J Clin Invest. 2024 Nov 1;134(21):e185865. doi: 10.1172/JCI185865.
Loss of enteric neurons leading to long-term gastrointestinal dysfunction is common to many diseases, and the path to functional recovery is unclear. In this issue of the JCI, Janova et al. report that West Nile virus killed enteric neurons and glia via CD4+ and CD8+ T cells acting through the perforin and Fas ligand pathways. Enteric glial cells contributed to neurogenesis and at least partial replacement of affected neurons. While neurogenesis is important for recovery, dysmotility and disruptions to the network structure persisted. Following enteric injury, the contribution of neurogenesis and the conditions that support restoration of enteric neural circuits for functional recovery remain for further investigation.
导致长期胃肠道功能障碍的肠神经元丧失是许多疾病的共同特征，而功能恢复的途径尚不清楚。在本期 JCI 中，Janova 等人报告称，西尼罗河病毒通过 CD4+和 CD8+T 细胞通过穿孔素和 Fas 配体途径杀死肠神经元和神经胶质细胞。肠神经胶质细胞有助于神经发生，并且至少部分替代受影响的神经元。虽然神经发生对于恢复很重要，但运动障碍和网络结构的破坏仍然存在。肠损伤后，神经发生的贡献以及支持恢复肠神经回路以实现功能恢复的条件仍需要进一步研究。
