology, 10th Edition

heart disease. Molecular mimicry may also cause the heart lesions
VetBooks.ir of rheumatic fever in children. Antibodies to the cell wall M-protein

of group A streptococci cross-react with cardiac myosin. Children
infected with certain strains of group A streptococci produce

antimyocardial antibodies and develop heart disease. Some strains
of streptococci may cause acute glomerulonephritis in children as a
result of the production of antibodies cross-reacting with
glomerular basement membranes. Other examples of molecular

mimicry include the Epstein-Barr virus DNA polymerase, which
cross-reacts with myelin basic protein and may be involved in the
induction of multiple sclerosis, and the poliovirus capsid protein
VP2, which cross-reacts with the acetylcholine receptor and may

induce myasthenia gravis.
The integrin CD11a/18 (LFA-1) shares an antigenic determinant
with the outer surface protein of the Lyme disease bacterium, B.
burgdorferi. Patients infected with this organism mount an initial

immune response that may then develop into autoimmunity. In
about 10% of patients with Lyme arthritis, antibiotics fail to resolve
the disease, suggesting that, once triggered, the autoimmune
process can proceed in the absence of the bacterium.

Antibodies against microbial heat-shock proteins are found in the
serum of humans and rats with rheumatoid arthritis, ankylosing
spondylitis, and SLE. Injection of killed Mycobacterium tuberculosis
in Freund's complete adjuvant can cause arthritis in rats, and T cells

from these animals can transfer arthritis to normal syngeneic
recipients. These T cells are responding to HSP 60, a mycobacterial
heat-shock protein (Chapter 26). It has been suggested that
molecular mimicry between microbial and mammalian HSP 60 may

be important in rheumatoid arthritis.
Ankylosing spondylitis is an autoimmune arthritis of humans
that affects the sacroiliac joints, spine, and peripheral joints. Patients
also develop acute anterior uveitis (inflammation of the iris and

neighboring structures in the eye). More than 95% of humans with
ankylosing spondylitis possess the MHC class I allele HLA-B27,
whereas in the normal population, the prevalence of this allele is
less than 8%. The disease results from molecular mimicry between
the hypervariable region of HLA-B27 and antigens found in

Klebsiella pneumoniae and related bacteria. K. pneumoniae is found

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