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Article ; Online: Anti-interferon-γ autoantibody-associated immunodeficiency.

Shih, Han-Po / Ding, Jing-Ya / Yeh, Chun-Fu / Chi, Chih-Yu / Ku, Cheng-Lung

2021 Volume 72, Page(s) 206–214

Abstract: Anticytokine autoantibodies are an emerging disease etiology, through the disturbance of physiological functions of cognate cytokines. Anti-interferon (IFN)-γ autoantibodies (AIGAs) were first identified in patients with severe mycobacterial infections, ... ...

Abstract	Anticytokine autoantibodies are an emerging disease etiology, through the disturbance of physiological functions of cognate cytokines. Anti-interferon (IFN)-γ autoantibodies (AIGAs) were first identified in patients with severe mycobacterial infections, and were considered to be an autoimmune phenocopy of inborn genetic errors of the IL-12/IFN-γ axis. More than 600 reported cases, most originating from Southeast Asia, have been diagnosed over the last decade. Specific HLA class II molecules are associated with these autoantibodies, which provide a genetic basis for the high prevalence of this immunodeficiency syndrome in certain ethnic groups. Salmonellosis and herpes zoster reactivation are observed in more than half the patients with AIGAs. Moreover, AIGAs have been shown to underlie severe Taralomyce marneffei infection in HIV-negative patients. AIGAs may, thus, be considered a new form of late-onset immunodeficiency conferring a predisposition not only to severe mycobacterial, but also to some bacterial and fungal infections.
MeSH term(s)	Animals ; Autoantibodies/immunology ; Autoimmune Diseases/immunology ; Autoimmunity ; Biomarkers ; Disease Susceptibility/immunology ; Humans ; Immunologic Deficiency Syndromes/diagnosis ; Immunologic Deficiency Syndromes/etiology ; Immunologic Deficiency Syndromes/metabolism ; Interferon-gamma/immunology
Chemical Substances	Autoantibodies ; Biomarkers ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2021-06-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2021.05.007
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Article ; Online: Targeting the elevated IFN-γ in vitiligo patients by human anti- IFN-γ monoclonal antibody hampers direct cytotoxicity in melanocyte.

Ng, Chau Yee / Chan, Yu-Pei / Chiu, Yen-Chuan / Shih, Han-Po / Lin, You-Ning / Chung, Pei-Han / Huang, Jing-Yi / Chen, Hung-Kai / Chung, Wen-Hung / Ku, Cheng-Lung

Journal of dermatological science

2023 Volume 110, Issue 3, Page(s) 78–88

Abstract: Background: Vitiligo is an autoimmune disease that progressively destroys melanocytes in the skin, resulting in patchy disfiguring depigmentation. The direct pathological effect of IFN-γ, CXCL10 to the melanocytes in vitiligo has been reported, but ... ...

Abstract	Background: Vitiligo is an autoimmune disease that progressively destroys melanocytes in the skin, resulting in patchy disfiguring depigmentation. The direct pathological effect of IFN-γ, CXCL10 to the melanocytes in vitiligo has been reported, but there are contradictory results to which cytokine exerts the critical cytotoxic effect on melanocytes. Objective: The overarching goal was to study the direct toxicity of highly expressed cytokine in vitiligo skin lesions to melanocytes. Methods: We obtained the interstitial fluid analyte from lesion and non-lesion skin of vitiligo patients and healthy control and sent for high sensitivity multiplex cytokine panel. We further performed functional study to identify the direct toxicity effect of the highly expressed cytokines. Results: We found a significant elevation of IFN-γ, CXCL9, CXCL10, CXCL11 in the vitiligo skin. Ex vivo melanocyte studies support the direct role of IFN-γ per se in melanocyte cell loss, increased oxidative stress and melanogenesis disruption. Interestingly, we found that IFN-γ regulated cell death through oxidative stress-related ferroptosis cell death, which may initiate autoimmunity in vitiligo. In contrast to blocking selected cell death pathway, our in vitro study supports the rescue effect of human anti-IFN-γ monoclonal antibody 2A6Q to IFN-γ induced cell death, oxidative stress, and loss of function in melanocytes by interrupting IFN-γ signaling, which may be a potential therapeutic option for vitiligo. Conclusion: This study further confirms the direct of toxicity effect of IFN-γ per se towards melanocyte in vitiligo skin and the potential utility of human anti-IFN-γ monoclonal antibody in treating vitiligo.
MeSH term(s)	Humans ; Vitiligo/pathology ; Melanocytes/metabolism ; Skin/pathology ; Interferon-gamma/metabolism ; Cytokines/metabolism ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal/pharmacology
Chemical Substances	Interferon-gamma (82115-62-6) ; Cytokines ; Antibodies, Monoclonal
Language	English
Publishing date	2023-04-25
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1024446-3
ISSN	1873-569X ; 0923-1811
ISSN (online)	1873-569X
ISSN	0923-1811
DOI	10.1016/j.jdermsci.2023.04.006
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Article ; Online: HAI-2 as a novel inhibitor of plasmin represses lung cancer cell invasion and metastasis.

