The NF-κB regulator Bcl-3 modulates inflammation during contact hypersensitivity reactions in radioresistant cells
Author:
Affiliation:
1. Laboratory of Molecular Immunology; National Institute of Allergy and Infectious Diseases, National Institutes of Health; Bethesda MD USA
2. Department of Dermatology; University of Minnesota; Minneapolis MN USA
Funder
National Institutes of Health and NIH
Publisher
Wiley
Subject
Immunology,Immunology and Allergy
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1002/eji.201444994/fullpdf
Reference36 articles.
1. Immunological mechanisms of contact hypersensitivity in mice;Christensen;APMIS,2012
2. Update of immune events in the murine contact hypersensitivity model: toward the understanding of allergic contact dermatitis;Honda;J. Invest. Dermatol.,2013
3. Shared principles in NF-kappaB signaling;Hayden;Cell,2008
4. Control of lymphocyte development by nuclear factor-kappaB;Siebenlist;Nat. Rev. Immunol.,2005
5. The candidate proto-oncogene bcl-3 is related to genes implicated in cell lineage determination and cell cycle control;Ohno;Cell,1990
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