Affiliation:
1. Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, United States
Abstract
The central question investigated in this study is why vascular endothelium remains inflamed and what underlying signaling is responsible. The new results show that the resolution of endothelial-controlled inflammation may be impaired or delayed because Janus kinase (JAK)/STAT activation is maintained autonomous of interferon (IFN)γ presence, and the late phase negative regulator suppressors of cytokine signaling (SOCS)1 fails to be induced.
Funder
American Society of Transplantation
HHS | NIH | National Institute of Allergy and Infectious Diseases
International Society for Heart and Lung Transplantation
UC | University of California, Los Angeles
Publisher
American Physiological Society
Cited by
1 articles.
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