Beta2-microglobulin deficient mice lack CD4-8+ cytolytic T cells

Article Abstract:

Beta2-microglobulin (beta2-m) is a protein that is structurally part of a number of molecules that are involved with the immune system, including the class I major histocompatibility complex (MHC) antigens, which are involved in the recognition of foreign antigens on cells. The MHC class I molecules are involved in the presentation of antigen to other cells of the immune system so that an immune response can occur. Beta2-m is also involved in the transport of immunoglobulins from mothers' milk across the membranes of the intestines of neonates. The beta2-m molecule has been disrupted by the insertion of a genetically engineered non-functional beta2-m gene into mouse embryos. Mice that were homozygous, or contained two copies of the non-functional gene were indistinguishable from mice that had received one copy or from the mice that did not receive the non-functional gene, except they did not express any beta2-m and expressed very little of the MHC class I heavy chains, which contain beta2-m. The mice did not have a function receptor which mediates the uptake of immunoglobulin across the intestines, nor did they possess cells that had the T cell receptor and the CD8+ molecule, which could cause destruction of other cells. This data shows that for cytotoxic T cells to develop, they must interact with MHC class I antigens, while the development of other subsets of T cells do not require this interaction. The mice in these experiments were kept in an environment free from pathogens. Future studies will show how they will be able to respond to pathogens or to ward off the development of tumors. The MHC class I molecules are also involved in the rejection of cells and organs that are transplanted. Therefore, these mice should be able to accept organ transplants without previous treatment with immunosuppressive agents. This study furthers the understanding of the immune system and provides information that may be applicable to clinical situations, such as the manipulation of the response to viral and bacteria infections and organ transplantation. (Consumer Summary produced by Reliance Medical Information, Inc.)

Transplantation immunology, CD8 lymphocytes

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Some savage cuts in defence

Article Abstract:

The disruption of a particular gene can lead to the understanding of the function of the gene. Beta2-microglobulin (beta2-m) is a protein that is structurally part of a number of molecules that are involved with the immune system, including the class I major histocompatibility complex (MHC) antigens, which are involved in the recognition of foreign antigens on cells. The disruption of a gene that codes for beta2-m was accomplished by the insertion of a genetically engineered non-functional beta2-m gene into mouse embryos. Mice that were homozygous, or contained two copies of the non-functional gene, were indistinguishable from mice that had received one copy or from mice that did not receive the non-functional gene, except they did not express any beta2-m and expressed very little of the MHC class I heavy chains, which contains beta2-m. It has been previously thought that cell-cell interactions during embryogenesis were programmed by molecules similar to beta2-m. Although this has been previously discredited, this study confirms that this is not true. There are two substantiated functions known to beta2-m. One function is the presentation of antigens by class I MHC molecules to T cells, which contain the T cell receptor, and another molecule known as CD8, which can destroy cells with foreign antigens. The other function is the transport of immunoglobulins from mothers' milk across the membranes of the intestines of neonates. Both functions are lacking in the mice which contain the nonfunctional beta2-m molecule. It is noteworthy that the mice appear normal except for the two missing functions, in part because complex organisms have evolved cells and molecules that are specialized, including those involved in immunity. The cells of the immune system are used sporadically, only when foreign agents are present. The mice in this study have been kept free from disease-causing organisms. Future studies will see how these mice can survive against pathogens. (Consumer Summary produced by Reliance Medical Information, Inc.)

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Transcription factor AP-2 essential for cranial closure and craniofacial development

Article Abstract:

The transcription factor AP-2 affects cranial closure and craniofacial development during embryogenesis. The AP-2(super -/-) mutant mice exhibit perinatal death with cranio-abdominoschisis and severe dismorphogenesis of the skull, face, sensory organs and cranial ganglia. Apoptosis in the midbrain and anterior hindbrain plus proximal mesenchyme of the first brachial arch increases with the failure of cranial closure between 9 and 9.5 days postcoitum. No loss of expression of twist occurred due to the failure of cranial closure.

Abnormalities, Physiological aspects, Genetic transcription, Transcription (Genetics), Skull

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