期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 12, 页码 8757-8766出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.12.8757
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资金
- NCCIH NIH HHS [AT 0006646] Funding Source: Medline
- NIAMS NIH HHS [AR 48781, R01 AR048781] Funding Source: Medline
- NICHD NIH HHS [HD 40939, R21 HD040939] Funding Source: Medline
- NIDCR NIH HHS [R01 DE015399] Funding Source: Medline
Although biomechanical signals generated during joint mobilization are vital in maintaining integrity of inflamed cartilage, the molecular mechanisms of their actions are little understood. In an experimental model of arthritis, we demonstrate that biomechanical signals are potent anti-inflammatory signals that repress transcriptional activation of proinflammatory genes and augment expression of anti-inflammatory cytokine IL-10 to profoundly attenuate localized joint inflammation.
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