Kimata H, Yoshida A
Department of Pediatrics, Kyoto University Hospital, Kyoto City, Japan.
Clin Immunol Immunopathol. 1996 May;79(2):197-202. doi: 10.1006/clin.1996.0068.
The effects of gangliosides on spontaneous immunoglobulin (Ig) production in human B cells were studied. Of the various gangliosides tested, including GM1, GM2, GM3, GD1a, GD1b, GD3, GT1b, and GQ1b, only GM2 inhibited Ig production, but not thymidine uptake, in human B cell lines. Moreover, the GM2-induced inhibition was blocked by anti-GM2 mAb, but not by control IgM. Of various cytokines, IL-10 and TNF-alpha each partially counteracted the GM2-induced inhibition, and addition of both IL-10 and TNF-alpha completely counteracted the inhibition. On the other hand, anti-IL-10 mAb plus anti-TNF-alpha mAb inhibited spontaneous Ig production. GM2 inhibited endogenous production of IL-10 and TNF-alpha without affecting the binding of IL-10 and TNF-alpha in B cell lines. GM2 also specifically inhibited spontaneous production of Ig, IL-10, and TNF-alpha in in vivo activated B cells obtained from normal donors. This inhibition was blocked by anti-GM2 mAb and was counteracted specifically by IL-10 plus TNF-alpha. Collectively, GM2 may inhibit spontaneous Ig production by inhibiting endogenous production of IL-10 and TNF-alpha in B cells.
研究了神经节苷脂对人B细胞中自发免疫球蛋白（Ig）产生的影响。在测试的各种神经节苷脂中，包括GM1、GM2、GM3、GD1a、GD1b、GD3、GT1b和GQ1b，只有GM2抑制人B细胞系中的Ig产生，但不抑制胸苷摄取。此外，GM2诱导的抑制作用被抗GM2单克隆抗体阻断，但不被对照IgM阻断。在各种细胞因子中，IL-10和TNF-α各自部分抵消了GM2诱导的抑制作用，同时添加IL-10和TNF-α则完全抵消了该抑制作用。另一方面，抗IL-10单克隆抗体加抗TNF-α单克隆抗体抑制自发Ig产生。GM2抑制B细胞系中IL-10和TNF-α的内源性产生，而不影响IL-10和TNF-α的结合。GM2还特异性抑制从正常供体获得的体内活化B细胞中Ig、IL-10和TNF-α的自发产生。这种抑制作用被抗GM2单克隆抗体阻断，并被IL-10加TNF-α特异性抵消。总体而言，GM2可能通过抑制B细胞中IL-10和TNF-α的内源性产生来抑制自发Ig产生。
