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PMID: 2112266 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Normal development of mice deficient in beta 2M, MHC class I proteins, and CD8+ T cells.

Science (New York, N.Y.) ·Vol. 248 ·No. 4960 ·1990-06-08 ·Pages 1227-30

Koller BH, Marrack P, Kappler JW, Smithies O

Abstract

Major histocompatibility class I proteins display viral and self antigens to potentially responsive cells and are important for the maturation of T cells; beta 2-microglobulin (beta 2M) is required for their normal expression. Mouse chimeras derived from embryonic stem cells with a disrupted beta 2M gene transmitted the inactivated gene to their progeny. Animals homozygous for the mutated beta 2M gene were obtained at expected frequencies after further breeding. The homozygotes appeared normal, although no class I antigens could be detected on their cells and the animals are grossly deficient in CD4- CD8+ T cells, which normally mediate cytotoxic T cell function.

MeSH Terms
Animals Antigens, Differentiation, T-Lymphocyte/genetics CD4 Antigens/genetics CD8 Antigens Chimera Gene Expression Genes Genes, MHC Class I Histocompatibility Antigens Class I/genetics Lymph Nodes/immunology Mice Mice, Inbred C57BL Mice, Mutant Strains Mutation Spleen/immunology T-Lymphocytes/immunology beta 2-Microglobulin/deficiency,genetics
Chemicals
Antigens, Differentiation, T-Lymphocyte CD4 Antigens CD8 Antigens Histocompatibility Antigens Class I beta 2-Microglobulin
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Koller B H
Department of Pathology, University of North Carolina, Chapel Hill 27599-7525.
Marrack P
Kappler J W
Smithies O
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
0036-8075
Published
1990-06-08
Pages
1227-30
Language
English
Region
United States
NLM ID
0404511
Subset
IM
Grants
NIAID NIH HHS · AI-18785 · United States
NIGMS NIH HHS · GM20069 · United States
NHLBI NIH HHS · HL37001 · United States
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