The induction of splenic suppressor T cells through an immune-privileged site requires an intact sympathetic nervous system

Abstract

Antigen injection into the eye's anterior chamber (AC) induces the antigen-specific suppression of delayed-type hypersensitivity (DTH) that is mediated by NKT cells and splenic CD8 + suppressor T cells. Because the AC, uveal tissues, the thymus and spleen required to induce anterior chamber-associated immune deviation (ACAID) have dense sympathetic innervations, we examined the effects of chemical sympathectomy of mice by 6-hydroxydopamine (6-OHDA) on the induction of the suppression of contact sensitivity to trinitrophenol (TNP) induced by the injection of TNP–bovine serum albumin (BSA) into the anterior chamber. DTH measured as contact sensitivity to picrylchloride was not induced in mice that received 6-OHDA before immunization with TNP-BSA. Although spleen cells from 6-OHDA-treated TNP-BSA-immunized mice produced IFN-γ when stimulated by TNP-BSA, the number of DTH-initiating hepatic NKT cells was reduced markedly in 6-OHDA-treated mice. Chemically denervated mice did not produce splenic suppressor T cells or thymic NKT cells that activate splenic suppressor T cells. We suggest that an intact sympathetic nervous system (SNS) is required to maintain cellular immunoregulation.