PubMed · 10467749
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T Beardsley. 1999. Calculating immunity.. https://doi.org/10.1038/scientificamerican0999-20
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Coeliac disease is a T-cell-mediated autoimmune disease of the small intestine that is induced by ingestion of gluten proteins from wheat, barley, or rye. We postulate that Candida albicans is a trigger in the onset of coeliac disease. The virulence factor of C albicans-hyphal wall protein 1 (HWP1)-contains aminoacid sequences that are identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes. HWP1 is a transglutaminase substrate, and is used by C albicans to adhere to the intestinal epithelium. Furthermore, tissue transglutaminase and endomysium components could become covalently linked to the yeast. Subsequently, C albicans might function as an adjuvant that stimulates antibody formation against HWP1 and gluten, and formation of autoreactive antibodies against tissue transglutaminase and endomysium.
The purpose of this review is to determine the effects of psychosocial stress on antibody response to vaccination in humans, consider possible mechanisms, and identify agenda for future research. Studies of the association between stress and vaccination response in humans were reviewed. There is evidence of a negative association between stress and antibody response to vaccination, which is most apparent with thymus-dependent vaccines and when measured at extended times after vaccination. Preliminary findings implicate the hypothalamic-pituitary-adrenal axis and sympathetic nervous system as potential mechanisms, although a role for unhealthy behaviours cannot be discounted at this stage. Results to date are sufficiently indicative to direct future research to untangling their theoretical ramifications, as well as realising their clinical implications.
The induction of tolerance is essential for the maintenance of immune homeostasis, for the prevention of autoimmune diseases, and to achieve transplantation tolerance. To induce tolerance, the immune system uses several mechanisms, including the deletion of autoreactive T cells, the induction of anergy, and active suppression of autoimmune responses. The mechanisms of thymic deletion and anergy of autoreactive T cells are well characterized, whereas active suppression by T-regulatory (Tr) cells, which has recently emerged as an essential component of the immune response to induce peripheral tolerance, is less well understood. Results from seminal studies by a number of laboratories have renewed interest in CD4+ T cells with regulatory properties. Although many aspects of the mechanisms by which these cells exert their effects have still to be elucidated, it is well established that T-regulatory cells suppress immune responses by means of cell-to-cell interactions or the production of interleukin (IL)-10, transforming growth factor (TGF)-beta, or both. Type-1 Tr (Tr1) cells are defined by their ability to produce high levels of IL-10 and TGF-beta. Tr1 cells specific for a variety of antigens arise in vivo but may also differentiate from naive CD4+ T cells in the presence of IL-10 in vitro. Tr1 cells have a low proliferative capacity. Tr1 cells suppress naive and memory T-helper type 1 or 2 responses by means of production of IL-10 and TGF-beta. Further characterization of Tr1 cells at the molecular level will define their mechanisms of action and clarify their relationship with other subsets of Tr cells. The use of Tr1 cells to identify novel targets for the development of new therapeutic agents, and as a cellular therapy to modulate peripheral tolerance, can be foreseen.