Abstract：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.
张彩勤, 师长宏. Hsp16.3在结核分枝杆菌潜伏感染中的作用[J]. 中国人兽共患病学报, 2019, 35(6): 493-497.
ZHANG Cai-qin, SHI Chang-hong. Role of Hsp16.3 in latent infection of Mycobacterium tuberculosis. Chinese Journal of Zoonoses, 2019, 35(6): 493-497.
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2019, Vol. 35 
