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Hu, Ming, Bassett, J H Duncan, Danks, Lynett, Howell, Peter G T, Xu, Ke, Spanoudakis, Emmanouil, Kotsianidis, Ioannis, Boyde, Alan, Williams, Graham R, Horwood, Nikki 
ORCID: https://orcid.org/0000-0002-6344-1677, Roberts, Irene A G and Karadimitris, Anastasios
(2011)
Activated invariant NKT cells regulate osteoclast development and function.
Journal of Immunology, 186 (5).
pp. 2910-2917.
ISSN 0022-1767
Abstract
Invariant NKT (iNKT) cells modulate innate and adaptive immune responses through activation of myeloid dendritic cells and macrophages and via enhanced clonogenicity, differentiation, and egress of their shared myeloid progenitors. Because these same progenitors give rise to osteoclasts (OCs), which also mediate the egress of hematopoietic progenitors and orchestrate bone remodeling, we hypothesized that iNKT cells would extend their myeloid cell regulatory role to the development and function of OCs. In this study, we report that selective activation of iNKT cells by α-galactosylceramide causes myeloid cell egress, enhances OC progenitor and precursor development, modifies the intramedullary kinetics of mature OCs, and enhances their resorptive activity. OC progenitor activity is positively regulated by TNF-α and negatively regulated by IFN-γ, but is IL-4 and IL-17 independent. These data demonstrate a novel role of iNKT cells that couples osteoclastogenesis with myeloid cell egress in conditions of immune activation.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | animals,immunology,immunology,cytology,immunology,physiology,immunology,physiology,cytology,mice,mice, inbred balb c,mice, inbred c57bl,mice, knockout,cytology,cytology,cytology,physiology,cytology,physiology,immunology |
| Faculty \ School: | Faculty of Medicine and Health Sciences > Norwich Medical School |
| UEA Research Groups: | Faculty of Medicine and Health Sciences > Research Centres > Metabolic Health |
| Depositing User: | LivePure Connector |
| Date Deposited: | 06 Mar 2019 10:30 |
| Last Modified: | 25 Sep 2024 13:57 |
| URI: | https://ueaeprints.uea.ac.uk/id/eprint/70140 |
| DOI: | 10.4049/jimmunol.1002353 |
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