MHC-linked protection from diabetes dissociated from clonal deletion of T cells

Article Abstract:

Insulin-dependent diabetes mellitus is generally considered to be an autoimmune disease which results when specific T cells invade the pancreatic islets and destroy the insulin-producing beta cells. Fortunately for medical scientists, a similar disease occurs in a strain of mice, called NOD for non-obese diabetes. Previous research has shown that particular alterations in the major histocompatibility complex are associated with the diabetes in these mice; there is an unusual sequence in the I-A complex (part of the murine class II genes), and the I-E complex is absent. Previous research has also shown that the restoration of the I-E complex through molecular biology results in protection from the development of diabetes. One possible hypothesis about the development of diabetes revolves around the concept of clonal deletion. In this process, which occurs early in development, clones of T cells which react with some of the body's own antigens are programmed to die, i.e. are deleted. In the case of diabetes, it might be imagined that clones of T cells which react with the insulin-producing cells were never deleted, and are thus available to cause the disease later in life. In experiments with the NOD mice, it might also be imagined that the restoration of the I-E complex is sufficient to cause the deletion of these clones and hence protection from diabetes. Researchers have now demonstrated, however, that the true situation is more complicated than this, and that clonal deletion is not sufficient to explain the protection of mice from diabetes by the I-E histocompatibility genes. Researchers demonstrated this by breeding transgenic NOD mice with either the natural I-E genes or artificial mutant I-E genes. Both the natural and the mutant I-E genes were subsets of immune cells, and both could mediate the elimination of T-cell clones in the thymus which occurs during clonal deletion. However, only the natural gene protects the mice against the lymphocyte invasion of the pancreas which results in diabetes. These results show that the protection from diabetes does not occur simply through the deletion of self-reactive T cells. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Diabetes, Diabetes mellitus, Genetic aspects, Autoimmune diseases, Histocompatibility antigens

---

Out, damned CLIP! Out , I say!

Article Abstract:

Researchers have advanced the understanding of how antigenic peptides are generated and bind to class II molecules within antigen-presenting cells (APCs). Antigen-processing human leukocyte antigen helps foreign peptides to be inserted into the peptide binding grove of class II molecules.

HLA histocompatibility antigens, Immune response, Immune response regulation, Immunogenetics

---

Immunology: selection for survival?

Article Abstract:

The human immune system is compartmentalized into general, or naive lymphocytes, and faster-responding antigen-stimulated lymphocytes. Work with naive CD8+ T cells indicates the thymus has a role in positive selection of faster-responding lymphocytes.

Methods, Lymphocytes, Immunological research, Immunologic research, CD8 lymphocytes

Similar abstracts:

• Abstracts: Medicine from plants. Pathological growth of regulations. Pharmaceuticals based on biotechnology
• Abstracts: Billion-dollar orphans: prescription for trouble. Anthropologists probe genes, brains at annual meeting. When it comes to evolution, humans are in the slow class
• Abstracts: Animal carcinogen testing challenged. Testing of autoimmune therapy begins
• Abstracts: Dissociation of gp120 from HIV-1 virions induced by soluble CD4. HIV receptors and the pathogenesis of AIDS
• Abstracts: Self-nonself discrimination by T cells. GAD, a Single Autoantigen for Diabetes. Close-up of a killer: new atomic-scale images of the receptor of a killer T cell detail how the immune protein recognizes infected cells

This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.