T-cell control of IL-12p75 production

T-cell control of IL-12p75 production
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DOI:
10.1111/j.1365-3083.2006.01767.x
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发表时间:
2006-08-01
影响因子:
3.7
通讯作者:
Matzinger, P.
Matzinger, P.
中科院分区:
医学4区
文献类型:
--
作者:
Abdi, K.;Singh, N.;Matzinger, P.

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目前认为,树突状细胞 (DC) 在受到细菌病原体或脂多糖 (LPS) 刺激后早期产生的 IL-12 充当促炎细胞因子,桥接先天性免疫反应和适应性免疫反应。然而,我们发现,响应 LPS 的早期大量分泌的只是 p40 亚基,而不是 IL-12p75 异二聚体。初始 T 细胞和各种微生物产物都无法诱导 IL-12p75 的产生,除非 DC 通过干扰素-γ (IFN-gamma) 的存在或与先前激活的 T 细胞相遇进行调节。初始 T 细胞或细菌产物无法诱导 IL-12,这与它作为先天性和适应性免疫反应的引发剂的早期作用相悖。
It is currently thought that IL-12, produced by dendritic cells (DC) early after stimulation by bacterial pathogens or lipopolysaccharide (LPS), acts as a pro-inflammatory cytokine bridging the innate and adaptive immune responses. We found, however, that it is only the p40 subunit and not the IL-12p75 heterodimer that is secreted early in copious amounts in response to LPS. Neither naive T cells, nor a variety of microbial products, were able to induce IL-12p75 production unless the DC were conditioned by the presence of interferon-gamma (IFN-gamma) or by encounter with previously activated T cells. The inability of naive T cells or of bacterial products to induce IL-12 argues against its early role as the initiator of innate and adaptive immune responses.