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Autoimmunity
1.
2. Immunological tolerance is a state of unresponsiveness for a particular
antigen. Tolerance mechanisms are needed because the immune system
randomly generates a vast diversity of antigen-specific receptors and some of
these will be self reactive; tolerance prevents harmful reactivity against the
body’s own tissues.
3.
4. Hashimoto’s thyroiditis is a disease of the thyroid that is most common in middle-
aged women and often leads to formation of a goiter and hypothyroidism. The gland
is infiltrated, sometimes to an extraordinary extent, with inflammatory lymphoid
cells. These are predominantly mononuclear phagocytes, lymphocytes and plasma
cells, and secondary lymphoid follicles are common.
The serum of patients with Hashimoto’s disease usually contains antibodies to
thyroglobulin. These antibodies are demonstrable by agglutination and by precipitin
reactions when present in high titer.
The antibodies associated with Hashimoto’s thyroiditis
and primary myxedema react only with the thyroid, so
the resulting lesion is highly localized.
By contrast, the serum from patients with diseases
such as systemic lupus erythematosus (SLE) reacts with
many, if not all, of the tissues in the body.
6. An individual may have more than one autoimmune disease
thyroid antibodies occur with a high frequency in patients with pernicious anemia who
have gastric autoimmunity, and these patients have a higher incidence of thyroid
autoimmune disease than the normal population;
similarly, patients with thyroid autoimmunity have a high incidence of stomach
autoantibodies and, to a lesser extent, the clinical disease itself, namely pernicious
anemia.
The mechanisms of immunopathological damage vary depending on where the disease lies in the spectrum:
where the antigen is localized in a particular organ, type II hypersensitivity (e.g.
autoimmune hemolytic anemia) and type IV cell-mediated reactions, as in type 1
insulin-dependent diabetes, are most important
in non-organ-specific autoimmune disorders such as SLE, type III immune complex
deposition leads to inflammation through a variety of mechanisms, including
complement activation and phagocyte recruitment
7.
8. Effect of neonatal thyroidectomy on Obese chickens
Possible model of T cell help via processing of intermolecular
complexes in the induction of autoimmunity
9.
10.
11. Factors that normally restrain potentially autoreactive cells may include:
regulatory T cells;
hormones (e.g. steroids);
cytokines (e.g. transforming growth factor-β [TGFβ]);
products of macrophages.
Deficiencies in any of these factors may increase susceptibility to
autoimmunity.
Cytokine dysregulation, inappropriate MHC expression, and
failure of suppression may induce autoimmunity
12. Autoimmune processes are often pathogenic. When autoantibodies are
found in association with a particular disease there are three possible
inferences:
the autoimmunity is responsible for producing the lesions of the disease;
there is a disease process that, through the production of tissue damage,
leads to the development of autoantibodies;
there is a factor that produces both the lesions and the autoimmunity.
Autoantibodies secondary to a lesion (the second possibility) are
sometimes found. For example, cardiac autoantibodies may develop after
myocardial infarction.