Regulation of immune cells by local-tissue oxygen tension: HIF1α and adenosine receptors
Author:
Publisher
Springer Science and Business Media LLC
Subject
Energy Engineering and Power Technology,Fuel Technology
Link
http://www.nature.com/articles/nri1685.pdf
Reference120 articles.
1. Sitkovsky, M. V. et al. Physiological control of immune response and inflammatory tissue damage by hypoxia inducible factors and adenosine A2A receptors. Annu. Rev. Immunol. 22, 657–682 (2004).
2. Cramer, T. et al. HIF-1α is essential for myeloid cell-mediated inflammation. Cell 112, 645–657 (2003). Using the Cre– loxP system with Cre expression under control of the lysozyme M promoter, the authors showed that HIF1α deficiency in macrophages causes metabolic defects as a consequence of inhibited glycolysis and results in an impaired inflammatory response.
3. Kojima, H. et al. Abnormal B lymphocyte development and autoimmunity in hypoxia-inducible factor 1α-deficient chimeric mice. Proc. Natl Acad. Sci. USA 99, 2170–2174 (2002). Using the RAG2-deficient blastocyst-complementation system, the authors examined HIF1α deficiency in T and B cells and showed that loss of HIF1α results in defects in the B-cell lineage, autoimmunity and tissue damage.
4. Caldwell, C. C. et al. Differential effects of physiologically relevant hypoxic conditions on T lymphocyte development and effector functions. J. Immunol. 167, 6140–6149 (2001).
5. Lukashev, D., Caldwell, C., Ohta, A., Chen, P. & Sitkovsky, M. Differential regulation of two alternatively spliced isoforms of hypoxia-inducible factor-1α in activated T lymphocytes. J. Biol. Chem. 276, 48754–48763 (2001).
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