IMPAIRED NK1.1(-CELLS DO NOT PREVENT THE DEVELOPMENT OF AN IGE-DEPENDENT ALLERGIC PHENOTYPE() T)

Background The induction of TH2 immune responses is critically depende nt on initial IL-4. Although crucial, the source of this early IL-4 ha s not been identified. One candidate is a CD1 restricted NK1.1(+) T ce ll subpopulation which is known to produce such early IL-4. Objectives and methods The necessity of NK1.1(+) T cells for the expression of a n IgE-dependent phenotype was investigated in a NK1.1(+) T cell defici ent mouse model. The allergic phenotype was defined as immediate cutan eous hypersensitivity. It was induced by immunization of mice with ova lbumin. Mouse strains used were C57BL/6 mice and C57BL/6 mice homozygo us for a targeted mutation of the beta(2) microglobulin gene with cons ecutive loss of CD1 expression, which leads to a drastic reduction of NK1.1(+) T cells. Manifestation of an allergic sensitization was asses sed by intradermal allergen challenge after i.v. injection of Evens bl ue solution. The blue stained weal formations were quantified with the Bonitur method. In addition, the Th-2 response was confirmed by the m easurement of cytokines and serum immunoglobulins. The capability to p roduce early IL-4 was tested through the assessment of IL-4 mRNA short ly after a single challenge, Results Wild type and mutated mice did no t differ in any of the immunological parameters measured. Conclusion A single exposure to antigen with or without adjuvant induces early IL- 4 production in C57BL/6 beta(2)m-/- mice. This early IL-4 is therefore independent of the presence of NK1.1(+) T cells and functional MHC cl ass I molecules and leads to IgE production and immediate cutaneous hy persensitivity.