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Gene Expression1
*
Center for Molecular Biology of Oral Diseases, and
Department of Biochemistry and Molecular Biology, University of Illinois, Chicago, IL 60612
We have previously shown that norepinephrine (NE) inhibits the in
vitro generation of anti-MOPC-315 CTL activity by spleen cells from
BALB/c mice rejecting a large MOPC-315 tumor as a consequence of
low-dose melphalan (L-phenylalanine mustard
(L-PAM)) treatment (L-PAM TuB spleen cells).
Since TNF-
plays a key role in the generation of antitumor CTL
activity in this system, we determined whether NE mediates this
inhibition through inhibition of TNF- production. Here, we show that
NE inhibits the production of TNF- protein and mRNA by
L-PAM TuB spleen cells stimulated in vitro with mitomycin
C-treated tumor cells. Flow cytometric analysis of intracellular
expression of TNF- revealed substantial NE-mediated decreases in the
percentages of TNF-+ cells among CD4+ and
CD8+ T cells and F4/80+ activated macrophages.
NE inhibition of CTL generation was largely overcome by addition of
TNF- to the stimulation cultures. When the ß-adrenergic antagonist
propranolol was added to the stimulation cultures of L-PAM
TuB spleen cells at a concentration that prevented NE-induced cAMP
elevation, the NE-mediated decrease in TNF- mRNA and NE-mediated
inhibition of CTL generation were reversed. Collectively, these results
suggest that NE inhibits antitumor CTL generation, at least in part, by
inhibiting TNF- synthesis through a mechanism(s) involving
ß-adrenergic receptor signaling.
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