Wu, Shang-Ru / Lin, Chia-Hao / Shih, Han-Po / Ko, Chun-Jung / Lin, Hsin-Ying / Lan, Shao-Wei / Lin, Hsin-Hsien / Tu, Hsin-Fang / Ho, Chao-Chi / Huang, Hsiang-Po / Lee, Ming-Shyue

British journal of cancer

2019 Volume 120, Issue 5, Page(s) 499–511

Abstract: Background: Dysregulation of pericellular proteolysis usually accounts for cancer cell invasion and metastasis. Isolation of a cell-surface protease system for lung cancer metastasis is an important issue for mechanistic studies and therapeutic target ... ...

Abstract	Background: Dysregulation of pericellular proteolysis usually accounts for cancer cell invasion and metastasis. Isolation of a cell-surface protease system for lung cancer metastasis is an important issue for mechanistic studies and therapeutic target identification. Methods: Immunohistochemistry of a tissue array (n = 64) and TCGA database (n = 255) were employed to assess the correlation between serine protease inhibitors (SPIs) and lung adenocarcinoma progression. The role of SPI in cell motility was examined using transwell assays. Pulldown and LC/MS/MS were performed to identify the SPI-modulated novel protease(s). A xenografted mouse model was harnessed to demonstrate the role of the SPI in lung cancer metastasis. Results: Hepatocyte growth factor activator inhibitor-2 (HAI-2) was identified to be downregulated following lung cancer progression, which was related to poor survival and tumour invasion. We further isolated a serum-derived serine protease, plasmin, to be a novel target of HAI-2. Downregulation of HAI-2 promotes cell surface plasmin activity, EMT, and cell motility. HAI-2 can suppress plasmin-mediated activations of HGF and TGF-β1, EMT and cell invasion. In addition, downregulated HAI-2 increased metastasis of lung adenocarcinoma via upregulating plasmin activity. Conclusion: HAI-2 functions as a novel inhibitor of plasmin to suppress lung cancer cell motility, EMT and metastasis.
MeSH term(s)	A549 Cells ; Adenocarcinoma of Lung/metabolism ; Adenocarcinoma of Lung/pathology ; Adenocarcinoma of Lung/secondary ; Animals ; Cell Line, Tumor ; Cell Movement ; Disease Progression ; Epithelial-Mesenchymal Transition ; Fibrinolysin/antagonists & inhibitors ; Fibrinolysin/metabolism ; Hepatocyte Growth Factor/metabolism ; Humans ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Membrane Glycoproteins/metabolism ; Mice ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Neoplasm Transplantation ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Membrane Glycoproteins ; SPINT2 protein, human ; Transforming Growth Factor beta1 ; Hepatocyte Growth Factor (67256-21-7) ; Fibrinolysin (EC 3.4.21.7)
Language	English
Publishing date	2019-02-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/s41416-019-0400-2
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Article ; Online: Pathogenic autoantibodies to IFN-γ act through the impedance of receptor assembly and Fc-mediated response.

