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SYNERGY BETWEEN STIMULATOR CELLS IN THE INDUCTION OF THE ANTI‐Mls a RESPONSE
Author(s) -
DeKruyff R. H.,
Laning J.,
Dorf M. E.
Publication year - 1988
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.1988.tb00415.x
Subject(s) - clone (java method) , biology , complementation , spleen , epitope , permissive , allele , immune system , haplotype , genetics , microbiology and biotechnology , antigen , immunology , gene , phenotype
SUMMARY We have identified two types of clones responsive to Mls determinants. One type responded vigorously to purified B cells from mice bearing Mls a ‐stimulatory determinants. The other type, including clone Lyl‐N5, responded vigorously to unfractionated spleen cells, but failed to respond to B cells alone or to spleenadherent cells (SAC) alone from the Mls a ‐bearing mice. Synergy between two stimulator cell types, B cells and SAC, was required to induce the Mls response of clone Lyl‐N5. The failure of clone Lyl‐N5 to respond to Mls a ‐bearing B cells was reversed by the addition of SAC taken from mice bearing the Mls b allele or the non‐stimulatory Mls b allele. B cells were required to provide the Mls a determinant. The Mls response of clone Ly1‐N5 is restricted by class II determinants shared by the H‐2 b , H‐2 d and H‐2 k haplotypes, but not the H‐2 q haplotype. The optimal response of the clone was obtained by using B cells bearing both Mls a and the permissive H‐2 alloantigen. However, complementation was also observed between B cells bearing Mls a and the non‐permissive Ia q and SAC bearing the non‐stimulatory Mls b , but a permissive la epitope, resulting in activation of the clone. Clone Ly1‐N5 responds to Mls a ‐bearing B cells only in the presence of SAC. The SAC provide an undefined signal required for the proliferation of certain clones such as clone Ly1‐N5, which is not provided by normal B cells. In this report, we show that the AKTB‐lb B‐cell tumour line stimulates the proliferation of clone Ly1‐N5, in the absence of SAC, suggesting that the tumour line has acquired the capacity to provide this signal.