MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I RELATED MOLECULES CONTROL THE DEVELOPMENT OF CD4+8- AND CD4-8- SUBSETS OF NATURAL-KILLER-1.1(+) T-CELL RECEPTOR-ALPHA/BETA(+) CELLS IN THE LIVER OF MICE

Normal mouse liver contains prominent subsets of CD4(+)8(-) and CD4(-)8(-) T cell receptor (TCR)-alpha/beta(+) cells with intermediate TCR levels. We show here that these cells express the natural killer (NK)1.1 surface antigen and have a restricted TCRV beta repertoire that is highly skewed to V beta 7 and V beta 8. Surprisingly, both CD4(+)8(-) and CD4(-)8(-) subsets of NK1.1(+)TCR-alpha/beta(+) cells are absent in the liver of beta 2-microglobulin deficient mice, which do not express major histocompatibility complex (MHC) class I or ''class I-like'' molecules. Analysis of reciprocal radiation bone marrow chimeras established with beta 2-microglobulin deficient and wild-type mice demonstrates that MHC class I expression on radiosensitive (presumably hematopoietic) cells is required for the development of NK1.1(+)TCR-alpha/beta(+) cells in the liver. In the liver of MHC class II deficient mice, the CD4(+)8(-) and CD4(-)8(-) subsets of NK1.1(+)TCR-alpha/beta(+) cells develop normally. Collectively our data suggest that NK1.1(+)TCR-alpha/beta(+) cells in liver require interaction with a MHC class I-related ligand on hematopoietic cells for their development. This unusual property of liver T cells is shared by a subset of CD4(-)8(-)NK1.1(+)TCR-alpha/beta(+) thymocytes, suggesting a common lineage independent of the mainstream of T cell development.