Shih, Han-Po / Ding, Jing-Ya / Sotolongo Bellón, Junel / Lo, Yu-Fang / Chung, Pei-Han / Ting, He-Ting / Peng, Jhan-Jie / Wu, Tsai-Yi / Lin, Chia-Hao / Lo, Chia-Chi / Lin, You-Ning / Yeh, Chun-Fu / Chen, Jiun-Bo / Wu, Ting-Shu / Liu, Yuag-Meng / Kuo, Chen-Yen / Wang, Shang-Yu / Tu, Kun-Hua / Ng, Chau Yee /

Lei, Wei-Te / Tsai, Yu-Huan / Chen, Jou-Han / Chuang, Ya-Ting / Huang, Jing-Yi / Rey, Félix A / Chen, Hung-Kai / Chang, Tse-Wen / Piehler, Jacob / Chi, Chih-Yu / Ku, Cheng-Lung

The Journal of experimental medicine

2022 Volume 219, Issue 9

Abstract: Anti-interferon (IFN)-γ autoantibodies (AIGAs) are a pathogenic factor in late-onset immunodeficiency with disseminated mycobacterial and other opportunistic infections. AIGAs block IFN-γ function, but their effects on IFN-γ signaling are unknown. Using ... ...

Abstract	Anti-interferon (IFN)-γ autoantibodies (AIGAs) are a pathogenic factor in late-onset immunodeficiency with disseminated mycobacterial and other opportunistic infections. AIGAs block IFN-γ function, but their effects on IFN-γ signaling are unknown. Using a single-cell capture method, we isolated 19 IFN-γ-reactive monoclonal antibodies (mAbs) from patients with AIGAs. All displayed high-affinity (KD < 10-9 M) binding to IFN-γ, but only eight neutralized IFN-γ-STAT1 signaling and HLA-DR expression. Signal blockade and binding affinity were correlated and attributed to somatic hypermutations. Cross-competition assays identified three nonoverlapping binding sites (I-III) for AIGAs on IFN-γ. We found that site I mAb neutralized IFN-γ by blocking its binding to IFN-γR1. Site II and III mAbs bound the receptor-bound IFN-γ on the cell surface, abolishing IFN-γR1-IFN-γR2 heterodimerization and preventing downstream signaling. Site III mAbs mediated antibody-dependent cellular cytotoxicity, probably through antibody-IFN-γ complexes on cells. Pathogenic AIGAs underlie mycobacterial infections by the dual blockade of IFN-γ signaling and by eliminating IFN-γ-responsive cells.
MeSH term(s)	Antibodies, Monoclonal ; Autoantibodies ; Electric Impedance ; Humans ; Interferon-gamma ; Mycobacterium Infections/genetics ; Mycobacterium Infections/microbiology ; Receptors, Interferon/genetics
Chemical Substances	Antibodies, Monoclonal ; Autoantibodies ; Receptors, Interferon ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2022-07-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20212126
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Article ; Online: Cryptococcus gattii Infection as the Major Clinical Manifestation in Patients with Autoantibodies Against Granulocyte-Macrophage Colony-Stimulating Factor.

Wang, Shang-Yu / Lo, Yu-Fang / Shih, Han-Po / Ho, Mao-Wang / Yeh, Chun-Fu / Peng, Jhan-Jie / Ting, He-Ting / Lin, Kuo-Hsi / Huang, Wen-Chi / Chen, Yi-Chun / Chiu, Yu-Hsin / Hsu, Chien-Wei / Tseng, Yu-Ting / Wang, Lih-Shinn / Lei, Wei-Yi / Lin, Chen-Yuan / Aoh, Yu / Chou, Chia-Huei / Wu, Tsai-Yi /

Ding, Jing-Ya / Lo, Chia-Chi / Lin, You-Ning / Tu, Kun-Hua / Lei, Wei-Te / Kuo, Chen-Yen / Chi, Chih-Yu / Ku, Cheng-Lung

Journal of clinical immunology

2022 Volume 42, Issue 8, Page(s) 1730–1741

Abstract: Purpose: Anti-granulocyte-macrophage colony-stimulating factor autoantibodies (anti-GM-CSF Abs) are a predisposing factor for pulmonary alveolar proteinosis (PAP) and Cryptococcus gattii cryptococcosis. This study aimed to investigate clinical ... ...

