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Journal of Immunology Research
Volume 2019, Article ID 1629258, 7 pages
https://doi.org/10.1155/2019/1629258
Research Article

Blockade Effects of Anti-Interferon- (IFN-) γ Autoantibodies on IFN-γ-Regulated Antimicrobial Immunity

1Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
2Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
3Dharma Husada Nursing Academy, Kediri, East Java, Indonesia
4Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
5Division of Infectious Diseases, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, Taipei 110, Taiwan
6Division of Infectious Diseases, Department of Internal Medicine, Taipei Medical University Hospital, Taipei 110, Taiwan
7School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
8Pulmonary Research Center, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan
9Cell Physiology and Molecular Image Research Center, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan
10Research Center of Thoracic Medicine, Taipei Medical University, Taipei 110, Taiwan

Correspondence should be addressed to Chiou-Feng Lin; wt.ude.umt@4102nilfc

Received 19 February 2019; Revised 2 April 2019; Accepted 10 April 2019; Published 30 May 2019

Guest Editor: Antonio Rivero

Copyright © 2019 Dyah Ika Krisnawati et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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.