Regulation of cytokine production by soluble CD23: costimulation of interferon gamma secretion and triggering of tumor necrosis factor alpha release.
Regulation of cytokine production by soluble CD23: costimulation of interferon gamma secretion and triggering of tumor necrosis factor alpha release.
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DOI：
10.1084/jem.180.3.1005
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发表时间：
1994-09-01
影响因子：
15.3
通讯作者：
Sarfati, Marika
中科院分区：
文献类型：
--
作者：
Armant, Myriam;Ishihara, Hideki;Rubio, Manuel;Delespesse, Guy;Sarfati, Marika
可溶性CD 23（sCD 23）具有多种IgE非依赖性生物学活性。在本研究中，我们研究了sCD 23对人外周血单个核细胞（PBMC）产生细胞因子的调节作用。我们发现，sCD 23增强约80倍的白细胞介素2（IL-2）诱导的干扰素γ（IFN-γ）的生产和约10倍的响应IL-12。这种增强活性是时间和剂量依赖性的，并且与对DNA合成的显著影响无关。sCD 23对IFN-γ合成的共刺激活性在单核细胞耗竭的PBMC中显著降低，表明单核细胞可能是sCD 23的靶点。这一假设得到以下观察结果的支持。首先，sCD 23单独是PBMC产生肿瘤坏死因子α（TNF-α）的有效诱导剂，这种作用在单核细胞耗竭后消失。TNF-α释放的触发被中和性抗CD 23单克隆抗体（mAb）特异性抑制。此外，IL-2和IL-12与sCD 23协同诱导TNF-α产生。其次，sCD 23触发其他炎症介质如IL-1 α、IL-1 β和IL-6的释放。最后，响应于IL-2和sCD 23的TNF-α产生先于IFN-γ，并且IFN-γ分泌被抗TNF-α mAb显著抑制，表明IFN-γ产生的sCD 23共刺激信号可能部分由TNF-α释放介导。有人提出，sCD 23是一种促炎细胞因子，此外，可能通过增强IFN-γ的产生在免疫反应的控制中发挥重要作用。
Soluble CD23 (sCD23) has multiple IgE-independent biological activities. In the present study, we examined the regulatory effect of sCD23 on cytokine production by human peripheral blood mononuclear cells (PBMC). We show that sCD23 enhances by about 80-fold the interleukin 2 (IL-2)-induced interferon gamma (IFN-gamma) production and by about 10-fold the response to IL-12. This potentiating activity is time and dose dependent and is not associated with a significant effect on DNA synthesis. The sCD23 costimulatory activity for IFN-gamma synthesis is drastically reduced in monocyte-depleted PBMC, suggesting that monocytes may be the target for sCD23. This hypothesis was supported by the following observations. First, sCD23 alone is a potent inducer of tumor necrosis factor alpha (TNF-alpha) production by PBMC and this effect disappears after monocyte depletion. The triggering of TNF-alpha release is specifically inhibited by neutralizing anti-CD23 monoclonal antibody (mAb). In addition, IL-2 and IL-12 synergize with sCD23 to induce TNF-alpha production. Second, sCD23 triggers the release of other inflammatory mediators such as IL-1 alpha, IL-1 beta, and IL-6. Finally, TNF-alpha production in response to IL-2 and sCD23 precedes IFN-gamma and IFN-gamma secretion is significantly inhibited by anti-TNF-alpha mAb, indicating that the sCD23 costimulatory signal for IFN-gamma production may be partially mediated by TNF-alpha release. It is proposed that sCD23 is a proinflammatory cytokine that, in addition, may play an important role in the control of the immune response via the enhancement of IFN-gamma production.
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DOI：
10.1084/jem.172.3.693
发表时间：
1990-09-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Letellier M;Nakajima T;Pulido-Cejudo G;Hofstetter H;Delespesse G
通讯作者：
Delespesse G
影响因子：
3.6
作者：
LETELLIER, M;SARFATI, M;DELESPESSE, G
通讯作者：
DELESPESSE, G
影响因子：
11.4
作者：
MOSSALAYI, MD;AROCK, M;SARFATI, M
通讯作者：
SARFATI, M
影响因子：
15.3
作者：
Alderson, M R;Armitage, R J;Tough, T W;Strockbine, L;Fanslow, W C;Spriggs, M K
通讯作者：
Spriggs, M K
影响因子：
56.9
作者：
FLORESROMO, L;SHIELDS, J;BONNEFOY, JY
通讯作者：
BONNEFOY, JY