Open AccessMost gamma delta T cells develop normally in beta 2-microglobulin-deficient mice.
Author(s) -
Isabel Correa,
Mark Bix,
NanShih Liao,
Maarten Zijlstra,
Rudolf Jaenisch,
David H. Raulet
Publication year - 1992
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.89.2.653
Subject(s) - beta (programming language) , beta 2 microglobulin , cd8 , biology , microbiology and biotechnology , major histocompatibility complex , t cell receptor , mhc class i , gamma delta t cell , delta , antigen , t cell , immunology , immune system , physics , astronomy , computer science , programming language
The specificity of T cells bearing gamma delta T-cell receptors (gamma delta+ T cells) is poorly characterized. Earlier studies suggest that like alpha beta+CD8+ T cells, some gamma delta+ T cells may recognize antigens associated with class I major histocompatibility complex molecules. alpha beta+CD8+ T cells are nearly absent in class I-deficient mice (mutant for beta 2-microglobulin), reflecting a requirement for intrathymic "positive selection" of these cells by class I molecules. Here, we examine whether the development of gamma delta+ T cells is altered in the beta 2-microglobulin mutant mice. We show that the cellularity, marker expression, repertoire, and functional competence of gamma delta+ T cells are not detectably deficient in beta 2-microglobulin mutant mice. We conclude that class I expression is unnecessary for the development of most gamma delta+ T cells.