''Superantigens'' may shed light on immune puzzle

Article Abstract:

One way bacteria and viruses cause disease is by means of toxins they manufacture that manage to escape the body's immune system. Staphylococcus and streptococcus produce toxins that both stimulate and suppress the immune system. An article in the May 11, 1990, issue of Science magazine details research on the subject of these toxins' effects. The toxins act in many ways like minor lymphocyte stimulating (Mls) antigens, a group discovered more than 20 years ago. When lymphocytes that carry the same major histocompatibility (MHC) proteins (proteins involved in graft rejection) were mixed, although no immune reaction was anticipated, one did occur. T cells, one type of lymphocyte, were stimulated to proliferate (increase in number). The existence of a 'minor' antigen was postulated and, today, researchers believe this antigen is likely to be a protein. Bacterial toxins, too, can stimulate massive T cell proliferation. They are so powerful, in fact, that they may be called 'superantigens'. Understanding how toxins and Mls work requires understanding the way antigens (foreign proteins) are presented to T cells. An antigen-presenting cell (a type of blood cell) displays fragments of the antigen combined with an MHC molecule on its surface. A molecule on the T cell (the receptor) 'recognizes' the complex and is thereby stimulated to respond. This receptor is composed of two molecular chains, with which the complex interacts. Mls antigens, however, complex with MHC proteins and interact with only one chain of the T cell receptor, making it possible to activate many more T cells. These antigens bind with the MHC complex in a way that may enhance their ability to attach antigen-presenting cells to T cells. Researchers believe that bacterial toxins may have evolved this structure to activate the immune system in a major way, and overwhelm it. While the mechanism of this is unknown, secretions from overstimulated immune systems can produce some of the symptoms associated with the toxins. Different ideas on possible functions of the Mls antigens are presented. It is not known whether these molecules exist in humans, although, from an evolutionary standpoint, it seems likely. (Consumer Summary produced by Reliance Medical Information, Inc.)

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The Staphylococcal enterotoxins and their relatives

Article Abstract:

Many types of bacteria, such as strains of Staphylococcus and Streptococcus, produce enterotoxins (toxins that cause symptoms in the digestive tract) leading to food poisoning and shock in people and animals. The mechanisms by which this occurs, however, have not been delineated. Recent work showing that the toxins bind to MHC (major histocompatibility) class II molecules proteins to form complexes has generated new ideas. These results are discussed. Normally an antigen-presenting cell (a type of blood cell) displays the antigen (foreign protein) in a complex with an MHC molecule to the T cell, thereby activating it and stimulating it to replicate. Bacterial toxins appear to do this, although they do not bind to MHC molecules in a conventional manner. They are capable of stimulating T cell replication (proliferation) very rapidly. This occurs because the toxin-MHC complex stimulates T cells via just one component of the T cell receptor molecule, rather than several, as is common for other complexes. Toxins act similarly to one type of naturally occurring molecule, the minor lymphocyte stimulating antigens, discovered many years ago. The similarities are discussed. Reasons for the pathogenic (disease-causing) nature of bacterial toxins are offered, including increased levels of factors produced by antigen-presenting cells, such as interleukin-1, or of factors produced by T cells themselves, such as lymphokines. Some of these factors are associated with symptoms similar to those resulting from exposure to the toxins. Possible evolutionary advantages for bacteria that make toxins are described. Research on the topic of staphylococcal toxins has yielded insights in several domains. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects

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Unraveling the genetics of fragile X syndrome

Article Abstract:

Fragile X syndrome is the most common inherited form of mental retardation. The area of the X chromosome where the site of this genetic defect is located has been identified. This will allow examination of fetuses for mutations (genetic changes) capable of causing this syndrome. With X-linked diseases, males inherit the disease state because they only have one X chromosome, while females are not affected because they have two X chromosomes, with the second, normal one compensating for the defect. However, 20 to 50 percent of the males that have this chromosomal mutation do not have symptoms of disease. Females and males who are asymptomatic carriers of the disease can pass on the defective genes to the next generation. Males can pass the defective gene to their daughters. The children of those daughters, including both males and females, can inherit the defect. Recent research has shown that the DNA (genetic material) segment from the site of the fragile X mutation is much larger in affected individuals then in male carriers without symptoms. The increase in size is large enough so that the area contains more than 20 times as much genetic material than normal. It is thought that the genes inherited from the father undergo a different chemical modification than those inherited from the mother. This chemical modification is called imprinting. It is thought by some scientists that this imprinting determines which genes are involved in the disease state and which are not. (Consumer Summary produced by Reliance Medical Information, Inc.)

Genetic aspects, Fragile X syndrome, Human chromosome abnormalities

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