Yasunobu Okuma* and Yasuyuki Nomura
Department of Pharmacology, Graduate School of Pharmaceutical Sciences,
Hokkaido University, Sapporo 060-0812, Japan
*Corresponding author. FAX: +81-11-706-4987
E-mail: okumay@pharm.hokudai.ac.jp
Abstract: Receptors for many neurotransmitters including catecholamines
and acetylcholine (ACh) have been detected on the cell surface of lymphocytes.
It has been demonstrated that a human T cell line synthesizes ACh and suggested
that ACh may be an autacoid modulating T cell-dependent immune responses.
However, the biochemical interactions of the ACh system with the immune
system have not been elucidated in detail. We have shown that m1 and m2
muscarinic receptor mRNAs are expressed in human peripheral blood lymphocytes
and in human T cell line Jurkat cells and that pretreatment of these cells
with a muscarinic receptor agonist enhances interleukin-2 (IL-2) production.
We also postulated possible intracellular signaling pathways via which muscarinic
receptors regulate IL-2 production in Jurkat cells. The findings suggest
that M1 muscarinic receptors are involved in muscarinic receptor-mediated
enhancement of IL-2 production in Jurkat cells and that the transcription
factor AP-1 and pathways via mitogen-activated protein kinase (MAPK) / extracellular
signal regulated protein kinase and c-Jun N-terminal kinase, but not via
p38 MAPK, may be involved in the muscarinic receptor-mediated enhancement
of IL-2 production. Our findings demonstrate a neuro-immune interaction
through muscarinic receptor signaling in immune cells.
Keywords: Neuroimmune interaction, Muscarinic receptor, Interleukin-2,
Jurkat cell
Copyright The Japanese Pharmacological Society
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