A proline deletion in IFNAR1 impairs IFN-signaling and underlies increased resistance to tuberculosis in humans

Lead researcher

This research was led by Dr Carl Feng, University of Sydney

Main finding

The main finding was that a single-nucleotide polymorphism found in the human IFNAR1 gene is associated with decreased susceptibility to tuberculosis and an increased risk of viral hepatitis in Chinese populations. This study therefore revealed the detrimental effect of IFN signaling in tuberculosis susceptibility. The work was a collaborative project between researchers at The Hudson Institute of Medical Research, four Medical Research Hospitals in China, The Centenary Institute, NSW and The University of Sydney.

Centre

Centre for Innate Immunity & Infectious Diseases

Research group

Interferon Structure and Function

Co-authors

Guoliang Zhang, Nicole A. deWeerd, Sebastian A. Stifter, Lei Liu, Boping Zhou, Wenfei Wang,
Yiping Zhou, Binwu Ying, Xuejiao Hu, Antony Y. Matthews, Magda Ellis, James A. Triccas,
Paul J. Hertzog, Warwick J. Britton, Xinchun Chen & Carl G. Feng

Journal and article title

Nature Communications

A proline deletion in IFNAR1 impairs IFN-signaling and underlies increased resistance to tuberculosis in humans

Most surprising

The study revealed for the first time the detrimental effect of IFN signaling in the human response to tuberculosis.

Future implications

Our research reveals that it may be beneficial to target IFN signaling in humans to reduce tuberculosis susceptibility.

Disease/health impact

Tuberculosis, IFN signaling