Abstract	Purpose: Anti-granulocyte-macrophage colony-stimulating factor autoantibodies (anti-GM-CSF Abs) are a predisposing factor for pulmonary alveolar proteinosis (PAP) and Cryptococcus gattii cryptococcosis. This study aimed to investigate clinical manifestations in anti-GM-CSF Ab-positive patients with C. gattii cryptococcosis and analyze the properties of anti-GM-CSF Abs derived from these patients and patients with PAP. Methods: Thirty-nine patients diagnosed with cryptococcosis (caused by C. neoformans or C. gattii) and 6 with PAP were enrolled in the present study. Clinical information was obtained from medical records. Blood samples were collected for analysis of autoantibody properties. We also explored the National Health Insurance Research Database (NHIRD) of Taiwan to investigate the epidemiology of cryptococcosis and PAP. Results: High titers of neutralizing anti-GM-CSF Abs were identified in 15 patients with cryptococcosis (15/39, 38.5%). Most anti-GM-CSF Ab-positive cryptococcosis cases had central nervous system (CNS) involvement (14/15, 93.3%). Eleven out of 14 (78.6%) anti-GM-CSF Ab-positive CNS cryptococcosis patients were confirmed to be infected with C. gattii, and PAP did not occur synchronously or metachronously in a single patient from our cohort. Exploration of an association between HLA and anti-GM-CSF Ab positivity or differential properties of autoantibodies from cryptococcosis patients and PAP yielded no significant results. Conclusion: Anti-GM-CSF Abs can cause two diseases, C. gattii cryptococcosis and PAP, which seldom occur in the same subject. Current biological evidence regarding the properties of anti-GM-CSF Abs cannot provide clues regarding decisive mechanisms. Further analysis, including more extensive cohort studies and investigations into detailed properties, is mandatory to better understand the pathogenesis of anti-GM-CSF Abs.
MeSH term(s)	Humans ; Autoantibodies ; Cryptococcosis/diagnosis ; Cryptococcosis/epidemiology ; Pulmonary Alveolar Proteinosis/diagnosis ; Pulmonary Alveolar Proteinosis/etiology ; Granulocyte-Macrophage Colony-Stimulating Factor/immunology
Chemical Substances	Autoantibodies ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2022-08-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-022-01341-2
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Article ; Online: Disseminated Cryptococcosis Due to Anti-Granulocyte-Macrophage Colony-Stimulating Factor Autoantibodies in the Absence of Pulmonary Alveolar Proteinosis.

Kuo, Chen-Yen / Wang, Shang-Yu / Shih, Han-Po / Tu, Kun-Hua / Huang, Wen-Chi / Ding, Jing-Ya / Lin, Chia-Hao / Yeh, Chun-Fu / Ho, Mao-Wang / Chang, Shi-Chuan / He, Chi-Ying / Chen, Hung-Kai / Ho, Chen-Hsuan / Lee, Chen-Hsiang / Chi, Chih-Yu / Ku, Cheng-Lung

Journal of clinical immunology

2017 Volume 37, Issue 2, Page(s) 143–152

Abstract: Introduction: Autoantibodies to granulocyte-macrophage colony-stimulating factor (GM-CSF) can cause acquired pulmonary alveolar proteinosis (PAP). Cases of acquired PAP susceptible to typical respiratory pathogens and opportunistic infections have been ... ...

