Mechanism of densensitization in DNCB-contact sensitive guinea pigs.
Contact sensitivity to dinitrochlorobenzene (DNCB) in guinea pigs could be rapidly suppressed by intravenous injection of dinitrobenzene sulfonic acid sodium salt (DNBSO3). This suppression is transient and antigen-specific. Macrophages from desensitized animals are not inactivated as shown by their ability to react, both in vivo and in vitro to lymphokines produced in a separate system. Therefore, effector lymphocytes are considered the target for the desensitizing antigen. Using an adoptive transfer system it was demonstrated that effector lymphocytes are inactivated by a direct effect of the hapten. Since this inactivation can be reversed by trypsin treatment, a receptor blockade of effector lymphocytes is proposed as the mechanism of desensitization of DNCB-contact sensitive guinea pigs. This does not exclude the possibility that additional mechanisms such as suppressor cells, compartmentalization or endogenous proliferation of lymph node lymphocytes may play an additional role.
D000818:Animals; D002464:Cell Migration Inhibition; D003877:Dermatitis, Contact / Q000276:immunology / Q000628:therapy*; D003888:Desensitization, Immunologic; D004136:Dinitrobenzenes / Q000627:therapeutic use; D004137:Dinitrochlorobenzene; D000939:Epitopes; D005260:Female; D006168:Guinea Pigs; D006241:Haptens; D008264:Macrophages / Q000276:immunology; D008297:Male; D009578:Nitrobenzenes; D013451:Sulfonic Acids / Q000627:therapeutic use; D013601:T-Lymphocytes / Q000276:immunology
D004136:Dinitrobenzenes; D004137:Dinitrochlorobenzene; D000939:Epitopes; D006241:Haptens; D009578:Nitrobenzenes; D013451:Sulfonic Acids