The induction of oxazolone-specific T suppressor afferent cells in mice by hapten-modified isologous IgG.
Injection of isologous 4(ethoxymethylene)-2-phenyl-oxazolin-5-one (oxazolone; OX)-substituted thymocytes or OX-labeled IgG (OX-IgG) into mice produces specific unresponsiveness in which immunization with homologous (OX), but not heterologous (picryl chloride), hapten on the skin does not result in significant contact sensitization. However, while injection of OX-substituted thymocytes triggers suppressor cells which inhibit the effector stage of contact sensitivity reaction, OX-IgG induces cells which suppress exclusively the afferent stage of reaction. In contrast to OX-IgG, OX-substituted F(ab')2 fragments, IgM, and albumin are ineffective. T suppressor afferent cells have Ly-2 and I-J surface markers and their precursors are resistant to cyclophosphamide treatment and adult thymectomy. We assume that T suppressor afferent cells recognize antigen in conjunction with intact IgG molecules, although the exact mechanism is unclear.
D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D005260:Female; D006241:Haptens / Q000494:pharmacology*; D007116:Immunization, Passive; D007074:Immunoglobulin G / Q000276:immunology*; D008297:Male; D051379:Mice; D010080:Oxazoles / Q000494:pharmacology*; D010081:Oxazolone / Q000494:pharmacology*; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects*
D006241:Haptens; D007074:Immunoglobulin G; D010080:Oxazoles; D010081:Oxazolone; D003520:Cyclophosphamide