Stimulation of protein tyrosine phosphorylation by the B-lymphocyte antigen receptor

Article Abstract:

Immunoglobulins are antibodies that are generally considered to be free-floating molecules of immunity. However, some immunoglobulins serve as membrane-bound antigen-binding receptors on the surface of B-cells. Signaling by membrane-bound immunoglobulin begins the sequence of B-cell maturation and activation in response to specific antigens. Research has shown that when the antigen receptors of immature B-cells are cross-linked, the cells are inactivated, a process that may prevent the development of antibodies to 'self' antigens. Conversely, the cross-linking of the receptors of mature B-cells, either with antigen or antibodies against the antibodies, result in the activation of the B-cells and the production of specific antibodies. Using cross-linking of the membrane receptors as an experimental model, researchers have investigated the cellular signals through which the membrane receptors exert their influence on the cell. They found that the process involves tyrosine phosphorylation, indicating that the activation of B-cells is another cellular signalling mechanism that involves phosphorylation. In this process, the activation of particular enzymes, called protein kinases, cause the attachment of a phosphate to tyrosine, an amino acid found in the backbone chain of most proteins. Once the tyrosines of a protein have been phosphorylated, the behavior of the protein changes, thus carrying the message that key events have occurred elsewhere in the cell. (Consumer Summary produced by Reliance Medical Information, Inc.)

Cellular signal transduction, Immunoglobulins, B cells, Cell receptors, Lymphocytes

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Tolerance: a second mechanism

Article Abstract:

The immune system is designed to recognize and destroy foreign substances, such as viruses and bacteria. It is critical that the immune system be able to distinguish between foreign invaders and substances that are naturally present in the body. If components of the self are mistaken for invaders and attacked by the immune system, autoimmune disease results. Thus the immune system must develop a tolerance for or unresponsiveness to components of the self; how this may occur is discussed. Substances that immune cells react to are called antigens, whether they are foreign or part of the self. Every time immune cells come in contact with an antigen, they evaluate whether it is native or foreign to the body. The critical issue for the health of the organism is whether the immune cells produce antibodies against the antigen; once specific antibodies are formed, they will attack the antigen upon subsequent contact with it. Immunological tolerance to self is acquired or developed by certain immune cells called T cells and B cells. Immature B or T lymphocytes are particularly open to developing long-lasting unresponsiveness to substances naturally present in the self. Scientists are questioning how the healthy unresponsiveness of immature lymphocytes is continued by mature lymphocytes. There is some evidence that mature B cells and mature helper T cells can become unresponsive when they come in contact with the antigen; as a result they do not produce antibodies that would destroy components of the self.

Development and progression, Immunologic diseases, Antigen-antibody reactions

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Loss of pancreatic islet tolerance induced by beta-cell expression of interferon-gamma

Article Abstract:

Previous research has shown that techniques of molecular biology can be used to attach the interferon-gamma gene to the insulin gene in mice to induce diabetes. The gene attachment was performed so that the insulin gene promoter would turn on interferon-gamma as well; the rationale is that this would occur only within the insulin-producing beta cells of the pancreatic islets, and thus these cells specifically would produce interferon-gamma within the living mouse. However, it is not clear from the original experiments whether the destruction of the beta cells and the subsequent diabetes were a result of some primary effect of the interferon gene or a result of the stimulation of the destruction of the beta cells by the mouse's own immune system. New experiments demonstrate that the presence of the interferon-gamma stimulates an immune reaction against the beta cells and destroys them. This was demonstrated by showing that normal, histocompatible, beta cells were also destroyed when implanted into the diabetic mice. This effect was clearly mediated by T cells. Furthermore, when lymphocytes from the affected mice were removed and challenged with normal beta cells, they destroyed these cells. The results suggest that the presence of interferon-gamma apparently breaks the normal tolerance of the immune system for the body's own pancreatic beta cells, which then begins the sequence of events leading to cell destruction. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models, Physiological aspects, Diabetes, Diabetes mellitus, Autoimmune diseases, Interferon, Islands of Langerhans, Islets of Langerhans

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