Fig. 15.13 Some autoimmune diseases that can be transferred across the placenta by pathogenic IgG autoantibodies. These diseases are caused mostly by autoantibodies against cell‑surface or tissue‑matrix molecules. This suggests that an important factor determining whether an autoantibody that crosses the placenta causes disease in the fetus or newborn baby is the accessibility of the antigen to the autoantibody. Autoimmune congenital heart block is caused by fibrosis of the developing cardiac conducting tissue, which expresses abundant Ro antigen. Ro protein is a constituent of an intracellular small cytoplasmic ribonucleoprotein. It is not yet known whether it is expressed at the cell surface of cardiac conducting tissue to act as a target for autoimmune tissue injury. Nevertheless, autoantibody binding leads to tissue damage and results in slowing of the heart rate (bradycardia).
Fig. 15.14 Antibody-mediated autoimmune diseases can is little lasting damage because the symptoms disappear along with appear in the infants of affected mothers as a consequence the maternal antibody. In Graves’ disease, the symptoms are caused of transplacental antibody transfer. In pregnant women, IgG by antibodies against the thyroid‑stimulating hormone receptor antibodies cross the placenta and accumulate in the fetus before (TSHR). Children of mothers making thyroid‑stimulating antibody are birth (see Fig. 10.30). Babies born to mothers with IgG‑mediated born with hyperthyroidism, but this can be corrected by replacing autoimmune disease therefore frequently show symptoms similar to the plasma with normal plasma (plasmapheresis), thus removing the those of the mother in the first few weeks of life. Fortunately, there maternal antibody.
the maternal antibody is catabolized, but in some cases the antibodies cause organ injury before they are removed, such as damage to the conducting tissue of the heart in babies of mothers with SLE or Sjögren’s syndrome. Antibody clearance can be accelerated by exchange of the infant’s blood or plasma (plasmapheresis), although this is not useful after permanent injury has occurred.
Figure 15.15 lists a selection of autoimmune diseases, along with the parts of the immune response that contribute to their pathogenesis. However, although the diseases noted above are clear examples that a particular effector function can drive disease, most autoimmune diseases are not caused solely by a single effector pathway. It is more useful to consider autoimmune responses, like immune responses to pathogens, as engaging the integrated immune system and typically involving T, B, and innate immune cells. Indeed,
Pathogenic Present, but role unclear Pathogenic Present, but role unclear T cells B cells AntibodyDisease Pathogenic Help for antibody Pathogenic Present antigen to T cells Present antigen to T cells Help for antibody Antibody secretion Pathogenic Present antigen to T cells Systemic lupus erythematosus Type 1 diabetes Myasthenia gravis Multiple sclerosis Autoimmune diseases involve all aspects of the immune response
Fig. 15.15 Autoimmune diseases involve all aspects of the immune response.
Although some autoimmune diseases have traditionally been thought to be mediated by B cells or T cells, it is useful to consider that, typically, all aspects of the immune system have a role. For four important autoimmune diseases, the figure lists the roles of T cells, B cells, and antibody. In some diseases, such as SLE, T cells can have multiple roles such as helping B cells to make autoantibody and directly promoting tissue damage. B cells can have two roles as well—presenting autoantigens to stimulate T cells and secreting pathogenic autoantibodies.