期刊
PLOS ONE
卷 11, 期 1, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0145983
关键词
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资金
- National Research University Project under Thailand's Office of the Higher Education Commission for Chiang Mai University
- Chiang Mai University Center of Excellence grant for Biomedical Technology Research Center
- Thailand Research Fund [TRG5780017]
- Chiang Mai University at the Biomedical Technology Research Center
Autoantibodies against interferon-gamma (IFN-gamma) 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-gamma autoantibodies (AAbs). Upon TCR activation, T cell proliferation and IL-2 receptor of the patients remained intact. Nonetheless, the Th1 cytokine (IFN-gamma and TNF-alpha) 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-gamma autoantibodies, alterations in the cellular immune functions may also contribute to this immunodeficiency.
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