Development of CD8 alpha alpha+ intestinal intraepithelial T cells in beta 2-microglobulin- and/or TAP1-deficient mice. NLM AIDSLINE Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.

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Development of CD8 alpha alpha+ intestinal intraepithelial T cells in beta 2-microglobulin- and/or TAP1-deficient mice.

J Immunol. 1996 Apr 15;156(8):2710-5. Unique Identifier : AIDSLINE MED/96183222
Fujiura Y; Kawaguchi M; Kondo Y; Obana S; Yamamoto H; Nanno M; Ishikawa H; Department of Microbiology, Keio University School of Medicine,; Tokyo, Japan.


Abstract: The development of CD8+ intestinal intraepithelial T lymphocytes (IEL) was analyzed in mice that are deficient in the expression of MHC class I molecules, owing to either a mutated beta 2-microglobulin (beta 2m) gene or a mutated transporter associated with Ag processing 1 (TAP1) gene, and in mice doubly homozygous for beta 2m and TAPI mutations. In all mutant mice, the population size of major CD8 alpha alpha+ and CD8 alpha beta+ alpha beta-IEL subsets was reduced drastically, and this resulted in a conspicuous decrease in the total number of alpha beta-IEL. Concomitantly, a compensatory two- to threefold increase in the number of gamma delta-IEL consisting mostly of CD8 alpha alpha+ subset was noted. In radiation bone marrow chimeras, this wild-type/mutant phenotype was determined by the genotype of radioresistant host cells, but was not determined by the genotype of reconstituting bone marrow-derived cells. In beta 2m X TCR-delta double mutant mice, however, the CD8 alpha alpha+ but not CD8 alpha beta+ alpha beta-IEL subset expanded dramatically. Thus, in the absence of gamma delta-IEL, alpha beta-IEL in beta 2m-deficient mice outnumbered those in wild-type littermates. These results indicate that the generation of CD8 alpha alpha+ lymphocyte population of alpha beta- and gamma delta-IEL is not dependent, but that of CD8 alpha beta+ lymphocyte population of alpha beta-IEL is dependent on beta 2m- and/or TAP1-dependent MHC class I molecules, expressed by the controlling cells present in the anatomical site, where the development of IEL takes place.
Keywords: beta 2-Microglobulin/*DEFICIENCY/*GENETICS Animal Antigens, CD8/*GENETICS/RADIATION EFFECTS ABC Transporters/*GENETICS Base Sequence Bone Marrow/IMMUNOLOGY Cell Differentiation/IMMUNOLOGY CD8-Positive T-Lymphocytes/*CLASSIFICATION/IMMUNOLOGY/RADIATION EFFECTS Epithelium/CYTOLOGY/IMMUNOLOGY/RADIATION EFFECTS Female Histocompatibility Antigens Class I/GENETICS Immunophenotyping Intestinal Mucosa/*CYTOLOGY/IMMUNOLOGY/RADIATION EFFECTS Lymphocyte Transformation/GENETICS Male Mice Mice, Inbred C57BL Mice, Mutant Strains Molecular Sequence Data Radiation Chimera Receptors, Antigen, T-Cell, alpha-beta/GENETICS Receptors, Antigen, T-Cell, gamma-delta/GENETICS Support, Non-U.S. Gov't Thymus Gland/CYTOLOGY JOURNAL ARTICLEKWDbeta2-microglobulin/KWDdeficiency/KWDgeneticsanimalantigens,cd8/KWDgenetics/radiationeffectsabctransporters/KWDgeneticsbasesequencebonemarrow/immunologycelldifferentiation/immunologycd8-positivet-lymphocytes/KWDclassification/immunology/radiationeffectsepithelium/cytology/immunology/radiationeffectsfemalehistocompatibilityantigensclassi/geneticsimmunophenotypingintestinalmucosa/
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Copyright © 1996 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

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