2012 Fiscal Year Final Research Report
Elucidation of a molecular mechanism of osteoporosis caused by a mutation in the STAT3 gene
| Project/Area Number |
22390205
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | The University of Tokushima (2012)
Tokyo Medical and Dental University (2010-2011) |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2012
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| Keywords | 免疫不全症 / 骨粗鬆症 / STAT3 |
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| Research Abstract |
Hyper-IgE syndrome is a primary immunodeficiency characterized by recurrent staphylococcal infections and atopic dermatitisassociated with elevated serum IgE levels. We recently identified dominant negative (DN) mutations in the STAT3gene is the most common cause of hyper-IgE syndrome associated with bone abnormalities. Here we established Stat3-DN knock-in mice and foundbone formation and osteoclast generation induced by osteoblasts were impaired in the Stat3-DN mice.
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[Journal Article] Deenick EK, Tangye SG. Functional STAT3 deficiency compromises the generation of human T follicular helper cells.2012
Author(s)
Ma CS, Avery DT, Chan A, Batten M, Bustamante J, Boisson-Dupuis S, Arkwright PD, Kreins AY, Averbuch D, Engelhard D, Magdorf K, Kilic SS, Minegishi Y, Nonoyama S, French MA, Choo S, Smart JM, Peake J, Wong M, Gray P, Cook MC, Fulcher DA
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Journal Title
Blood
Volume: 119
Pages: 3997-4008
DOI
Peer Reviewed
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[Journal Article] Defective IL-10 signaling in hyper-IgE syndrome results in impaired generation of tolerogenic dendritic cells and induced regulatory T cells2011
Author(s)
Saito M, Nagasawa M, Takada H, Hara T, Tsuchiya S, Agematsu K, Yamada M, Kawamura N, Ariga T, Tsuge I, Nonoyama S, Karasuyama H, Minegishi Y
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Journal Title
J Exp Med
Volume: 208
Pages: 235-249
DOI
Peer Reviewed
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