Abstract	Introduction: Autoantibodies to granulocyte-macrophage colony-stimulating factor (GM-CSF) can cause acquired pulmonary alveolar proteinosis (PAP). Cases of acquired PAP susceptible to typical respiratory pathogens and opportunistic infections have been reported. Anti-GM-CSF autoantibodies have been reported in a few patients with cryptococcal meningitis. This study evaluated the presence of neutralizing anti-GM-CSF autoantibodies in patients without known congenital or acquired immunodeficiency with severe pulmonary or extrapulmonary cryptococcal infection but without PAP. Methods: We took a clinical history and performed an immunologic evaluation and screening of anti-cytokine autoantibodies in patients with cryptococcal meningitis. The impact of autoantibodies to GM-CSF on immune function was assessed by intracellular staining of GM-CSF-induced STAT5 phosphorylation and MIP-1α production in normal peripheral blood mononuclear cells incubated with plasma from patients or normal control subjects. Results: Neutralizing anti-GM-CSF autoantibodies were identified in four patients with disseminated cryptococcosis, none of whom exhibited PAP. Plasma from patients blocked GM-CSF signaling and inhibited STAT5 phosphorylation and production of MIP-1α. One patient died of disseminated cryptococcosis involving the central nervous system, which was associated with defective GM-CSF activity. Conclusions: Anti-GM-CSF autoantibodies increase susceptibility to cryptococcal infection in adults without PAP. Cryptococcal central nervous system infection associated with anti-GM-CSF autoantibodies could result in neurological sequelae or be life-threatening. Therefore, timely detection of neutralizing anti-GM-CSF autoantibodies and development of an effective therapy are necessary to prevent deterioration of cryptococcal infection in these patients.
Language	English
Publishing date	2017-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-016-0364-4
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Article ; Online: Anti-IFN-γ autoantibodies underlie disseminated Talaromyces marneffei infections.

Guo, Jing / Ning, Xin-Qiang / Ding, Jing-Ya / Zheng, Yan-Qing / Shi, Na-Na / Wu, Feng-Yao / Lin, You-Kun / Shih, Han-Po / Ting, He-Ting / Liang, Gang / Lu, Xiang-Chan / Kong, Jin-Ling / Wang, Ke / Lu, Yi-Bo / Fu, Yu-Jiao / Hu, Rong / Li, Tian-Min / Pan, Kai-Su / Li, Xiu-Ying /

Huang, Chun-Yang / Lo, Yu-Fang / Chang, Ian Yi-Feng / Yeh, Chun-Fu / Tu, Kun-Hua / Tsai, Yu-Huan / Ku, Cheng-Lung / Cao, Cun-Wei

The Journal of experimental medicine

2020 Volume 217, Issue 12

Abstract: Talaromyces marneffei causes life-threatening opportunistic infections, mainly in Southeast Asia and South China. T. marneffei mainly infects patients with human immunodeficiency virus (HIV) but also infects individuals without known immunosuppression. ... ...

Abstract	Talaromyces marneffei causes life-threatening opportunistic infections, mainly in Southeast Asia and South China. T. marneffei mainly infects patients with human immunodeficiency virus (HIV) but also infects individuals without known immunosuppression. Here we investigated the involvement of anti-IFN-γ autoantibodies in severe T. marneffei infections in HIV-negative patients. We enrolled 58 HIV-negative adults with severe T. marneffei infections who were otherwise healthy. We found a high prevalence of neutralizing anti-IFN-γ autoantibodies (94.8%) in this cohort. The presence of anti-IFN-γ autoantibodies was strongly associated with HLA-DRB116:02 and -DQB105:02 alleles in these patients. We demonstrated that adult-onset acquired immunodeficiency due to autoantibodies against IFN-γ is the major cause of severe T. marneffei infections in HIV-negative patients in regions where this fungus is endemic. The high prevalence of anti-IFN-γ autoantibody-associated HLA class II DRB116:02 and DQB105:02 alleles may account for severe T. marneffei infections in Southeast Asia. Our findings clarify the pathogenesis of T. marneffei infection and pave the way for developing novel treatments.
MeSH term(s)	Adult ; Aged ; Alleles ; Autoantibodies/blood ; Autoantibodies/immunology ; Case-Control Studies ; Female ; HLA-DRB1 Chains/immunology ; Humans ; Interferon-gamma/immunology ; Male ; Middle Aged ; Mycoses/blood ; Mycoses/immunology ; Mycoses/microbiology ; Talaromyces/physiology ; Young Adult
Chemical Substances	Autoantibodies ; HLA-DRB1 Chains ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2020-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20190502
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Article ; Online: Identification of a major epitope by anti-interferon-γ autoantibodies in patients with mycobacterial disease.

