Blockade effects of anti-interferon- (ifn-) γ autoantibodies on ifn- γ -regulated antimicrobial immunity

Dyah Ika Krisnawati, Yung Ching Liu, Yuarn Jang Lee, Yun Ting Wang, Chia Ling Chen, Po Chun Tseng, Ting Jing Shen, Chiou Feng Lin

研究成果: 雜誌貢獻文章同行評審

11 引文 斯高帕斯(Scopus)


The interferon- (IFN-) γ expression is elicited in response to microbial infections and activates immune surveillance by antimicrobial immune elements to induce microbial killing. Patients with adult-onset immunodeficiency who suffer from recurrent infections with microbes, particularly nontuberculous mycobacteria (NTM), commonly display genetic defects in IFN-γ signaling as well as the generation of anti-IFN-γ autoantibodies (autoAbs). Because IFN-γ is an activator of macrophage differentiation and a proinflammatory activator of innate immunity, the blockade effects of the autoAbs present in NTM patient serum on IFN-γ are hypothesized to regulate the antimicrobial function of macrophages. In the presence of patient serum, IFN-γ-induced type 1 macrophage (M1) differentiation was inhibited in PMA-stimulated human monocytic THP-1 cells. Treatment with patient serum significantly blocked the production of proinflammatory factors, including cytokines/chemokines and reactive oxygen/nitrogen species, by M1 macrophages. Importantly, IFN-γ-facilitated phagocytosis and degradation of heat-killed mycobacterium were decreased by cotreatment with patient serum. These results show the blockade activity of anti-IFN-γ autoAbs on IFN-γ-mediated antimicrobial immunity in macrophages.

期刊Journal of Immunology Research
出版狀態已發佈 - 1月 1 2019

ASJC Scopus subject areas

  • 免疫學和過敏
  • 免疫學


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