Mouse alloantibodies capable of blocking cytotoxic T-cell function. I. Relationship between the antigen reactive with blocking antibodies and the Lyt-2 locus.

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Abstract
To produce alloantibodies [allo-Ab] to cytotoxic T[thymus-derived]-cell receptors, hyperimmune anti-lymphocyte antisera were raised in mice of various strain combinations and were tested for their ability to block allogeneic cell-mediated lymphocytotoxicity (CML) in the absence of complement at the T killer cell level. Most sera failed to show any significant and reproducible inhibitory effects. Among C3H anti-B10.BR antisera, some sera could significantly inhibit CML. This effect was attributable to Ab reacting with the killer population rather than the target cells, because the sera inhibited B10 anti-C3H CML but not C3H anti-B10 CML. Among mouse strains tested, A/J, BALB/c, B10 and B6 strains were sensitive to the inhibitory effect of the sera whereas AKR, CBA, C3H and DBA/2 strains were insensitive. This sensitivity of killer cells to the inhibitory effect correlated well with the strain distribution of the Lyt-2.2 antigen. In the presence of complement, these same sera were toxic to 100% of spleen cells of AKR, BALB/c, B10 and DBA/2 strains, with comparable cytotoxic titers. The inhibitory activity of the sera could not be explained by non-specific effects of high-titered Ab. To study the relationship between the antigen(s) responsible for the blocking effect and Lyt-2-linked genes, killer cells from Lyt-2 congenic strains were tested and conventional anti-Lyt-2.2 antisera were raised in an appropriate congenic strain combination. Killer cells from B6, but not from B6.Ly2.1 animals, were significantly sensitive to the blocking effects of the inhibitory C3H anti-B10.BR sera. The conventional anti-Lyt.2.2 sera did produce CML blocking, although there was no apparent correlation between such blocking and the anti-Lyt-2.2 cytotoxic titer. The target molecules responsible for blocking of killer cells may be encoded or regulated by genes that are closely linked to or identical with Lyt-2.

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