title: Immune Alterations in Patients with Anti-Interferon-γ Autoantibodies.
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.
authors.affiliation: 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.
authors.forename: Nuttapol
authors.initials: N
authors.lastname: Chruewkamlow
authors.affiliation: 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.
authors.forename: Kodchakorn
authors.initials: K
authors.lastname: Mahasongkram
authors.affiliation: 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.|Department of Medical Technology, Division of Clinical Immunology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, Thailand.
authors.forename: Supansa
authors.initials: S
authors.lastname: Pata
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
authors.forename: Romanee
authors.initials: R
authors.lastname: Chaiwarith
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
authors.forename: Parichart
authors.initials: P
authors.lastname: Salee
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.|Research Institute for Health Sciences, Chiang Mai University, Chiang Mai, Thailand.
authors.forename: Khuanchai
authors.initials: K
authors.lastname: Supparatpinyo
authors.affiliation: 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.|Department of Medical Technology, Division of Clinical Immunology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, Thailand.
authors.forename: Watchara
authors.initials: W
authors.lastname: Kasinrerk
mesh_terms: D001323:Autoantibodies / Q000097:blood*; D016022:Case-Control Studies; D016207:Cytokines / Q000096:biosynthesis; D006801:Humans; D007111:Immunity, Cellular; D007153:Immunologic Deficiency Syndromes / Q000276:immunology*; D007371:Interferon-gamma / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D001323:Autoantibodies; D016207:Cytokines; D007371:Interferon-gamma