No abstract

There has been some speculation that the T-cell-dependent contact hypersensitivity reactions contain elements of both immediate and delayed hypersensitivity. This has been provoked by the finding that the swelling reactions of contact sensitivity can be detected as early as 4 h after challenge (1) and by the demonstration that basophils constitute a significant proportion of the inflammation in contact sensitivity (2). Also lymphocytes have been shown to release a product capable of giving peritoneal exudate cells the ability to passively transfer contact sensitivity (3). The capacity of the sensitized peritoneal cells to passively transfer contact sensitivity was abrogated by treatment with antiimmunoglobulin sera. Askenase (4) has also reported that serum from mice painted with oxazolone can transfer a basophil inflammation when recipient mice were challenged 2 h after serum transfer. This reaction required 24 h after challenge to develop.More recently the possible contribution of immediate hypersensitivity reactions in contact sensitivity was emphasized by the investigation of Gershon et al. (5) who found that skin sites where contact sensitivity reactions are most easily elicited are particularly rich in mast cells. In addition mice with mast cells depleted of 5-hydroxytryptamine by reserpine could not manifest delayed hypersensitivity reactions although they had sensitized cells capable of passively transferring delayed hypersensitivity to normal recipients. They also showed that serum from mice repeatedly painted with oxazolone could produce a passive cutaneous anaphylaxis reaction in mice if challenged within 2 h of intradermal transfer. This early reaction in mice has been attributed to weak IgG homocytotrophic antibody (6). This communication shows that mice can produce reaginic antibody within a week of sensitization with contact sensitizing agents and therefore have a strong homocytotrophic antibody capable of arming the basophils in contact sensitivity reactions. The reaginic antibody was unusual in that it was elicited by large doses of antigen without adjuvant and could be boosted by repeated challenge. Materials and MethodsMice. 6-to 12-wk-old mice bred at the Clinical Research Centre were used. Application of Picryl Chloride and Oxazolone. Mice were shaved on the thorax and abdomen and usually painted with either 0.1 ml of 5% picryl chloride (BDH, Poole, Dorset, Great Britain) or 0.1 ml of 3% oxazolone (2-phenyl-4-ethoxymethylene oxazolone) (Sigma Chemical Co., St. Louis, Mo.) on the shaven areas and forepaws. The contact sensitizers were dissolved in ethanol just before application.

This report describes IgM, IgG and IgE antibody and contact sensitivity responses of strains of mice congenic at the major histocompatibility complex (MHC) to skin painting with picryl chloride or oxazolone. B10 had low responses of all classes to picryl chloride. This was also reflected by the DNA synthesis occurring in their draining lymph nodes after painting. B10BR were high responders to picryl chloride for all classes but B10A and B10D2 were high responders for all classes except IgE. This presents evidence that genes in the MHC can selectively control antibody classes. The contact sensitivity response of the congenics to oxazolone confirmed the low previously described responsiveness of B10 mice. Antibody responses to oxazolone (agglutinin and reagin) were low for all congenics with B10 backgrounds.

No abstract

No abstract