| Arthritis Research & Therapy | |
| Collagen-induced arthritis is exacerbated in IL-10-deficient mice | |
| Alison Finnegan4  Charles D Kaplan4  Yanxia Cao2  Hermann Eibel1  Tibor T Glant3  Jian Zhang3  | |
| [1] Klinische Forschergruppe fur Rheumatologie, Freiburg, Germany | |
| [2] Department of Medicine, Section of Rheumatology, Rush Presbyterian–St Luke's Medical Center, Chicago, Illinois, USA | |
| [3] Department of Orthopedic Surgery and Department of Biochemistry, Rush Presbyterian–St Luke's Medical Center, Chicago, Illinois, USA | |
| [4] Department of Immunology and Microbiology, Rush Presbyterian–St Luke's Medical Center, Chicago, Illinois, USA | |
| 关键词: cytokines; autoimmunity; arthritis; antibody; | |
| Others : 1101419 DOI : 10.1186/ar601 |
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| received in 2002-07-11, accepted in 2002-09-11, 发布年份 2002 | |
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【 摘 要 】
IL-10 is a potent immunoregulatory cytokine attenuating a wide range of immune effector and inflammatory responses. In the present study, we assess whether endogenous levels of IL-10 function to regulate the incidence and severity of collagen-induced arthritis. DBA/1 wildtype (WT), heterozygous (IL-10+/-) and homozygous (IL-10-/-) IL-10-deficient mice were immunized with type II collagen. Development of arthritis was monitored over time, and collagen-specific cytokine production and anticollagen antibodies were assessed. Arthritis developed progressively in mice immunized with collagen, and 100% of the WT, IL-10+/-, and IL-10-/- mice were arthritic at 35 days. However, the severity of arthritis in the IL-10-/- mice was significantly greater than that in WT or IL-1+/- animals. Disease severity was associated with reduced IFN-γ levels and a dramatic increase in CD11b-positive macrophages. Paradoxically, both the IgG1 and IgG2a anticollagen antibody responses were also significantly reduced. These data demonstrate that IL-10 is capable of controlling disease severity through a mechanism that involves IFN-γ. Since IL-10 levels are elevated in rheumatoid arthritis synovial fluid, these findings may have relevance to rheumatoid arthritis.
【 授权许可】
2003 Finnegan et al., licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any non-commercial purpose, provided this notice is preserved along with the article's original URL.
【 预 览 】
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| 20150131130313254.pdf | 91KB | ||
| Figure 4. | 38KB | Image | |
| Figure 3. | 69KB | Image | |
| Figure 2. | 38KB | Image | |
| Figure 1. | 79KB | Image |
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