Chomarat P, Rissoan M C, Banchereau J, Miossec P
Laboratory for Immunological Research, Schering-Plough, Dardilly, France.
J Exp Med. 1993 Feb 1;177(2):523-7. doi: 10.1084/jem.177.2.523.
Interleukin 10 (IL-10) was first described for its ability to inhibit interferon gamma (IFN-gamma) production. Herein, we studied the balance between IFN-gamma and IL-10 production by human peripheral blood mononuclear cells (PBMC) in response to Staphylococcus aureus Cowan (SAC) or lipopolysaccharide (LPS). Monocyte depletion reduced IL-10 production by 90% and resulted in an increased IFN-gamma production. Addition of anti-IL-10 antibody to PBMC cultures also strongly increased IFN-gamma production. In contrast, among various cytokines, only IFN-gamma strongly reduced IL-10 synthesis by SAC- or LPS-activated PBMC and monocytes. Thus, IFN-gamma has proinflammatory effects through the combination of two mechanisms: (a) induction of early tumor necrosis factor alpha (TNF-alpha) and IL-1 beta synthesis; and (b) inhibition of the delayed production of IL-10, an inhibitor of TNF-alpha and IL-1 beta synthesis. Taken together, the present data indicate that IFN-gamma and IL-10 antagonize each other's production and function.
白细胞介素10（IL-10）最初因其抑制γ干扰素（IFN-γ）产生的能力而被描述。在此，我们研究了人外周血单个核细胞（PBMC）在响应金黄色葡萄球菌考恩株（SAC）或脂多糖（LPS）时，IFN-γ和IL-10产生之间的平衡。单核细胞耗竭使IL-10产生减少90%，并导致IFN-γ产生增加。向PBMC培养物中添加抗IL-10抗体也强烈增加了IFN-γ的产生。相反，在各种细胞因子中，只有IFN-γ能强烈降低SAC或LPS激活的PBMC和单核细胞的IL-10合成。因此，IFN-γ通过两种机制的结合具有促炎作用：（a）诱导早期肿瘤坏死因子α（TNF-α）和IL-1β合成；（b）抑制IL-10的延迟产生，IL-10是TNF-α和IL-1β合成的抑制剂。综上所述，目前的数据表明IFN-γ和IL-10相互拮抗彼此的产生和功能。
