INTERLEUKIN-12 REGULATES THE PROLIFERATION OF TH1, BUT NOT TH2 OR TH0, CLONES
INTERLEUKIN-12 REGULATES THE PROLIFERATION OF TH1, BUT NOT TH2 OR TH0, CLONES
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DOI：
10.1002/eji.1830241002
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发表时间：
1994-10-01
影响因子：
5.4
通讯作者：
GRABSTEIN, KH
中科院分区：
文献类型：
--
作者：
KENNEDY, MK;PICHA, KS;GRABSTEIN, KH
我们的结果表明，白介素12是小鼠Th1克隆抗原依赖性增殖的重要共刺激因子。此外，我们证明IL-10抑制依赖于脾抗原提呈细胞(APC)的Th1克隆的增殖，至少部分是通过下调APC来源的IL-12来实现的。此外，激活的B细胞不能通过IL-12提供共刺激，这是它们无法支持Th1克隆的最佳增殖反应的原因。我们还表明，IL-12调节Th1克隆对IL-4的反应能力，并在对IL-2、IL-7或IL-15的反应中促进其增殖。相反，Th2和Th0克隆似乎难以抵抗IL-12对抗原依赖或生长因子诱导的增殖的影响。
Our results indicate that interleukin (IL)-12 is an important costimulator of antigen-dependent proliferation of murine Th1 clones. In addition, we demonstrate that IL-10 inhibits splenic antigen-presenting cell (APC)-dependent proliferation of Th1 clones, at least in part, via down-regulation of APC-derived IL-12. Moreover, the failure of activated B cells to provide costimulation via IL-12 accounts for their inability to support optimal proliferative responses of Th1 clones. We also show that IL-12 regulates the ability of Th1 clones to respond to IL-4 and enhances their proliferation in response to IL-2, IL-7, or IL-15. In contrast, Th2 and Th0 clones appear refractory to the effects of IL-12 on antigen-dependent or growth factor-induced proliferation.