A role for gamma/delta T cells in a mouse model of fracture healing.
A role for gamma/delta T cells in a mouse model of fracture healing.
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DOI:
10.1002/art.24520
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发表时间:
2009-06
影响因子:
--
通讯作者:
Tuan, Rocky S.
中科院分区:
文献类型:
--
作者:
Colburn, Nona T.;Zaal, Kristien J. M.;Wang, Francis;Tuan, Rocky S.
Fractures can initiate an immune response that disturbs osteoblastic and osteoclastic cellular homeostasis through cytokine production and release. The aim of our study was to investigate γδ T-cells, innate lymphocytes known to be involved in tissue repair, as potential cellular components of the osteoimmune’s system response to an in-vivo model of bony injury. The absence of such cells or their effector cytokines influences the fate of other responder cells in proliferation, differentiation, matrix production, and ultimate callus formation. Tibia fractures were created in 60 γδ T-cell receptor knockout and 60 control C57BL/6 mice. Analysis included radiographs, basic histology, mechanical testing, flow cytometry, and immunohistochemical localization of γδ positive subsets from control animals, and of CD 44 from both groups, as well as ELISA for the effector cytokines, IL-2, interferon-γ, and IL-6, respectively. γδ knockout animals demonstrated more mature histological elements and quantitative increases in the expression of major bone (bone sialoprotein) and cartilage (collagen type II) matrix proteins, and bone morphogenetic protein-2 at a critical reparative phase. Moreover, only knockout animals had a decrease in osteoprogenitor antiproliferative cytokines, IL-6 and interferon-γ. The result was improved stability at the repair site and an overall superior biomechanical strength in knockout mice as compared with controls. The evidence for γδ T-cells in the context of skeletal injury demonstrates the importance of the immune system’s impact on bone biology, relevant to the field of osteoimmunlogy, and offers a potential molecular platform from which to develop essential therapeutic strategies.
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影响因子:
3.1
作者:
Daniel, TanJanika;Thobe, Ljoern M.;Schwacha, Martin G.
通讯作者:
Schwacha, Martin G.
影响因子:
64.8
作者:
FERRICK, DA;SCHRENZEL, MD;LEPPER, H
通讯作者:
LEPPER, H
DOI:
10.3109/17453679408995493
发表时间:
1994-08-01
期刊:
ACTA ORTHOPAEDICA SCANDINAVICA
影响因子:
--
作者:
ANDREW, JG;ANDREW, SM;MARSH, DR
通讯作者:
MARSH, DR
影响因子:
4.4
作者:
Corthay, A;Johansson, Å;Holmdahl, R
通讯作者:
Holmdahl, R
影响因子:
1.9
作者:
GEBHARD, JS;JOHNSTONJONES, K;MEALS, RA
通讯作者:
MEALS, RA