Lin, Chia-Hao / Chi, Chih-Yu / Shih, Han-Po / Ding, Jing-Ya / Lo, Chia-Chi / Wang, Shang-Yu / Kuo, Chen-Yen / Yeh, Chun-Fu / Tu, Kun-Hua / Liu, Shou-Hsuan / Chen, Hung-Kai / Ho, Chen-Hsuan / Ho, Mao-Wang / Lee, Chen-Hsiang / Lai, Hsin-Chin / Ku, Cheng-Lung

Nature medicine

2016 Volume 22, Issue 9, Page(s) 994–1001

Abstract: The binding of autoantibodies (autoAbs) to interferon (IFN)-γ in people with mycobacterial diseases has become an emerging medical concern. Many patients display specific human leukocyte antigen (HLA) class II haplotypes, which suggests that a common T ... ...

Abstract	The binding of autoantibodies (autoAbs) to interferon (IFN)-γ in people with mycobacterial diseases has become an emerging medical concern. Many patients display specific human leukocyte antigen (HLA) class II haplotypes, which suggests that a common T cell-dependent and B cell-dependent mechanism might underlie the production of specific anti-IFN-γ autoAbs. We show here that these autoAbs target a major epitope (amino acids 121-131, designated position (P)121-131) in a region crucial for IFN-γ receptor (IFN-γR) activation to impair IFN-γ-mediated activities. The amino acid sequence of this epitope is highly homologous to a stretch in the Noc2 protein of Aspergillus spp., which was cross-reactive with autoAbs from patients. Rats immunized with Aspergillus Noc2 developed antibodies that reacted with human IFN-γ. We generated an epitope-erased variant of IFN-γ (EE-IFN-γ), in which the major neutralizing epitope region was altered. The binding affinity of anti-IFN-γ autoAbs for EE-IFN-γ was reduced by about 40%, as compared to that for IFN-γ1-131. Moreover, EE-IFN-γ activated the IFN-γR downstream signaling pathway ex vivo, irrespectively of anti-IFN-γ autoAbs. In conclusion, we identified a common, crucial B cell epitope that bound to anti-IFN-γ autoAbs in patients, and we propose a molecular-mimicry model for autoAb development. In addition, treatment with EE-IFN-γ might be worth investigating in patients producing anti-IFN-γ autoAbs.
MeSH term(s)	Animals ; Antibodies, Neutralizing/immunology ; Aspergillus ; Autoantibodies/immunology ; Autoantigens/immunology ; Case-Control Studies ; Cross Reactions ; Enzyme-Linked Immunosorbent Assay ; Epitope Mapping ; Epitopes/immunology ; Epitopes, B-Lymphocyte ; Fungal Proteins/immunology ; HLA-DR Antigens/immunology ; Haplotypes ; Histocompatibility Antigens Class II/genetics ; Humans ; Immunization ; Immunoblotting ; Interferon-gamma/immunology ; Interleukin-12 Subunit p40/immunology ; Mycobacterium Infections ; Rats ; Receptors, Interferon/immunology ; Interferon gamma Receptor
Chemical Substances	Antibodies, Neutralizing ; Autoantibodies ; Autoantigens ; Epitopes ; Epitopes, B-Lymphocyte ; Fungal Proteins ; HLA-DR Antigens ; Histocompatibility Antigens Class II ; Interleukin-12 Subunit p40 ; Receptors, Interferon ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2016-08-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm.4158
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Article ; Online: Anti-IFN-γ autoantibodies are strongly associated with HLA-DR15:02/16:02 and HLA-DQ05:01/05:02 across Southeast Asia.

The Journal of allergy and clinical immunology

2016 Volume 137, Issue 3, Page(s) 945–8.e8

MeSH term(s)	Alleles ; Asia, Southeastern ; Asian Continental Ancestry Group/genetics ; Autoantibodies/immunology ; Genetic Association Studies ; HLA-DQ Antigens/genetics ; HLA-DQ Antigens/immunology ; HLA-DQ beta-Chains/genetics ; HLA-DQ beta-Chains/immunology ; HLA-DR Antigens/genetics ; HLA-DR Antigens/immunology ; HLA-DRB1 Chains/genetics ; HLA-DRB1 Chains/immunology ; Histocompatibility Testing ; Humans ; Interferon-gamma/antagonists & inhibitors
Chemical Substances	Autoantibodies ; HLA-DQ Antigens ; HLA-DQ beta-Chains ; HLA-DQB1 antigen ; HLA-DR Antigens ; HLA-DRB1 Chains ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2015.09.018
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Article ; Online: Clinical manifestations, course, and outcome of patients with neutralizing anti-interferon-γ autoantibodies and disseminated nontuberculous mycobacterial infections.

