Equivalence of conventional anti-picryl T suppressor factor in the contact sensitivity system and monoclonal anti-NP TsF3: their final non-specific effect via the T acceptor cell.
There is considerable confusion over whether the antigen-specific T suppressor factors (TsF) described by different authors are indeed equivalent. This paper investigates whether monoclonal TsF3, obtained from hybridomas derived from mice injected subcutaneously with NP derived spleen cells, is functionally equivalent to the conventional T suppressor factor, produced by mice injected intravenously with chemically reactive, water soluble haptene (picrylsulphonic acid and oxazolone thioglycolic acid). Comparison of monoclonal anti-NP TsF3 with conventional anti-picryl and anti-oxazolone T suppressor factor showed that both armed the non-specific T acceptor cell (Tacc) which was sensitive to cyclophosphamide and adult thymectomy. Moreover, non-specific inhibitor (nsINH) of the transfer of contact sensitivity was released when antigen, together with major histocompatibility complex products (MHC), reacted with conventional or monoclonal TsF on the surface of the non-specific T acceptor cell. The interaction of monoclonal TsF3 with antigen, which led to the release of NsINH, required the presence of MHC and was I-J restricted. However, there was no Igh-1 restriction. The equivalence of conventional anti-picryl and anti-oxazolone TsF has been demonstrated by arming the Tacc with a mixture of these two suppressor factors, and then triggering the release of nsINH with the mixed haptene 'picryl-oxazolone-lysine' which crosslinks separate molecules of TsF. A similar equivalence of conventional anti-oxazolone TsF and monoclonal anti-NP TsF3 was demonstrated using the mixed hapten 'NP-oxazolone-lysine' to trigger the release of nsINH. It was concluded that monoclonal TsF3 and conventional TsF were equivalent, and that both had an indirect mode of action through the non-specific T acceptor cell which led to the production of non-specific inhibitor.
D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D003877:Dermatitis, Contact / Q000276:immunology*; D006241:Haptens / Q000276:immunology*; D006825:Hybridomas / Q000276:immunology*; D007116:Immunization, Passive; D008222:Lymphokines / Q000096:biosynthesis / Q000276:immunology*; D008285:Major Histocompatibility Complex; D051379:Mice; D008815:Mice, Inbred Strains; D009596:Nitrophenols / Q000276:immunology*; D010081:Oxazolone / Q000276:immunology; D010648:Phenylacetates; D010853:Picryl Chloride / Q000276:immunology; D013491:Suppressor Factors, Immunologic; D013601:T-Lymphocytes / Q000276:immunology*; D013934:Thymectomy
D006241:Haptens; D008222:Lymphokines; D009596:Nitrophenols; D010648:Phenylacetates; D013491:Suppressor Factors, Immunologic; C026242:4-hydroxy-5-nitrophenyl acetic acid; D010081:Oxazolone; D003520:Cyclophosphamide; D010853:Picryl Chloride