Hsp16.3在结核分枝杆菌潜伏感染中的作用

结核病(Tuberculosis,TB)主要是结核分枝杆菌(Mycobacterium tuberculosis,Mtb)引起的细菌感染性疾病。当宿主免疫力减弱,潜伏感染的Mtb得以复苏,导致TB感染的复发。巨噬细胞自噬作为宿主先天性和适应性免疫反应的重要组成部分,在保护宿主抗Mtb感染方面发挥着重要作用。热休克蛋白16.3(Hsp16.3)是Mtb潜伏感染(LTBI)期间表达的重要蛋白,它可能通过抑制巨噬细胞自噬而维持Mtb长期生存,从而导致LTBI的发生。本文综述了Hsp16.3在LTBI中调控巨噬细胞自噬的作用,期望Hsp16.3能够成为LTBI的生物标志物和抗结核药物的新靶点。

Role of Hsp16.3 in latent infection of Mycobacterium tuberculosis

Tuberculosis (TB) is a bacterial infectious disease caused by Mycobacterium tuberculosis (Mtb). When the immune system of the host weakened, the latently infected Mtb was recovered. That results to the recurrence of TB infection. As an important component of the host’s innate and adaptive immune response, macrophage autophagy plays an important role in protecting the host against Mtb infection. Heat shock protein 16.3 (Hsp16.3) is an important protein expressed during MTB latent infection (LTBI). It may maintain MTB long-term survival by inhibiting macrophage autophagy, and lead to the occurrence of LTBI. This article reviews the role of Hsp16.3 on regulating macrophage autophagy in LTBI. It is expected that Hsp16.3 can become a new biomarker for LTBI and a new target for anti-tuberculosis drugs.