Impaired NK1.1+ T cells do not prevent the development of an IgE-dependent allergic phenotype

The induction of TH2 immune responses is critically dependent on initial IL-4. Although crucial, the source of this early IL-4 has not been identified. One candidate is a CD1 restricted NK1.1+ T cell subpopulation which is known to produce such early IL-4.

The necessity of NK1.1+ T cells for the expression of an IgE-dependent phenotype was investigated in a NK1.1+ T cell deficient mouse model. The allergic phenotype was defined as immediate cutaneous hypersensitivity. It was induced by immunization of mice with ovalbumin. Mouse strains used were C57BL/6 mice and C57BL/6 mice homozygous for a targeted mutation of the beta2 microglobulin gene with consecutive loss of CD1 expression, which leads to a drastic reduction of NK1.1+ T cells. Manifestation of an allergic sensitization was assessed by intradermal allergen challenge after i.v. injection of Evans blue solution. The blue stained weal formations were quantified with the Bonitur method. In addition, the Th2 response was confirmed by the measurement of cytokines and serum immunoglobulins. The capability to produce early IL-4 was tested through the assessment of IL-4 mRNA shortly after a single challenge.

Wild type and mutated mice did not differ in any of the immunological parameters measured.

A single exposure to antigen with or without adjuvant induces early IL-4 production in C57BL/6 beta2m-/- mice. This early IL-4 is therefore independent of the presence of NK1.1+ T cells and functional MHC class I molecules and leads to IgE production and immediate cutaneous hypersensitivity.