分子与细胞免疫学C1q和抗C1qR　mAb抑制U937细胞产生TNF－α

C1q AND AN ANTI-C1qR MONOCLONAL ANTIBODY INHIBIT PMA/LPS-INDUCED TNF-α PRODUCTION BY U937 CELLS

人Ｍ 系Ｕ９３７细胞可在ＰＭＡ／ＬＰＳ诱导下产生ＴＮＦ－α。这种ＴＮＦ－α的诱生可被Ｃ１ｑ以剂量依赖方式所抑制，而且多聚Ｃ１ｑ的抑制作用比单体Ｃ１ｑ强约１０倍。将Ｃ１ｑ热灭活或加入抗人Ｃ１ｑＦ（ａｂ＇）２，Ｃ１ｑ的抑制作用即消失，证实该作用是Ｃ１ｑ特异的。此外，抗人Ｃ１ｑＲｍＡｂＥ８能模拟Ｃ１ｑ诱导类似的抑制效应。这些资料揭示了Ｃ１ｑ／Ｃ１ｑＲ系统的一项新功能，提供了该系统与细胞因子网络联系的直接证据。

A novel functional role of the C1q/C1qR system was reported.The human M line U937 cells did not generate TNF-α constitutively, but did in response to PMA/LPS. Treatment with monomeric or aggregated C1q resulted in a dose-dependent inhibition of TNF-αproduction in PMA/LPS-primed U937 cells, in which the aggreated C1q, in contrast to the monomeric, was 10 times more active. The inhibitory effect of C1q on TNF-αproduction was abrogated when the C1q was heat inactivated or the C1q was incubated with U937 cell in presence of anti-C1q F(ab')2. An inhibition of TNF-α production by the anti-C1qR monoclonal antibody E8 was also demonstrated. The data provide the first direct evidence that there is a connection between the C1q/C1qR system and the cytokine network.