Immune System and Autoimmune Diseases

They act in a sequential proteolytic cascade which gives tremendous amplification of the response.

Parietal cell antibodies detected by immunofluorescence in stomach sections are important markers of inflammatory atrophic gastritis and subsequent pernicious anaemia.

The constant region of IgM and of IgGI, IgG2 and IgG3 antibodies binds C1q after the antibody has complexed with antigen. 

Both T-cells and B-cells possess antigen specific receptors.

5 days or more are required for B-cell proliferation, differentiation into plasma cells, and the secretion of a large enough amount of antibody for it to be readily detected systemically.

Adoptive transfer experiments helped establish that immunological memory, one of the hallmarks of the adaptive immune response, is a property of small lymphocyte.

SLE is a disease involving antibodies to non-organ specific antigens.

Tolerance is a specific immunological non-responsiveness. Whilst tolerance can be induced to any antigen, the mechanism is thought to have evolved as a means of preventing the maturation of pathogenic self-reactive lymphocytes.

These mice spontaneously develop an inflammatory attack on the islets of Langerhans.

Individuals with HLA-DR2 are more at risk of developing multiple sclerosis than those with other HLA-DR specificities. 

Natural antibodies are low affinity IgM.

Transfection with rearranged genes encoding a red cell autoantibody causes early disease in normal animals.

Graves' disease is a fairly frequent organ-specific disease and is often found in association with pernicious anaemia.

In order to be T-cell epitopes, i.e. peptides, they must be derived by antigen processing. Qualitative and/or quantitative alterations in processing can lead to greatly increased production of cryptic peptides and thus, may trigger autoimmune disease.

The mutation of the antibody variable region genes in B-cells in the germinal centre produces a range of antibody affinities, and those B-cells bearing higher affinity antibody will be favourably selected for further stimulation by antigen.

Recurrent foetal loss is a characteristic of antiphospholipid syndrome. In experimental situation, passive transfer of cardiolipin antibodies into mice also results in recurrent foetal loss.

Macrophages have an impressive range of functions but appear unable to prime naive lymphocytes. 

The normally acquired tolerance to the dietary protein wheat gluten breaks down in celiac disease. 

In Graves' disease, there is hyperthyroidism due to stimulating autoantibodies to the TSH receptor, which continuously mimic the effect of TSH but which are not subject to the feedback mechanisms which lower the level of TSH, once sufficient thyroid hormone has been produced. 

Transient neonatal autoimmune diseases are seen due to the transplacental transfer of maternal IgG autoantibodies in those diseases in which IgG is the effector component of the autoimmune response. The disease will be of the same type as seen in the mother because the autoantibodies will determine the target organ specificity. The neonatal disease resolves after a few weeks as the maternal IgG is catabolised.