Muhammad Asghar Pasha
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Muhammad Asghar Pasha has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Angela Haczku
University of California
1 shared publication Angelica Costello
Department of Immunology and Microbial Disease, Albany Medical College, Albany, NY 12208
1 shared publicationAvinash Bhandoola
T-Cell Biology and Development Unit, Laboratory of Genome Integrity, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
1 shared publicationChristian W. Siebel
Department of Discovery Oncology, Genentech, South San Francisco, CA 94080
1 shared publication- Ivan Maillard
University of Pennsylvania
1 shared publication - Jinfang Zhu
National Institute of Allergy and Infectious Diseases, National Institutes of Health 1 Molecular and Cellular Immunoregulation Section, Laboratory of Immune System Biology, Division of Intramural Research Bethesda, MD
1 shared publication
Latest Publications
- 1 March 2017
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 198 (5) , 1798-1803
Cutting Edge: Notch Signaling Promotes the Plasticity of Group-2 Innate Lymphoid Cells
The mechanisms underlying lymphocyte lineage stability and plasticity remain elusive. Recent work indicates that innate lymphoid cells (ILC) possess substantial plasticity. Whereas natural ILC2 (nILC2) produce type-2 cytokines, plastic inflammatory ILC2 (iILC2) can coproduce both type-2 cytokines and the ILC3-characteristic cytokine, IL-17. Mechanisms that elicit this lineage plasticity, and the importance in health and disease, remain unclear. In this study we show that iILC2 are potent inducers of airway inflammation in response to acute house dust mite challenge. We find that Notch signaling induces lineage plasticity of mature ILC2 and drives the conversion of nILC2 into iILC2. Acute blockade of Notch signaling abolished functional iILC2, but not nILC2, in vivo. Exposure of isolated nILC2 to Notch ligands induced Rorc expression and elicited dual IL-13/IL-17 production, converting nILC2 into iILC2. Together these results reveal a novel role for Notch signaling in eliciting ILC2 plasticity and driving the emergence of highly proinflammatory innate lymphocytes.
- 1 March 2017
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 198 (5) , 1798-1803
Cutting Edge: Notch Signaling Promotes the Plasticity of Group-2 Innate Lymphoid Cells
The mechanisms underlying lymphocyte lineage stability and plasticity remain elusive. Recent work indicates that innate lymphoid cells (ILC) possess substantial plasticity. Whereas natural ILC2 (nILC2) produce type-2 cytokines, plastic inflammatory ILC2 (iILC2) can coproduce both type-2 cytokines and the ILC3-characteristic cytokine, IL-17. Mechanisms that elicit this lineage plasticity, and the importance in health and disease, remain unclear. In this study we show that iILC2 are potent inducers of airway inflammation in response to acute house dust mite challenge. We find that Notch signaling induces lineage plasticity of mature ILC2 and drives the conversion of nILC2 into iILC2. Acute blockade of Notch signaling abolished functional iILC2, but not nILC2, in vivo. Exposure of isolated nILC2 to Notch ligands induced Rorc expression and elicited dual IL-13/IL-17 production, converting nILC2 into iILC2. Together these results reveal a novel role for Notch signaling in eliciting ILC2 plasticity and driving the emergence of highly proinflammatory innate lymphocytes.