Nature Communications (Dec 2016)
Fas/CD95 prevents autoimmunity independently of lipid raft localization and efficient apoptosis induction
- Anthony C. Cruz,
- Madhu Ramaswamy,
- Claudia Ouyang,
- Christopher A. Klebanoff,
- Prabuddha Sengupta,
- Tori N. Yamamoto,
- Françoise Meylan,
- Stacy K. Thomas,
- Nathan Richoz,
- Robert Eil,
- Susan Price,
- Rafael Casellas,
- V. Koneti Rao,
- Jennifer Lippincott-Schwartz,
- Nicholas P. Restifo,
- Richard M. Siegel
Affiliations
- Anthony C. Cruz
- Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), Intramural Research Program, National Institutes of Health (NIH)
- Madhu Ramaswamy
- Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), Intramural Research Program, National Institutes of Health (NIH)
- Claudia Ouyang
- Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), Intramural Research Program, National Institutes of Health (NIH)
- Christopher A. Klebanoff
- Center for Cell Engineering and Department of Medicine, Memorial Sloan Kettering Cancer Center
- Prabuddha Sengupta
- Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), NIH
- Tori N. Yamamoto
- Center For Cancer Research, National Cancer Institute (NCI), NIH
- Françoise Meylan
- Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), Intramural Research Program, National Institutes of Health (NIH)
- Stacy K. Thomas
- Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), Intramural Research Program, National Institutes of Health (NIH)
- Nathan Richoz
- Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), Intramural Research Program, National Institutes of Health (NIH)
- Robert Eil
- Center For Cancer Research, National Cancer Institute (NCI), NIH
- Susan Price
- Clinical Genomics Unit, National Institute of Allergy and Infectious Diseases (NIAID), NIH
- Rafael Casellas
- Genomics and Immunity Branch, NIAMS
- V. Koneti Rao
- Clinical Genomics Unit, National Institute of Allergy and Infectious Diseases (NIAID), NIH
- Jennifer Lippincott-Schwartz
- Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), NIH
- Nicholas P. Restifo
- Center For Cancer Research, National Cancer Institute (NCI), NIH
- Richard M. Siegel
- Immunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), Intramural Research Program, National Institutes of Health (NIH)
- DOI
- https://doi.org/10.1038/ncomms13895
- Journal volume & issue
-
Vol. 7,
no. 1
pp. 1 – 15
Abstract
Fas drives apoptosis and mutations in this receptor can cause autoimmunity through failure of cell death. Here, the authors uselpr/lprmice with palmitoylation-defective mutant Fas to provide evidence that Fas might limit spontaneous autoimmunity through a non-apoptotic mechanism.
