| First Author | Fujiura Y | Year | 1996 |
| Journal | J Immunol | Volume | 156 |
| Issue | 8 | Pages | 2710-5 |
| PubMed ID | 8609387 | Mgi Jnum | J:111566 |
| Mgi Id | MGI:3654409 | Doi | 10.4049/jimmunol.156.8.2710 |
| Citation | Fujiura Y, et al. (1996) Development of CD8 alpha alpha+ intestinal intraepithelial T cells in beta 2-microglobulin- and/or TAP1-deficient mice. J Immunol 156(8):2710-5 |
| abstractText | 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. |
