Outcomes of RIP Kinase Signaling During Neuroinvasive Viral Infection.
Outcomes of RIP Kinase Signaling During Neuroinvasive Viral Infection.
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DOI：
10.1007/82_2020_204
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发表时间：
2023
影响因子：
--
通讯作者：
Oberst A
中科院分区：
文献类型：
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作者：
Daniels BP;Oberst A
神经侵袭性病毒性疾病是全球公共卫生的一个相当大的和日益增长的负担。尽管如此，这些感染仍然知之甚少，并且控制对感染的保护性与病理性神经炎症反应的分子机制是一个深入研究的问题。最近的证据表明，坏死性凋亡，免疫原性形式的程序性细胞死亡，可能有助于病毒性脑炎的发病机制。然而，协调坏死性凋亡的受体相互作用蛋白（RIP）激酶RIPK1和RIPK3似乎在中枢神经系统（CNS）中也具有意想不到的非细胞死亡依赖性功能，可在神经侵袭性感染期间促进有益的神经炎症。在这里，我们回顾了这一领域的新证据，并对最近的工作进行了额外的讨论，这些工作研究了RIPK信号传导和坏死性凋亡在CNS非感染性病理过程中的作用，因为这些研究为RIP激酶的专门神经免疫功能的潜力提供了重要的额外见解。
Neuroinvasive viral diseases are a considerable and growing burden on global public health. Despite this, these infections remain poorly understood, and the molecular mechanisms that govern protective versus pathological neuroinflammatory responses to infection are a matter of intense investigation. Recent evidence suggests that necroptosis, an immunogenic form of programmed cell death, may contribute to the pathogenesis of viral encephalitis. However, the receptor-interacting protein (RIP) kinases that coordinate necroptosis, RIPK1 and RIPK3, also appear to have unexpected, cell death-independent functions in the central nervous system (CNS) that promote beneficial neuroinflammation during neuroinvasive infection. Here, we review the emerging evidence in this field, with additional discussion of recent work examining roles for RIPK signaling and necroptosis during noninfectious pathologies of the CNS, as these studies provide important additional insight into the potential for specialized neuroimmune functions for the RIP kinases.