Characterization of murine immune responses to allergenic diisocyanates.

Chemicals may cause contact allergy. Some allergens may, in addition, cause respiratory sensitization. In previous investigations we have found that contact and respiratory sensitizers induce differential immune responses in mice characteristic of TH1 and TH2 T helper cell activation, respectively. In the present study we have examined immune responses in mice following topical exposure to three allergenic diisocyanates; diphenylmethane-4,4'-diisocyanate (MDI), dicyclohexylmethane-4,4'-diisocyanate (HMDI), and isophorone diisocyanate (IPDI). All three chemicals are contact allergens. MDI is in addition a known human respiratory allergen. HMDI and IPDI appear not to induce respiratory sensitization or at least do so very rarely. Exposure of mice to all chemicals resulted in a vigorous lymphocyte proliferative response in lymph nodes draining the site of application, and each caused contact sensitization. In common with other respiratory allergens, MDI induced an increase in the serum concentration of IgE and provoked considerably more IgG2b than IgG2a anti-hapten antibody; responses consistent with a preferential activation of TH2 cells. In contrast, under conditions where both caused lymph node cell proliferation and contact sensitization, neither HMDI nor IPDI induced a measurable antibody response of any class. These data provide additional evidence that different classes of chemical allergen cause divergent immune responses in mice. The possibility that these characteristics may facilitate not only the identification, but also classification, of chemical allergens is discussed.