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Lymphocyte signaling and activation by the CARMA1-BCL10-MALT1 signalosome

机译：CARMA1-BCL10-MALT1信号体的淋巴细胞信号传导和激活

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The CARMA1-BCL10-MALT1 (CBM) signalosome triggers canonical NF-kappa B signaling and lymphocyte activation upon antigen-receptor stimulation. Genetic studies in mice and the analysis of human immune pathologies unveiled a critical role of the CBM complex in adaptive immune responses. Great progress has been made in elucidating the fundamental mechanisms that dictate CBM assembly and disassembly. By bridging proximal antigen-receptor signaling to downstream signaling pathways, the CBM complex exerts a crucial scaffolding function. Moreover, the MALT1 subunit confers a unique proteolytic activity that is key for lymphocyte activation. Deregulated 'chronic' CBM signaling drives constitutive NF-kappa B signaling and MALT1 activation, which contribute to the development of autoimmune and inflammatory diseases as well as lymphomagenesis. Thus, the processes that govern CBM activation and function are promising targets for the treatment of immune disorders. Here, we summarize the current knowledge on the functions and mechanisms of CBM signaling in lymphocytes and how CBM deregulations contribute to aberrant signaling in malignant lymphomas.
机译：CARMA1-BCL10-MALT1（CBM）信号小体在抗原受体刺激后触发经典的NF-κB信号和淋巴细胞活化。小鼠的基因研究和人体免疫病理分析揭示了CBM复合物在适应性免疫反应中的关键作用。在阐明决定CBM组装和拆卸的基本机制方面已取得了巨大进展。通过将近端抗原受体信号传导桥接到下游信号传导途径，CBM复合物发挥了关键的支架作用。此外，MALT1亚基赋予独特的蛋白水解活性，这是淋巴细胞激活的关键。失控的“慢性” CBM信号驱动组成型NF-κB信号和MALT1激活，这有助于自身免疫和炎性疾病的发展以及淋巴瘤的发生。因此，控制CBM激活和功能的过程是治疗免疫疾病的有希望的目标。在这里，我们总结了有关淋巴细胞中CBM信号传导的功能和机制的当前知识，以及CBM失调如何导致恶性淋巴瘤中异常信号传导的知识。

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