The ability of mice to mount an immune response against hen egg white lysozyme (HEL) is determined by genes linked to the H-2 complex. The cellular basis for this observation was analyzed in cellular cooperation experiments in which isolated T cells and B cells from parent →F1 and F1[ parent bone marrow chimeras were used. The results suggest the defect in the nonresponder (NR) mice carrying the H-2b haplotype involves a deficient stimulation of antigen-specific helper T cells. Significant immune responses to HEL were obtained only when responder of nonresponder B cells were stimulated in the presence of responder (R) T cells and responder antigen-presenting cells in a responder host environment. Thus, R → F1 and F1 → R chimeras responded well to HEL whereas NR → F1 and F1 → NR chimeras were nonresponders to HEL. In addition, maturation of nonresponder cells in the presence of responder cells did not reverse either parental phenotype. Thus, after transfer to another sublethally irradiated F1 host, isolated nonresponder cells obtained from (NR + R) → F1 chimeras were still unable to respond to HEL while responder cells from such chimeras maintained their ability to respond to HEL. Because nonresponder B cells were able to produce HEL-specific antibody in the presence of responder, F1, T cell help, and there was no evidence for H-2b-induced suppressor activity, at least one defect in the H-2b nonresponder can be placed at the level of interaction between the antigen-presenting cell and the T cell.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Immunology|
|State||Published - Jan 1 1982|
ASJC Scopus subject areas
- Immunology and Allergy