Autoantibody Responses

Some clinically important autoantibodies are directed against hormone receptors, for example thyrotoxicosis in Basedow's disease is caused by autoantibodies that stimulate the TSH receptor, and myasthenia gravis is caused by blockage of the acetylcholine receptor by specific autoantibodies. Other antibody-induced diseases mediated by antibodies, directed against hormones and other cellular self antigens, include Hashimoto thyroiditis (induced by anti-thyroglobulin and anti-mitochondrial autoantibodies), pernicious anemia (anti-intrinsic factor), pemphigus vulgaris (anti-desmosome) Guillain-Barre syndrome (ascending paralysis caused by specific myelin auto-antibodies), and scleroderma (involving anti-collagen antibodies). Other immunopathologies involving autoantibodies include transplant rejection as a result of endothelial damage (especially in xenogeneic transplants), and tumor rejection caused by antibodies against tumor-associated antigens present on neoplastic cells (especially relevant for lymphohematopoietic

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The Pathological Immune Response 111 Table 2.12 Mechanisms Of Autoantibody Induction

Possible mechanisms

Autoimmune pathology or immunopathology

Polyclonal B-cell activation

Lipopolysaccharides, viruses, chronic parasitic infection

Anti-tat (HTLV-1), anti-H. pylori, or anti-streptococcus crossreacting with self-antigens

Molecular mimicry (overall very rare)

Exposure of hidden autoantigens Cytopathic effects of infectious agents tumors). However, in general the detection of autoantibodies does not necessarily correlate with evidence of pathological changes or processes. In fact, our detection methods often measure low-avidity autoantibodies that may have no direct disease-causing effects.

Exactly how autoantibody responses are induced remains to be clarified. As explained earlier (in the discussion of immunological tolerance) such IgG responses cannot be induced without T help. Thus, intensive research is currently focused on those mechanisms by which T cell help for autoreactive B cells is regulated; Table 2.12 sums up some of the possible mechanisms.

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