MTS-32 monoclonal antibody defines CD4+8- thymocyte subsets that differ in their maturation level, lymphokine secretion, and selection patterns.

We have previously described MTS-32 as identifying an Ag on both thymic stromal cells and thymocytes. In contrast with CD4+8+ and CD4-8+ thymocytes, of which the vast majority are MTS-32+, a notable subset of CD4+8- thymocytes is MTS-32-. Here we show that with regard to heat-stable Ags, Qa-2, and CD69 expression CD4+8- MTS-32- thymocytes are phenotypically enriched in mature cells when compared with their MTS-32+ counterparts.

Tissue distribution and polymorphism of minor histocompatibility antigens involved in GVHR.

A graft-vs-host reaction (GVHR) develops after major histocompatibility complex (MHC)-compatible bone marrow-transplantation. In the genetic combination studied, B10.D2 donor cells differed from those of (DBA/2 x B10.

A kinetic study on the deletion of thymic, peripheral, and gut-associated V beta 6+ T cells in an Mls-1b BALB/c colony infected with an exogenous mouse mammary tumor virus.

Mls-1a expression results in the deletion of T cells bearing V beta 6 chains of the TCR. However, V beta 6+ T cells are also deleted in Mls-1b BALB/c mice that have been infected with an exogenous mouse mammary tumor virus (swiss mice) via maternal milk intake, and whose open reading frame region is markedly similar to that of the provirus Mtv-7. In this report we describe the kinetics of V beta 6+ T cell deletion in the thymus, spleen, lymph nodes, and gut-associated lymphoid populations of these BALB/c mice from the early weeks of life to 6 mo of age.

Tissue distribution of Mtv-7-like exogenous retroviral transcripts and clonal deletion of V beta 6+ T cells in Mls-1b BALB/c mice.

We have previously described an Mls-1a-like clonal deletion of mature CD4+ T cells which express V beta 6 and V beta 8.1 chains of the TCR in half of the mice of a BALB/c, Mls-1b colony (BALB/c IC). This occurs in the absence of the Mtv-7 provirus which is responsible for the clonal deletion in Mls-1a mice.