B cells are not required for T cell priming in low zone tolerance to contact allergens and contact hypersensitivity

Abstract

Low zone tolerance (LZT) to contact allergens is induced by epicutaneous exposure to haptens in subsensitizing doses resulting in an inhibition of contact hypersensitivity (CHS), which, in contrast, occurs after sensitization with immunogenic doses of allergens. Performing the protocol of tolerance induction resulted in robust LZT to allergens in B cell‐deficient mice in vivo, indicating that B cells are not required for the induction and effector phase of LZT. However, CHS reactions in vivo were restricted in B cell‐deficient mice as compared to wild‐type (WT) mice. In contrast, analysis of hapten‐specific T cell activation in vitro revealed a strong proliferative response of T cells derived from both WT and B cell‐deficient sensitized mice. Similar to WT animals, T cells obtained from tolerized B cell‐deficient mice produced a Tc2 cytokine pattern of LZT with high levels of IL‐4 and IL‐10, whereas sensitization of B cell‐deficient mice resulted in the typical Tc1 cytokine profile of CHS. Adoptive transfer of CD8⁺ effector T cells from tolerized or sensitized B cell‐deficient mice induced significant LZT or CHS reactions, respectively, in WT recipients, demonstrating that the development of hapten‐specific effector CD8⁺ T cells of LZT and CHS is independent of B cells.