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dc.contributor.authorSarah K. Browneen_US
dc.contributor.authorPeter D. Burbeloen_US
dc.contributor.authorPloenchan Chetchotisakden_US
dc.contributor.authorYupin Suputtamongkolen_US
dc.contributor.authorSasisopin Kiertiburanakulen_US
dc.contributor.authorPamela A. Shawen_US
dc.contributor.authorJennifer L. Kirken_US
dc.contributor.authorKamonwan Jutivorakoolen_US
dc.contributor.authorRifat Zamanen_US
dc.contributor.authorLi Dingen_US
dc.contributor.authorAmy P. Hsuen_US
dc.contributor.authorSmita Y. Patelen_US
dc.contributor.authorKenneth N. Olivieren_US
dc.contributor.authorViraphong Lulitanonden_US
dc.contributor.authorPiroon Mootsikapunen_US
dc.contributor.authorSiriluck Anunnatsirien_US
dc.contributor.authorNasikarn Angkasekwinaien_US
dc.contributor.authorBoonmee Sathapatayavongsen_US
dc.contributor.authorPo Ren Hsuehen_US
dc.contributor.authorChi Chang Shiehen_US
dc.contributor.authorMargaret R. Brownen_US
dc.contributor.authorWanna Thongnoppakhunen_US
dc.contributor.authorReginald Claypoolen_US
dc.contributor.authorElizabeth P. Sampaioen_US
dc.contributor.authorCharin Thepthaien_US
dc.contributor.authorDuangdao Waywaen_US
dc.contributor.authorCamilla Dacombeen_US
dc.contributor.authorYona Reizesen_US
dc.contributor.authorAdrian M. Zelaznyen_US
dc.contributor.authorPaul Saleeben_US
dc.contributor.authorLindsey B. Rosenen_US
dc.contributor.authorAllen Moen_US
dc.contributor.authorMichael Iadarolaen_US
dc.contributor.authorSteven M. Hollanden_US
dc.contributor.otherNational Institute of Allergy and Infectious Diseasesen_US
dc.contributor.otherNational Institute of Dental and Craniofacial Researchen_US
dc.contributor.otherNational Institutes of Health, Bethesdaen_US
dc.contributor.otherSystexen_US
dc.contributor.otherKhon Kaen Universityen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherChulalongkorn Universityen_US
dc.contributor.otherUniversity of Oxforden_US
dc.contributor.otherNational Taiwan Universityen_US
dc.contributor.otherNational Cheng Kung Universityen_US
dc.contributor.otherFundacao Oswaldo Cruzen_US
dc.contributor.otherColgate Universityen_US
dc.date.accessioned2018-06-11T05:06:30Z-
dc.date.available2018-06-11T05:06:30Z-
dc.date.issued2012-08-23en_US
dc.identifier.citationNew England Journal of Medicine. Vol.367, No.8 (2012), 725-734en_US
dc.identifier.issn15334406en_US
dc.identifier.issn00284793en_US
dc.identifier.other2-s2.0-84865300679en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84865300679&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/14687-
dc.description.abstractBACKGROUND: Autoantibodies against interferon-γ are associated with severe disseminated opportunistic infection, but their importance and prevalence are unknown. METHODS: We enrolled 203 persons from sites in Thailand and Taiwan in five groups: 52 patients with disseminated, rapidly or slowly growing, nontuberculous mycobacterial infection (group 1); 45 patients with another opportunistic infection, with or without nontuberculous mycobacterial infection (group 2); 9 patients with disseminated tuberculosis (group 3); 49 patients with pulmonary tuberculosis (group 4); and 48 healthy controls (group 5). Clinical histories were recorded, and blood specimens were obtained. RESULTS: Patients in groups 1 and 2 had CD4+ T-lymphocyte counts that were similar to those in patients in groups 4 and 5, and they were not infected with the human immunodeficiency virus (HIV). Washed cells obtained from patients in groups 1 and 2 had intact cytokine production and a response to cytokine stimulation. In contrast, plasma obtained from these patients inhibited the activity of interferon-γ in normal cells. High-titer anti-interferon-γ autoantibodies were detected in 81% of patients in group 1, 96% of patients in group 2, 11% of patients in group 3, 2% of patients in group 4, and 2% of controls (group 5). Forty other anticytokine autoantibodies were assayed. One patient with cryptococcal meningitis had autoantibodies only against granulocyte-macrophage colony-stimulating factor. No other anticytokine autoantibodies or genetic defects correlated with infections. There was no familial clustering. CONCLUSIONS: Neutralizing anti-interferon-γ autoantibodies were detected in 88% of Asian adults with multiple opportunistic infections and were associated with an adult-onset immunodeficiency akin to that of advanced HIV infection. (Funded by the National Institute of Allergy and Infectious Diseases and the National Institute of Dental and Craniofacial Research; ClinicalTrials.gov number, NCT00814827.) Copyright © 2012 Massachusetts Medical Society.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84865300679&origin=inwarden_US
dc.subjectMedicineen_US
dc.titleAdult-onset immunodeficiency in Thailand and Taiwanen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1056/NEJMoa1111160en_US
Appears in Collections:Scopus 2011-2015

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