Besser M, Wank R
Institute of Immunology, University of Munich, Munich, Germany.
J Immunol. 1999 Jun 1;162(11):6303-6.
Neurotrophins, such as neurotrophin-3 (NT-3) and brain-derived neurotrophic factor (BDNF), are potent regulators of neuronal functions. Here we show that human immune cells also produce NT-3 mRNA, secrete BDNF, and express their specific receptors trkB and trkC. The truncated trkB receptor, usually expressed in sensory neurons of the central nervous system, was also constitutively expressed in unstimulated Th cells. Full-length trkB was detectable in stimulated PBMC, B cell lines, and Th1, but not in Th2 and Th0 cell clones. Clonally restricted expression was also observed for trkC, until now not detected on blood cells. The Th1 cytokine IL-2 stimulated production of trkB mRNA but not of trkC, whereas the Th2 cytokine IL-4 enhanced NT-3 but not BDNF mRNA expression. Microbial Ags, which influence the Th1/Th2 balance, could therefore modulate the neurotrophic system and thereby affect neuronal synaptic activity of the central nervous system.
神经营养因子，如神经营养因子-3（NT-3）和脑源性神经营养因子（BDNF），是神经元功能的强效调节因子。我们在此表明，人类免疫细胞也产生NT-3 mRNA、分泌BDNF，并表达其特异性受体trkB和trkC。截短的trkB受体通常在中枢神经系统的感觉神经元中表达，在未受刺激的Th细胞中也组成性表达。全长trkB在受刺激的外周血单核细胞（PBMC）、B细胞系和Th1细胞中可检测到，但在Th2和Th0细胞克隆中未检测到。trkC也观察到克隆限制性表达，此前在血细胞上未检测到。Th1细胞因子白细胞介素-2（IL-2）刺激trkB mRNA的产生，但不刺激trkC的产生，而Th2细胞因子IL-4增强NT-3但不增强BDNF mRNA的表达。因此，影响Th1/Th2平衡的微生物抗原可能调节神经营养系统，从而影响中枢神经系统的神经元突触活动。
