IFI44L as a Forward Regulator Enhancing Host Antituberculosis Responses | Zendy

Haiqin Jiang | Zendy; Lemuel ShuiLun Tsang | Zendy; Hongsheng Wang | Zendy; Changhong Liu | Zendy

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IFI44L as a Forward Regulator Enhancing Host Antituberculosis Responses

Author(s) -

Haiqin Jiang,

Lemuel ShuiLun Tsang,

Hongsheng Wang,

Changhong Liu

Publication year - 2021

Publication title -

journal of immunology research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.315

H-Index - 83

eISSN - 2314-8861

pISSN - 2314-7156

DOI - 10.1155/2021/5599408

Subject(s) - mycobacterium tuberculosis , tuberculosis , rifampicin , gene knockdown , intracellular , regulator , downregulation and upregulation , antimicrobial , interferon gamma , microbiology and biotechnology , biology , intracellular parasite , interferon , immunology , gene , cytokine , medicine , antibiotics , pathology , biochemistry

Interferon-induced protein 44-like (IFI44L) gene is a type I interferon-stimulated gene (ISG) that plays a critical role in antiviral activity and constitutes a promising diagnostic marker. However, its precise role and function in tuberculosis have not been unveiled. This study showed that IFI44L acts as an antimicrobial target and positive modulator in human macrophages. Knockdown of IFI44L led to increased Mycobacterium tuberculosis intracellular survival. Moreover, IFI44L was significantly upregulated, and it restricted the intracellular survival of M. tuberculosis H37Rv strains at 72 h after rifampicin treatment. Individuals with cutaneous tuberculosis (CTB) were found to have significantly higher IFI44L expression after 6 months of rifampicin therapy than after only 1 month. These results demonstrated that IFI44L induced positive regulation and clearance of M. tuberculosis from human macrophages. This antimicrobial activity of IFI44L makes it a possible target for therapeutic applications against M. tuberculosis .

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