Fujiwara R, Yokoyama M M
Department of Immunology, Kurume University School of Medicine, Fukuoka, Japan.
Ann N Y Acad Sci. 1994 Nov 25;741:244-51. doi: 10.1111/j.1749-6632.1994.tb39666.x.
We previously demonstrated that plaque-forming cell (PFC) production in the spleen of mice immunized with sheep red blood cells (SRBC) was enhanced by pain stimulation. This phenomenon was due to activation of antigen nonspecific L3T4-/Lyt-2- T lymphocytes (double-negative T cells) by the beta-adrenergic action of endogenous catecholamines released from the adrenal gland after pain stimulation. Further study also demonstrated that interleukin-2 (IL-2) production of spleen cells was enhanced in mice by pain stimulation. In this study spleen cells of BALB/c mice were cultured with Con A and SRBC, respectively, and the IL-2 level was measured by incorporation of 3H-thymidine into CTLL-2 cells during culture for 24 hours. Interleukin-2 production of spleen cells from mice given pain stimulation was significantly increased compared with spleen cells of normal mice. The IL-2 production of spleen cells of normal mice was also markedly enhanced by the mixed culture with spleen cells from pain-stimulated mice. Enhancement of IL-2 production in the spleen cells of mice given pain stimulation did not occur with anti-Thy-1.2 antibody and complement treatment, but production was maintained by treatment with anti-L3T4 antibody and complement. These data suggest that the enhanced production of IL-2 in mice given pain stimulation resulted from the activation of L3T4- T cells by endogenous catecholamines released from the adrenal gland after pain stimulation. It can be assumed that activated L3T4- T cells interact with antigen-specific L3T4+ T cells and lead to enhanced IL-2 production.
我们先前证明，用绵羊红细胞（SRBC）免疫的小鼠脾脏中形成斑块细胞（PFC）的产生会因疼痛刺激而增强。这种现象是由于疼痛刺激后肾上腺释放的内源性儿茶酚胺的β-肾上腺素能作用激活了抗原非特异性L3T4-/Lyt-2- T淋巴细胞（双阴性T细胞）。进一步的研究还表明，疼痛刺激可增强小鼠脾脏细胞白细胞介素-2（IL-2）的产生。在本研究中，分别用刀豆蛋白A（Con A）和SRBC培养BALB/c小鼠的脾脏细胞，并在24小时培养期间通过将3H-胸腺嘧啶掺入CTLL-2细胞来测量IL-2水平。与正常小鼠的脾脏细胞相比，给予疼痛刺激的小鼠脾脏细胞的IL-2产生显著增加。正常小鼠脾脏细胞与来自疼痛刺激小鼠的脾脏细胞混合培养也显著增强了IL-2的产生。给予疼痛刺激的小鼠脾脏细胞中IL-2产生的增强在抗Thy-1.2抗体和补体处理后未出现，但用抗L3T4抗体和补体处理可维持其产生。这些数据表明，给予疼痛刺激的小鼠中IL-2产生的增强是由于疼痛刺激后肾上腺释放的内源性儿茶酚胺激活了L3T4- T细胞。可以推测，活化的L3T4- T细胞与抗原特异性L3T4+ T细胞相互作用并导致IL-2产生增强。
