Osteoimmunology in Bone Fracture Healing

被引:159
作者
Ono, Takehito [1 ]
Takayanagi, Hiroshi [2 ,3 ]
机构
[1] Tokyo Med & Dent Univ, Dept Cell Signaling, Grad Sch Med & Dent Sci, Bunkyo Ku, Yushima 1-5-45, Tokyo 1138549, Japan
[2] Univ Tokyo, Dept Immunol, Grad Sch Med, Bunkyo Ku, Hongo 7-3-1, Tokyo 1130033, Japan
[3] Univ Tokyo, Fac Med, Bunkyo Ku, Hongo 7-3-1, Tokyo 1130033, Japan
关键词
Bone repair; Inflammation; gamma delta T cell; Cytokine; Bone formation; Osteoblast; MESENCHYMAL STEM-CELLS; ANTI-INTERLEUKIN-17A MONOCLONAL-ANTIBODY; PROMOTES OSTEOGENIC DIFFERENTIATION; ANTAGONIST-DEFICIENT MICE; TUMOR-NECROSIS-FACTOR; DELTA T-CELLS; GAMMA-DELTA; OSTEOBLAST DIFFERENTIATION; TNF-ALPHA; B-CELLS;
D O I
10.1007/s11914-017-0381-0
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of Review In the process of bone fracture healing, inflammation is thought to be an essential process that precedes bone formation and remodeling. We review recent studies on bone fracture healing from an osteoimmunological point of view. Recent Findings Based on previous observations that many types of immune cells infiltrate into the bone injury site and release a variety of molecules, recent studies have addressed the roles of specific immune cell subsets. Macrophages and interleukin (IL)-17-producing gamma delta T cells enhance bone healing, whereas CD8(+) T cells impair bone repair. Additionally, IL-10-producing B cells may contribute to bone healing by suppressing excessive and/or prolonged inflammation. Although the involvement of other cells and molecules has been suggested, the precise underlying mechanisms remain elusive. Summary Accumulating evidence has begun to reveal the deeper picture of bone fracture healing. Further studies are required for the development of novel therapeutic strategies for bone fracture.
引用
收藏
页码:367 / 375
页数:9
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