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dc.contributor.authorNuttapol Chruewkamlowen_US
dc.contributor.authorKodchakorn Mahasongkramen_US
dc.contributor.authorSupansa Pataen_US
dc.contributor.authorRomanee Chaiwarithen_US
dc.contributor.authorParichart Saleeen_US
dc.contributor.authorKhuanchai Supparatpinyoen_US
dc.contributor.authorWatchara Kasinrerken_US
dc.date.accessioned2018-09-05T02:51:20Z-
dc.date.available2018-09-05T02:51:20Z-
dc.date.issued2016-01-04en_US
dc.identifier.issn19326203en_US
dc.identifier.other2-s2.0-84953896550en_US
dc.identifier.other10.1371/journal.pone.0145983en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84953896550&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/55053-
dc.description.abstract© 2016 Chruewkamlow et al. 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.en_US
dc.subjectAgricultural and Biological Sciencesen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleImmune alterations in patients with anti-interferon-γ autoantibodiesen_US
dc.typeJournalen_US
article.title.sourcetitlePLoS ONEen_US
article.volume11en_US
article.stream.affiliationsChiang Mai Universityen_US
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