Publication: Adult-onset immunodeficiency in Thailand and Taiwan
dc.contributor.author | Sarah K. Browne | en_US |
dc.contributor.author | Peter D. Burbelo | en_US |
dc.contributor.author | Ploenchan Chetchotisakd | en_US |
dc.contributor.author | Yupin Suputtamongkol | en_US |
dc.contributor.author | Sasisopin Kiertiburanakul | en_US |
dc.contributor.author | Pamela A. Shaw | en_US |
dc.contributor.author | Jennifer L. Kirk | en_US |
dc.contributor.author | Kamonwan Jutivorakool | en_US |
dc.contributor.author | Rifat Zaman | en_US |
dc.contributor.author | Li Ding | en_US |
dc.contributor.author | Amy P. Hsu | en_US |
dc.contributor.author | Smita Y. Patel | en_US |
dc.contributor.author | Kenneth N. Olivier | en_US |
dc.contributor.author | Viraphong Lulitanond | en_US |
dc.contributor.author | Piroon Mootsikapun | en_US |
dc.contributor.author | Siriluck Anunnatsiri | en_US |
dc.contributor.author | Nasikarn Angkasekwinai | en_US |
dc.contributor.author | Boonmee Sathapatayavongs | en_US |
dc.contributor.author | Po Ren Hsueh | en_US |
dc.contributor.author | Chi Chang Shieh | en_US |
dc.contributor.author | Margaret R. Brown | en_US |
dc.contributor.author | Wanna Thongnoppakhun | en_US |
dc.contributor.author | Reginald Claypool | en_US |
dc.contributor.author | Elizabeth P. Sampaio | en_US |
dc.contributor.author | Charin Thepthai | en_US |
dc.contributor.author | Duangdao Waywa | en_US |
dc.contributor.author | Camilla Dacombe | en_US |
dc.contributor.author | Yona Reizes | en_US |
dc.contributor.author | Adrian M. Zelazny | en_US |
dc.contributor.author | Paul Saleeb | en_US |
dc.contributor.author | Lindsey B. Rosen | en_US |
dc.contributor.author | Allen Mo | en_US |
dc.contributor.author | Michael Iadarola | en_US |
dc.contributor.author | Steven M. Holland | en_US |
dc.contributor.other | National Institute of Allergy and Infectious Diseases | en_US |
dc.contributor.other | National Institute of Dental and Craniofacial Research | en_US |
dc.contributor.other | National Institutes of Health, Bethesda | en_US |
dc.contributor.other | Systex | en_US |
dc.contributor.other | Khon Kaen University | en_US |
dc.contributor.other | Mahidol University | en_US |
dc.contributor.other | Chulalongkorn University | en_US |
dc.contributor.other | University of Oxford | en_US |
dc.contributor.other | National Taiwan University | en_US |
dc.contributor.other | National Cheng Kung University | en_US |
dc.contributor.other | Fundacao Oswaldo Cruz | en_US |
dc.contributor.other | Colgate University | en_US |
dc.date.accessioned | 2018-06-11T05:06:30Z | |
dc.date.available | 2018-06-11T05:06:30Z | |
dc.date.issued | 2012-08-23 | en_US |
dc.description.abstract | BACKGROUND: 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.identifier.citation | New England Journal of Medicine. Vol.367, No.8 (2012), 725-734 | en_US |
dc.identifier.doi | 10.1056/NEJMoa1111160 | en_US |
dc.identifier.issn | 15334406 | en_US |
dc.identifier.issn | 00284793 | en_US |
dc.identifier.other | 2-s2.0-84865300679 | en_US |
dc.identifier.uri | https://hdl.handle.net/20.500.14594/14687 | |
dc.rights | Mahidol University | en_US |
dc.rights.holder | SCOPUS | en_US |
dc.source.uri | https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84865300679&origin=inward | en_US |
dc.subject | Medicine | en_US |
dc.title | Adult-onset immunodeficiency in Thailand and Taiwan | en_US |
dc.type | Article | en_US |
dspace.entity.type | Publication | |
mu.datasource.scopus | https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84865300679&origin=inward | en_US |