Spleen cells from H-2(b,k,d) C57Bl/10 congenic mice were sensitized in vitro to trinitrobenzenesulfonate (TNBS)-modified autologous spleen cells. Cold target competition studies at the lytic phase demonstrated three distinct patterns of cytotoxic responsiveness: (a) H-2b spleen cells generated approximately equivalent CTL responses against Kb and Db modified self products, (b) H-2(d) spleen cells generated preferential responses against D(d) modified self products, and (c) H-2(k) spleen cells generated cytotoxic responses which could only be detected against K(k) self products in association with TNP. F1 spleen cells were sensitized against autologous TNBS-treated cells. The results showed that, although H-2b parental cells generated aproximately equivalent Kb-TNP- and Db-TNP-specific CTL, the presence of the H-2b haplotype did not result in the generation of (a) D(k)-TNP CTL response by (H-2bxH-2(k)) spleen cells, nor (b) a Db CTL response by (H-2bxH-2a) F1 spleen cells. Additionally, (H-2(d)xH-2(k)) F1 cells failed to generate detectable D(d)-TNP-specific CTL, although H-2(d) parental cells generated D-regional-specific CTL. The findings demonstrated that these F1 response patterns paralleled those of the H-2(k) and H-2a parents, i.e. weak or no D-region TNP-specific CTL were induced. Because (H-2(d)xH-2a) F1 responders stimulated with H-2(d) TNBS-treated cells did generate good D(d) TNP responses, the results illustrated that the presence of responder genes was not sufficient to result in a D-region TNP CML. It is suggested that the absence of K(k) alleles on the stimulating population is necessary for the generation of D-region TNP CTL in these F1's. Mechanisms which could account for these response patterns in parental F1 mice are discussed including immunodominance, suppression, T-cell response, and Ir-gene defects.
ASJC Scopus subject areas
- Immunology and Allergy