IL-23 is critical for induction of arthritis, osteoclast formation, and maintenance of bone mass.
IL-23 is critical for induction of arthritis, osteoclast formation, and maintenance of bone mass.
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DOI：
10.4049/jimmunol.1003986
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发表时间：
2011-07-15
期刊：
影响因子：
--
通讯作者：
Bowman EP
中科院分区：
文献类型：
--
作者：
Adamopoulos IE;Tessmer M;Chao CC;Adda S;Gorman D;Petro M;Chou CC;Pierce RH;Yao W;Lane NE;Laface D;Bowman EP
通过体内流体动力输送IL-23微环DNA和IL-23基因缺陷小鼠的全身IL-23暴露，研究了IL-23在关节炎和骨代谢中的作用。全身IL-23暴露可导致慢性关节炎、严重的骨丢失和骨髓和脾中的骨髓生成，导致破骨细胞分化增加和全身骨丢失。IL-23的作用部分依赖于CD4+T细胞、IL-17A和肿瘤坏死因子，但不能通过体内IL-17A的过表达来实现。在IL-23诱导的关节炎中，髓系细胞的增殖和活性起着关键作用。在体外破骨细胞生成实验中，IL-23p19−/−小鼠的骨髓巨噬细胞向破骨细胞的成熟较慢，抗酒石酸酸性磷酸酶阳性细胞和牙本质吸收能力降低。这与26周龄雄性IL-23p19−/−小鼠与对照组相比，多核破骨细胞样细胞减少，骨小梁体积和数量增加有关。总而言之，我们的数据表明，系统性IL-23暴露诱导髓系破骨细胞前体的扩张，靶向IL-23途径可能对抗类风湿性关节炎和其他自身免疫性关节炎中观察到的炎症驱动的骨破坏。免疫学杂志，2011,187：951-959。
The role of IL-23 in the development of arthritis and bone metabolism was studied using systemic IL-23 exposure in adult mice via hydrodynamic delivery of IL-23 minicircle DNA in vivo and in mice genetically deficient in IL-23. Systemic IL-23 exposure induced chronic arthritis, severe bone loss, and myelopoiesis in the bone marrow and spleen, which resulted in increased osteoclast differentiation and systemic bone loss. The effect of IL-23 was partly dependent on CD4+ T cells, IL-17A, and TNF, but could not be reproduced by overexpression of IL-17A in vivo. A key role in the IL-23–induced arthritis was made by the expansion and activity of myeloid cells. Bone marrow macrophages derived from IL-23p19−/− mice showed a slower maturation into osteoclasts with reduced tartrate-resistant acid phosphatase-positive cells and dentine resorption capacity in in vitro osteoclastogenesis assays. This correlated with fewer multinucleated osteoclast-like cells and more trabecular bone volume and number in 26-wk-old male IL-23p19−/− mice compared with control animals. Collectively, our data suggest that systemic IL-23 exposure induces the expansion of a myeloid lineage osteoclast precursor, and targeting IL-23 pathway may combat inflammation-driven bone destruction as observed in rheumatoid arthritis and other autoimmune arthritides. The Journal of Immunology, 2011, 187: 951–959.
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影响因子：
30.8
作者：
Nair RP;Duffin KC;Helms C;Ding J;Stuart PE;Goldgar D;Gudjonsson JE;Li Y;Tejasvi T;Feng BJ;Ruether A;Schreiber S;Weichenthal M;Gladman D;Rahman P;Schrodi SJ;Prahalad S;Guthery SL;Fischer J;Liao W;Kwok PY;Menter A;Lathrop GM;Wise CA;Begovich AB;Voorhees JJ;Elder JT;Krueger GG;Bowcock AM;Abecasis GR;Collaborative Association Study of Psoriasis
通讯作者：
Collaborative Association Study of Psoriasis
DOI：
10.1084/jem.20061775
发表时间：
2006-11-27
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Sato K;Suematsu A;Okamoto K;Yamaguchi A;Morishita Y;Kadono Y;Tanaka S;Kodama T;Akira S;Iwakura Y;Cua DJ;Takayanagi H
通讯作者：
Takayanagi H
DOI：
10.1084/jem.190.12.1741
发表时间：
1999-12-20
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Arai F;Miyamoto T;Ohneda O;Inada T;Sudo T;Brasel K;Miyata T;Anderson DM;Suda T
通讯作者：
Suda T
影响因子：
4.9
作者：
Adamopoulos IE;Chao CC;Geissler R;Laface D;Blumenschein W;Iwakura Y;McClanahan T;Bowman EP
通讯作者：
Bowman EP
影响因子：
5.4
作者：
Chen, Li;Wei, Xiao-Qing;Aeschlimann, Daniel
通讯作者：
Aeschlimann, Daniel