Involvement of 4F2 antigen expressed on the MHC-negative target cells in the recognition of murine CD3+CD4-CD8- alpha beta (V alpha 4/V beta 2) T cells.

T cells of an unique phenotype (CD3+CD4-CD8- alpha beta TCR+) develop in vitro from the hematopoietic progenitors, the majority of which carry homologous alpha beta TCR (V alpha 4J alpha 28/V beta 2D beta 1.1J beta 2.6). In the present study, antigen corresponding to the particular alpha beta TCR was investigated, taking advantage of the fact that growth of T cell hybridomas was arrested by their TCR stimulation. Results indicated that both syngeneic and allogeneic thymocytes, particularly from newborn mice, could specifically inhibit the proliferation of a T cell hybridoma with the V alpha 4/V beta 2 TCR (15H1.2). Proliferation of neither TCR-missing hybridoma subclones nor those with unrelated alpha beta TCRs was affected at all. It was also found that embryonal carcinoma (EC) cells without classical MHC antigens could specifically inhibit the proliferation of 15H1.2 cells. We then raised a mAb, 14.37, against an EC line, OTF9, that could interfere with the ability of them to inhibit the growth of 15H1.2. Pretreatment of 15H1.2 cells with anti-V beta 2 and OTF9 cells with 14.37 mAb respectively completely abrogated the growth inhibition of 15H1.2 by OTF9. The 14.37 antigen was a 120 kDa heterodimer glycoprotein consisting of 85 and 36 kDa proteins. In normal lymphoid tissues, the expression of 14.37 antigen exhibited an apparently inverse relationship with that of class I MHC antigens. Thus, ontogenically it was strongly expressed in fetal and newborn mice, rather rapidly declined thereafter, and remained at very low levels in adult organs. In a given stage, the distribution of 14.37 antigen and class I MHC was rather exclusive to each other.(ABSTRACT TRUNCATED AT 250 WORDS)