Immunological mechanisms of the antitumor effects of supplemental oxygenation

Author:

Hatfield Stephen M.1,Kjaergaard Jorgen1,Lukashev Dmitriy1,Schreiber Taylor H.2,Belikoff Bryan1,Abbott Robert1,Sethumadhavan Shalini1,Philbrook Phaethon1,Ko Kami1,Cannici Ryan1,Thayer Molly1,Rodig Scott3,Kutok Jeffrey L.3,Jackson Edwin K.4,Karger Barry5,Podack Eckhard R.2,Ohta Akio1,Sitkovsky Michail V.16

Affiliation:

1. New England Inflammation and Tissue Protection Institute, Northeastern University, 360 Huntington Avenue, Boston, MA 02115, USA.

2. Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.

3. Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, 20 Shattuck Street, Boston, MA 02115, USA.

4. Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA.

5. Barnett Institute of Chemical and Biological Analysis, Northeastern University, Boston, MA 02115, USA.

6. Cancer Vaccine Center, Dana-Farber Cancer Institute, Harvard Institutes of Medicine, 44 Binney Street, Boston, MA 02115, USA.

Abstract

Respiratory hyperoxia stimulates lung tumor regression by promoting T cell infiltration into the tumors and decreasing immunosuppression.

Funder

NIH

National Cancer Institute

National Institute of Allergy and Infectious Diseases

Bankhead-Coley Postdoctoral Fellowship

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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