Mitogenic signals are not required to circumvent the cyclosporin-induced inhibition of TNP-specific B memory cell expression.
Previous studies have shown that TNP-LPS-induced B memory cells can be recalled by either TNP-LPS or DNP-Ficoll and that cyclosporin A (CsA) prevents the expression of these B memory cells when DNP-Ficoll and not TNP-LPS is the challenging antigen. The possibility that the mitogenic signal delivered by TNP-LPS circumvents the inhibition exerted by CsA was investigated. It is demonstrated here that TNP-LPS, in its non-mitogenic (polymyxin-B-treated) as well as in its mitogenic form, is capable of driving TNP-specific B memory cells into the antibody-secreting stage, regardless of the presence or absence of CsA. It is suggested that both forms of TNP-LPS activate the same CsA-resistant subpopulation of B memory cells. The lack of DNP-Ficoll-induced memory expression in the presence of CsA is related to an intrinsic sensitivity to CsA inhibition of a subpopulation of B memory cells.
D000818:Animals; D001402:B-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D003524:Cyclosporins / Q000494:pharmacology*; D004347:Drug Interactions; D005260:Female; D005362:Ficoll / Q000031:analogs & derivatives / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008938:Mitosis / Q000187:drug effects; D011112:Polymyxin B / Q000494:pharmacology
D003524:Cyclosporins; C031007:DNP-Ficoll; D005362:Ficoll; D011112:Polymyxin B