Immune Alterations in Patients with Anti-Interferon-γ Autoantibodies

Nuttapol Chruewkamlow; Kodchakorn Mahasongkram; Supansa Pata; Romanee Chaiwarith; Parichart Salee; Khuanchai Supparatpinyo; Watchara Kasinrerk

doi:10.1371/journal.pone.0145983

Immune Alterations in Patients with Anti-Interferon-γ Autoantibodies

PLoS One. 2016 Jan 4;11(1):e0145983. doi: 10.1371/journal.pone.0145983. eCollection 2016.

Authors

Nuttapol Chruewkamlow¹, Kodchakorn Mahasongkram¹, Supansa Pata^{1

2}, Romanee Chaiwarith³, Parichart Salee³, Khuanchai Supparatpinyo^{3

4}, Watchara Kasinrerk^{1

2}

Affiliations

¹ Biomedical Technology Research Center, National Center for Genetic Engineering and Biotechnology, National Sciences and Technology Development Agency at the Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, Thailand.
² Department of Medical Technology, Division of Clinical Immunology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, Thailand.
³ Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
⁴ Research Institute for Health Sciences, Chiang Mai University, Chiang Mai, Thailand.

Abstract

Autoantibodies against interferon-gamma (IFN-γ) can cause immunodeficiency and are associated with various opportunistic infections. In the present study, we investigated other cellular immune parameters for a better understanding of the immunodeficiency condition in the patients. The numbers of WBC, monocytes and NK cells were increased in patients with anti-IFN-γ autoantibodies (AAbs). Upon TCR activation, T cell proliferation and IL-2 receptor of the patients remained intact. Nonetheless, the Th1 cytokine (IFN-γ and TNF-α) production was up-regulated. The production of Th2 (IL-4) and Th17 (IL-17) cytokines was unchanged. We suggest that, in addition to the presence of anti-IFN-γ autoantibodies, alterations in the cellular immune functions may also contribute to this immunodeficiency.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Autoantibodies / blood*
Case-Control Studies
Cytokines / biosynthesis
Humans
Immunity, Cellular
Immunologic Deficiency Syndromes / immunology*
Interferon-gamma / immunology*
T-Lymphocytes / immunology

Substances

Autoantibodies
Cytokines
Interferon-gamma

Supplementary concepts

Immune Deficiency Disease

Grants and funding

This work was supported by the National Research University Project under Thailand’s Office of the Higher Education Commission for Chiang Mai University to KS, Chiang Mai University Center of Excellence grant for Biomedical Technology Research Center to KW, and Thailand Research Fund [TRG5780017] to SP. NC is a postdoctoral researcher supported by Chiang Mai University at the Biomedical Technology Research Center. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.