人CD4- CD8-不变性自然杀伤T细胞通过抗原受体交联刺激B细胞分泌IgG

T. Miyasaka, Y. Watanabe, Y. Akahori, Namiko Miyamura, K. Ishii, Y. Kinjo, Y. Miyazaki, Tianyi Liu, Y. Uemura, K. Kawakami
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引用次数: 0

摘要

免疫球蛋白(Ig) M的产生可以由胸腺非依赖性2型抗原(TI-2)与B细胞Ag受体(bcr)相互作用诱导,而无需常规T细胞的参与;然而,通过相同的过程产生IgG,则需要第二个信号。先前的研究报道,不变性自然杀伤T (iNKT)细胞可能负责IgG产生的第二个信号。在本研究中,我们在体外研究了人iNKT细胞是否可以参与对抗TI-2 Ag的Ig的产生。人类iNKT细胞的两个主要不同亚群,CD4+ CD8β- (CD4)和CD4- CD8β-[双阴性(DN)]细胞,从健康志愿者的外周血单核细胞中产生。由抗IgM抗体刺激触发的BCR接合,在这里作为由TI-2 Ag触发的BCR接合的模型进行了研究,诱导B细胞产生大量的IgM。CD4和DN iNKT细胞均以剂量依赖性的方式减少IgM的产生,相反地增加IgG的产生。此外,CD19+CD27-(幼稚)和CD19+CD27+(记忆)B细胞的IgG产生主要是由DNiNKT细胞而不是CD4 iNKT细胞促进的;然而,两种B细胞亚群的IgM产生同样被iNKT细胞亚群中的任何一个减少。这些结果表明,DN iNKT亚群可能在TI-2 Ag刺激下优先促进B细胞的Ig类转换。
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Human CD4- CD8- Invariant Natural Killer T Cells Promote IgG Secretion from B Cells Stimulated by Cross-Linking of Their Antigen Receptors
Immunoglobulin (Ig) M production can be induced by the interaction of thymus-independent type-2 (TI-2) antigen (Ag) with B cell Ag receptors (BCRs) without the involvement of conventional T cells; for IgG production through the same process, however, a second signal is required. Previous studies have reported that invariant natural killer T (iNKT) cells may be responsible for the second signal involved in IgG production. In the present study, we addressed whether human iNKT cells could participate in the production of Ig against TI-2 Ag in vitro. Two major distinct subsets of human iNKT cells, CD4+ CD8β- (CD4) and CD4- CD8β- [double negative (DN)] cells, were generated from peripheral blood monocytes from a healthy volunteer. BCR engagement, triggered by anti-IgM antibody stimulation, examined here as a model of BCR engagement triggered by TI-2 Ag, induced abundant IgM production by B cells. Both CD4 and DN iNKT cells reduced IgM production and conversely enhanced IgG production in a dose-dependent manner. In addition, IgG production by CD19+CD27- (naive) and CD19+CD27+ (memory) B cells was predominantly promoted by DNiNKT cells rather than CD4 iNKT cells; nevertheless, IgM production by both B cell subsets was similarly reduced by either subset of iNKT cells. These results suggest that the DN iNKT subsets may preferentially promote Ig class switching by B cells upon stimulation with TI-2 Ag.
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