Sympathetic neural modulation of the immune system. I. Depression of T cell immunity in vivo and vitro following chemical sympathectomy.
Chemical sympathectomy of adult mice with 6-hydroxydopamine (6-OHDA) either prior to or following epicutaneous sensitization with the trinitrophenyl (TNP) hapten decreased the delayed hypersensitivity (DH) response to ear challenge. To determine if uptake of 6-OHDA into sympathetic nerve terminals, and their subsequent destruction, was required for suppression of DH, the catecholamine uptake blocker, desipramine, was employed to block 6-OHDA-induced sympathetic denervation. Pretreatment with desipramine prevented the depression of DH. In vivo treatment with the beta blocker, propranolol, did not alter the 6-OHDA effect, eliminating the potential contribution of released catecholamines, acting on beta-adrenoceptors, to DH reduction. Sympathectomy before sensitization also diminished hapten-specific T cell reactivity of sensitized lymph node (LN) cells, as measured in vitro by IL-2 production and CTL generation. In vivo DNA synthesis in draining LN in response to immunization was modestly decreased following 6-OHDA. Thus, sympathetic denervation appears to impair T cell activity in vivo and in vitro. Overall, these results indicate the SNS plays a role in generation of cell-mediated immunity.
Madden
K S
KS
Department of Microbiology, University of Rochester Medical Center, New York 14642.
Felten
S Y
SY
Felten
D L
DL
Sundaresan
P R
PR
Livnat
S
S
D000818:Animals; D006892:Hydroxydopamines; D006968:Hypersensitivity, Delayed; D007107:Immune System / Q000502:physiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D009498:Neurotoxins; D016627:Oxidopamine; D013563:Sympathectomy, Chemical; D013564:Sympathetic Nervous System / Q000502:physiology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*
D006892:Hydroxydopamines; D009498:Neurotoxins; D016627:Oxidopamine