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Skewing of the population balance of lymphoid and myeloid cells by secreted and intracellular osteopontin.

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Date
2017-09
Authors
Kanayama, Masashi
Xu, Shengjie
Danzaki, Keiko
Gibson, Jason R
Inoue, Makoto
Gregory, Simon G
Shinohara, Mari L
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Abstract
The balance of myeloid populations and lymphoid populations must be well controlled. Here we found that osteopontin (OPN) skewed this balance during pathogenic conditions such as infection and autoimmunity. Notably, two isoforms of OPN exerted distinct effects in shifting this balance through cell-type-specific regulation of apoptosis. Intracellular OPN (iOPN) diminished the population size of myeloid progenitor cells and myeloid cells, and secreted OPN (sOPN) increase the population size of lymphoid cells. The total effect of OPN on skewing the leukocyte population balance was observed as host sensitivity to early systemic infection with Candida albicans and T cell-mediated colitis. Our study suggests previously unknown detrimental roles for two OPN isoforms in causing the imbalance of leukocyte populations.
Type
Journal article
Subject
Lymphocytes
T-Lymphocytes
Myeloid Cells
Animals
Mice, Knockout
Mice
Candida albicans
Infection
Candidiasis
Colitis
Autoimmune Diseases
Protein Isoforms
Enzyme-Linked Immunosorbent Assay
Flow Cytometry
Reverse Transcriptase Polymerase Chain Reaction
Apoptosis
Lymphopoiesis
Myelopoiesis
Cell Proliferation
Osteopontin
Real-Time Polymerase Chain Reaction
Permalink
https://hdl.handle.net/10161/17648
Published Version (Please cite this version)
10.1038/ni.3791
Publication Info
Kanayama, Masashi; Xu, Shengjie; Danzaki, Keiko; Gibson, Jason R; Inoue, Makoto; Gregory, Simon G; & Shinohara, Mari L (2017). Skewing of the population balance of lymphoid and myeloid cells by secreted and intracellular osteopontin. Nature immunology, 18(9). pp. 973-984. 10.1038/ni.3791. Retrieved from https://hdl.handle.net/10161/17648.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Gregory

Simon Gray Gregory

Professor in Neurosurgery
Dr. Gregory is a tenured Professor and Director of the Brain Tumor Omics Program (BTOP) in the Duke Department of Neurosurgery, the Vice Chair of Research in the Department of Neurology, and Director of the Molecular Genomics Core at the Duke Molecular Physiology Institute.  As a neurogenomicist, Dr. Gregory applies the experience gained from leading the sequencing of chromosome 1 for the Human Genome Project to elucidating the mechanisms underlying multi-factorial
Shinohara

Mari L. Shinohara

Professor of Integrative Immunobiology
Shinohara Lab WebsiteImmune responses against pathogens are essential for host protection, but excessive and uncontrolled immune reactions can lead to autoimmunity. How does our immune system keep the balance fine-tuned? This is a central question being asked in my laboratory. The immune system needs to detect pathogens quickly and effectively. This is performed by the innate immune system, which includes cells such as mac
Xu

Shengjie Xu

Research Assistant, Ph D Student
Program Start Year:  2013Mari Shinohara Laboratory"Novel Heterogeneous Alveolar Macrophage Subpopulations during Early Fungal Infection"
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