Chi, Chih-Yu / Lin, Chia-Hao / Ho, Mao-Wang / Ding, Jing-Ya / Huang, Wen-Chi / Shih, Han-Po / Yeh, Chun-Fu / Fung, Chang-Phone / Sun, Hsin-Yun / Huang, Ching-Tai / Wu, Ting-Shu / Chang, Chih-Yen / Liu, Yuag-Meng / Feng, Jia-Yih / Wu, Wei-Kai / Wang, Lih-Shinn / Tsai, Chung-Hao / Ho, Cheng-Mao / Lin, Huang-Shen /

Chen, Hung-Jen / Lin, Po-Chang / Liao, Wei-Chin / Chen, Wei-Ting / Lo, Chia-Chi / Wang, Shang-Yu / Kuo, Chen-Yen / Lee, Chen-Hsiang / Ku, Cheng-Lung

Medicine

2016 Volume 95, Issue 25, Page(s) e3927

Abstract: Neutralizing anti-interferon-γ autoantibody (nAIGA)-associated immunodeficiency is an emerging medical issue worldwide. In the present study, we describe and discuss the clinical features and outcomes of patients with nAIGAs and disseminated infections ... ...

Abstract	Neutralizing anti-interferon-γ autoantibody (nAIGA)-associated immunodeficiency is an emerging medical issue worldwide. In the present study, we describe and discuss the clinical features and outcomes of patients with nAIGAs and disseminated infections by nontuberculous mycobacteria (dNTM).We thoroughly reviewed the medical records of all patients. Microorganisms and nAIGAs were identified using previously described methods with modifications. All data were calculated and analyzed using SPSS software.Among 46 adult patients with dNTM infections, we identified 45 cases (97.8%) with nAIGAs. The average patient age was 58.6 years, and there was no sex predominance. Cervical lymphadenitis (81.8%) was the most common clinical manifestation. Endocrine disorder was the leading comorbidity (7 cases). Malignancies were found in 4 patients, and all of the malignancies originated from the T-cell/macrophage lineage. More than half of the identifiable isolates were slow-growing NTMs. Twenty-eight (62.2%) and 18 (40.0%) patients had a history of zoster and salmonellosis, respectively. A high proportion of patients with recurrent episodes of NTM infection or a history of zoster and dNTM infection had initial nAIGA titers ≥10 dilution (P < 0.05). Twenty-seven patients (60.0%) required long-term antimycobacterial therapy and had at least 1 episode of recurrent NTM disease. No mortality was related to dNTM infection.In Taiwan, nAIGAs are a recently recognized mechanism of dNTM infection. Long term of antibiotic treatment and adherence to medical advice are necessary to improve the clinical outcome of patients with nAIGAs.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Anti-Bacterial Agents/therapeutic use ; Antibodies, Anti-Idiotypic/immunology ; Autoantibodies/immunology ; Female ; Follow-Up Studies ; Humans ; Incidence ; Interferon-gamma/immunology ; Male ; Middle Aged ; Mycobacterium Infections, Nontuberculous/drug therapy ; Mycobacterium Infections, Nontuberculous/epidemiology ; Mycobacterium Infections, Nontuberculous/immunology ; Nontuberculous Mycobacteria/immunology ; Prognosis ; Retrospective Studies ; Taiwan/epidemiology ; Time Factors
Chemical Substances	Anti-Bacterial Agents ; Antibodies, Anti-Idiotypic ; Autoantibodies ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2016-06-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	80184-7
ISSN	1536-5964 ; 0025-7974
ISSN (online)	1536-5964
ISSN	0025-7974
DOI	10.1097/MD.0000000000003927
Database	MEDical Literature Analysis and Retrieval System OnLINE

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