期刊
CELLULAR IMMUNOLOGY
卷 262, 期 2, 页码 84-88出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2010.02.013
关键词
Rheumatoid arthritis; Inflammation; Hyaluronan; Macrophages; Interferon gamma; Interleukin-10; Interleukin-12; Tumor necrosis factor; c-Jun
资金
- NIH [T32AR007603, U24DE1650901, R01HD032259, R01A165265]
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD032259] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI065265] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [T32AR007603] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [U24DE016509] Funding Source: NIH RePORTER
The objective was to assess outcomes of IFN gamma-priming upon macrophage activation by the synovial macromolecule high molecular weight hyaluronan [HMW-HA] in the context of rheumatoid arthritis inflammation. Human macrophages primed by IFN gamma and activated by HMW-HA were evaluated for cytokine secretion by ELISA and Milliplex assay and activation profiles by nuclear transcription factor EIA. IFN gamma-primed, HMW-HA-activated macrophages produced elevated levels of TNF and secreted the TH1 cytokine IL-12p70, while IFN gamma suppressed HMW-HA-induced secretion of the regulatory cytokine IL-10 and activation of the transcription factor c-Jun. IFN gamma modulates the HMW-HA-induced cytokine response profile promoting macrophage activation and inflammatory TH1 cytokine secretion. (C) 2010 Elsevier Inc. All rights reserved.
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