Conclusion The biological effects of mutant is higher than that of original TNFR blocking peptide.
结论突变肽的生物学效应强于原肽。
The molecular switch that sends the call to immune cells is termed the tumor necrosis factor receptor (TNFR).
给免疫细胞发送信息的分子开关又被称为肿瘤坏死因子受体（TNFR）。
The researchers found that astrocytes in mice were producing chemokines in response to activation of their TNFR molecules.
研究人员发现，小鼠的星形胶质细胞可以产生化学增活素作为对TNFR激活以后的应答。
We hypothesized that TNF induces opposing inflammatory and remodeling responses in HF that are TNF-receptor (TNFR) specific.
我们的研究假设是TNF通过特异的TNF受体(TNFR)诱导相反的炎症和重构反应。
When TNFR is activated, it causes cells to send out signal molecules called chemokines that direct immune cells to the site of damage or infection.
当TNFR被激活以后，它使细胞释放出信号分子-化学增活素，化学增活素引导免疫细胞到达破坏或感染的位点。
In recent years, tumor necrosis factor receptor (TNFR) family member-OX40 (CD134), as a key co-stimulatory molecule, involved in maintenance of activation, proliferation, survival of CD4 + t cells.
近年来，肿瘤坏死因子受体超家族成员-OX40 (CD134)，作为一共刺激分子对于维持CD 4 +T细胞的活化、增值、存活起到关键性作用。
In recent years, tumor necrosis factor receptor (TNFR) family member-OX40 (CD134), as a key co-stimulatory molecule, involved in maintenance of activation, proliferation, survival of CD4 + t cells.
近年来，肿瘤坏死因子受体超家族成员-OX40 (CD134)，作为一共刺激分子对于维持CD 4 +T细胞的活化、增值、存活起到关键性作用。
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