gammadelta T-cell-deficient mice do not differ from normal controls in their induction or expression of type 2 dominant responses to exogenous antigen.

Abstract

The roles that gammadelta T cells play in shaping initial CD4 T cell activation, and sensitivity to development of atopic diseases, remain controversial. Using a genetic knockout model of gammadelta T-cell deficiency, we investigated the role of these cells in initiation of exogenous antigen specific murine cytokine and antibody responses. Given that the most widely distributed and clinically prominent class of allergens are soluble protein antigens, we utilized OVA to examine the role played by gammadelta T cells in shaping the induction and expression of exogenous Ag specific immune responses. Focusing on immunization conditions that stimulate in vivo induction of type 2 dominant immunity, we report that gammadelta deficient and intact C57Bl6 mice exhibit similar OVA-specific responses as indicated by the (i) intensity of initial T-cell activation (ii) the type1 vs. type 2 balance of exogenous Ag specific cytokine synthesis and the (iii) intensity and the relative balance of the resulting IgE vs. IgG(2a) responses in vivo seen in these strains. Taken together, the data are consistent with the hypothesis that gammadelta T cells do not play an essential role in shaping induction of systemic immune responses to soluble exogenous antigen in type 2 dominated responses.