The Ma Li team of the School of Laboratory and Biotechnology published a paper in the Science sub-publication to reveal a new mechanism of Viperin's immunity against tuberculosis infection

On October 4, 2022, the Ma Li team from the Institute of Molecular Immunology of the School of Laboratory and Biotechnology published a research paper
entitled "Viperin impairs the innate immune response through the IRAK1-TRAF6-TAK1 axis to promote Mtb infection" online at Science signaling 。 Science Signaling is a comprehensive sub-journal of Science and a Top Journal of the Chinese Academy of Sciences District 1 (IF 9.
517
).
Professor Ma Li is the corresponding author, and Associate Professor Zhou Xinying and Master Zhang Zelin are the first authors
.
This research is supported
by the National Natural Science Foundation of China and the Natural Science Foundation of Guangdong Province.

As one of the important interferon-stimulated genes (ISGs), Viperin has both antiviral and proviral effects, and plays an important role in the natural immune defense and homeostasis maintenance of macrophages (Mφ) and dendritic cells (DC), However, whether it is involved in regulating the immune response of Mφ against Mycobacterium tuberculosis (Mtb) infection has not been previously reported
。 Professor Ma Li's team found that Viperin expressed upregulation in Mtb-infected mice and primary Mφ, and by binding to IRAK1 and TAK1, blocked the formation of IRAK1-TRAF6-TAK1 complex, inhibited the activation of downstream TAK1-IKKα/β signaling pathways, and negatively regulated the production of pro-inflammatory cytokines such as NO and IL-6, IL-1β, TNF-α, etc.
, thereby inhibiting innate immune response and promoting Mtb infection
。 Viperin plays an important role in modulating host defenses against TB and is expected to be a potential target
for anti-tuberculosis dominant therapy (HDT).

In recent years, Professor Ma Li's team has conducted a series of studies on the effects and mechanisms of ISGs on host immune regulation against tuberculosis infection, and found that IRF1 can eliminate Mtb infection in Mφ by inhibiting the mTOR signaling pathway and its downstream p70 S6.
2019,79(3):262-76.
IF 38.
637), MxA can promote Mtb infection in Mφ by inhibiting cytokine production mediated by the TAK1-IKKα/β-NF-κB signaling pathway (J Infect.
2020,81(2):231-41.
IF 38.
637）
。 Studies have revealed that different ISGs have very different
regulatory effects and mechanisms on immunity to TB infection.
In the future, Professor Ma Li's team will continue to work on analyzing the immune regulatory mechanism of host-TB bacteria interactions, and provide scientific and technological assistance
for the development of new drugs and therapies for tuberculosis immunotherapy.

Paper Link: