Autocrine and paracrine regulation of lymphocyte CB2 receptor expression by TGF-β
Autocrine and paracrine regulation of lymphocyte CB2 receptor expression by TGF-β
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DOI：
10.1006/bbrc.2001.6179
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发表时间：
2002-01-11
影响因子：
3.1
通讯作者：
Dubinett, SM
中科院分区：
文献类型：
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作者：
Gardner, B;Zu, LX;Dubinett, SM
大麻衍生的大麻素δ(9)-四氢大麻酚（THC）已被证明具有免疫抑制作用。我们报道四氢大麻酚通过人外周血淋巴细胞（PBL）诱导免疫抑制细胞因子tgf - β。四氢大麻酚刺激tgf - β产生的能力被CB2受体特异性拮抗剂SR144528阻断，而不被CB1特异性拮抗剂AM251阻断。此外，我们的数据表明tgf - β以自分泌和旁分泌的方式积极调节淋巴细胞CB2受体的表达。在PBL培养物中加入重组tgf - β可下调CB2受体的表达，而抗tgf - β抗体处理可提高CB2受体的表达。我们得出结论，四氢大麻酚促进免疫抑制的一个机制是通过刺激淋巴细胞tgf - β的增强产生。(C) 2002 Elsevier Science。
The marijuana-derived cannabinoid Delta(9)-tetrahydrocannabinol (THC) has been shown to be immunosuppressive. We report that THC induces the immunosuppressive cytokine TGF-beta by human peripheral blood lymphocytes (PBL). The ability of THC to stimulate TGF-beta production was blocked by the CB2 receptor specific antagonist SR144528 but not by the CB1 specific antagonist AM251. Furthermore, our data suggest that TGF-beta actively regulates lymphocyte CB2 receptor expression in an autocrine and paracrine manner. Whereas the addition of recombinant TGF-beta to PBL cultures downregulated CB2 receptor expression, anti-TGF-beta antibody treatment increased CB2 receptor expression. We conclude that one mechanism by which THC contributes to immune suppression is by stimulating an enhanced production of lymphocyte TGF-beta. (C) 2002 Elsevier Science.