Blockade Effects of Anti-Interferon- (IFN-) γ Autoantibodies on IFN-γ-Regulated Antimicrobial Immunity
Autor: | Dyah Ika Krisnawati, Yung-Ching Liu, Yuarn-Jang Lee, Yun-Ting Wang, Chia-Ling Chen, Po-Chun Tseng, Ting-Jing Shen, Chiou-Feng Lin |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: | |
Zdroj: | Journal of Immunology Research, Vol 2019 (2019) |
Druh dokumentu: | article |
ISSN: | 2314-8861 2314-7156 |
DOI: | 10.1155/2019/1629258 |
Popis: | 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. |
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