A precise balance between cellular apoptosis and cellular survival is essential for the proper functioning of the immune system. Whereas apoptosis eliminates self-reactive or supernumerary lymphocytes, survival signaling that counteracts apoptotic programs is needed to allow B and T lymphocytes that recognize pathogens to become activated and expand in response to infection. A major regulator of lymphocyte survival and activation is the transcription factor NF-kappaB. Controlled activation of NF-kappaB is essential for normal innate and adaptive immune responses, and dysregulated NF-kappaB signaling in lymphocytes contributes to diseases ranging from chronic inflammation and autoimmunity to lymphoma. The core NF-kappaB activating machinery composed of the NF-kappaB, IkappaB and IKK proteins is relatively well-characterized, but it is less clear how distinct upstream stimuli activate NF-kappaB in a tissue-, time- and signal-specific manner. In this review, we discuss recent insights into the specific signal transduction pathways leading to NF-kappaB activation that are triggered by engagement of the antigen receptors of T and B cells. We focus mainly on T cell receptor (TCR)-mediated NF-kappaB activation and draw parallels to B cell receptor (BCR)-mediated NF-kappaB activation where appropriate.

中文翻译：

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从抗原到激活：将抗原受体连接到NF-κB的特定信号转导途径。

细胞凋亡与细胞存活之间的精确平衡对于免疫系统的正常运转至关重要。凋亡消除了自身反应性或数量过多的淋巴细胞，但需要抵消凋亡程序的生存信号，才能使识别病原体的B和T淋巴细胞响应感染而被激活和扩增。淋巴细胞存活和激活的主要调节因子是转录因子NF-κB。NF-κB的受控激活对于正常的先天和适应性免疫反应至关重要，并且淋巴细胞中NF-κB信号失调会导致疾病，从慢性炎症，自身免疫到淋巴瘤。由NF-kappaB，IkappaB和IKK蛋白组成的核心NF-kappaB激活机制相对较为成熟，但尚不清楚不同的上游刺激如何以组织，时间和信号特异性方式激活NF-κB。在这篇综述中，我们讨论了对导致NF-κB活化的特定信号转导途径的最新见解，这些信号传导途径是由T细胞和B细胞的抗原受体的结合触发的。我们主要集中在T细胞受体（TCR）介导的NF-kappaB激活，并在适当的情况下与B细胞受体（BCR）介导的NF-kappaB激活平行。