结核分枝杆菌诱导IFN-β产生在免疫调控中的作用

结核分枝杆菌是导致结核病的病原体，也是影响全球数百万人健康的病原体之一。机体中多种模式识别受体(pattern recognition receptor,PRR)可识别入侵的结核分枝杆菌，如DNA和RNA传感器，从而激活天然免疫系统并诱导干扰素-β(interferon-β, IFN-β)产生。虽然IFN-β是先天抗病毒应答的主要效应因子，但其在结核分枝杆菌感染中的作用仍具有争议。结核分枝杆菌感染诱导的IFN-β产生可以促进细菌生长，并增强细菌在宿主中的存活率，但用IFN-β处理细胞后再感染结核分枝杆菌，则可增强抗菌作用，保护宿主。因此，本综述将重点关注可识别结核分枝杆菌并诱导的IFN-β产生的PRR及其下游信号通路，并着重探讨IFN-β在介导结核分枝杆菌调控免疫功能中的作用，尤其是IFN-β与IL-1β之间的相互抑制性调节，旨在为进一步揭示结核分枝杆菌致病机制及结核病治疗药物研发提供新思路。

Research progress in the role of IFN-β production induced by Mycobacterium tuberculosis in immune regulation

Mycobacterium tuberculosis (Mtb), the pathogen of tuberculosis (TB), threatens the health of millions of people worldwide. The pattern recognition receptors (PRRs) including DNA and RNA sensors on immune cells recognize the invaded Mtb to activate the innate immune system and induce the production of interferon-beta (IFN-β). IFN-β is a major effector cytokine in innate antiviral response, while its role in the host response to Mtb infection remains controversial. IFN-β induced by Mtb can promote bacterial growth and improve the bacterial survival in the host. However, IFN-β treatment before Mtb infection can protect the host from bacterial infection. Focusing on the PRR signaling pathways that can recognize Mtb and mediate the IFN-β production, this review expounds the role of IFN-β in mediating the regulation of immune function by Mtb, especially the mutual inhibitory effect between IFN-β and IL-1β, aiming to reveal the pathogenic mechanism of Mtb and facilitate future research and development of anti-TB drugs.