儿茶酚胺调节免疫功能的细胞和分子机制  

Cellular and Molecular Mechanisms of Regulation of Immune Functions by Catecholamines

作　　者：邱一华[1] 彭聿平[1] 王建军[1] 

机构地区：[1]南京大学生物科学与技术系,南京210093

出　　处：《生理科学进展》2003年第4期303-308,共6页Progress in Physiological Sciences

基　　金：江苏省高校自然科学基金 ( 0 2KJB180 0 0 1);国家自然科学基金( 30 0 70 2 5 0 )资助课题

摘　　要：目前认为儿茶酚胺 (catecholamines ,CAs)不只是引起普遍的免疫抑制 ,而是抑制细胞免疫但促进体液免疫。CAs可抑制 1型辅助T(Thelper 1,Th1)细胞、细胞毒性T(Tcytotoxic ,Tc)细胞、自然杀伤 (naturalkiller,NK)细胞和单核细胞的作用 ,并增强Th2和B细胞的作用。CAs通过免疫细胞上的 β2 肾上腺素受体 (β2 adrenoreceptors ,β2 ARs)引起细胞内cAMP增加 ,cAMP激活蛋白激酶A(proteinkinaseA ,PKA) ,后者调节核转录因子的活性 ,从而影响细胞因子的基因表达 ,即抑制白介素 2 (interleukin 2 ,IL 2 )、肿瘤坏死因子 α(tumornecrosisfactor α ,TNF α)和IL 12的基因转录 ;增强IL 6、IL 10和ILAn increasing body of evidence suggests that catecholamines (CAs) do not only cause a general immunosuppression as previously believed, but suppress cellular immunity and boost humoral response. CAs can inhibit T helper 1 cells, T cytotoxic cells, natural killer cells and monocytes, but enhance T helper 2 cells and B cells through their direct regulation of these immune cells. In addition, CAs may modulate the gene transcription for cytokines in immune cells through stimulation of β 2 adrenoreceptors and increase of cAMP, subsequently, activation of protein kinase A and alteration of the activity of nuclear transcription factors. Through these molecular mechanisms, the production of interleukin 2 (IL 2), tumor necrosis factor α and IL 12 is decreased, but the production of IL 6, IL 10 and IL 4 is increased.

关 键 词：儿茶酚胺 免疫细胞 细胞因子 核转录因子 β2-肾上腺素受体 

分 类 号：R392[医药卫生—免疫学]