NDLI: Myeloid-derived suppressor cells are involved in lysosomal acid lipase deficiency-induced endothelial cell dysfunctions.

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Myeloid-derived suppressor cells are involved in lysosomal acid lipase deficiency-induced endothelial cell dysfunctions.

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Myeloid-derived suppressor cells are involved in lysosomal acid lipase deficiency-induced endothelial cell dysfunctions.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhao, Ting Ding, Xinchun Yan, Cong Du, Hong
Description	Author Affiliation: Zhao T ( Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202); Ding X ( Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202); Du H ( Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202); Yan C ( Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202)
Abstract	The underlying mechanisms that lysosomal acid lipase (LAL) deficiency causes infiltration of myeloid-derived suppressor cells (MDSCs) in multiple organs and subsequent inflammation remain incompletely understood. Endothelial cells (ECs), lining the inner layer of blood vessels, constitute barriers regulating leukocytes transmigration to the site of inflammation. Therefore, we hypothesized that ECs are dysfunctional in LAL-deficient (lal(-/-)) mice. We found that Ly6G(+) cells transmigrated more efficiently across lal(-/-) ECs than wild-type (lal(+/+)) ECs, which were associated with increased levels of PECAM-1 and MCP-1 in lal(-/-) ECs. In addition, lal(-/-) ECs showed enhanced migration and proliferation, decreased apoptosis, but impaired tube formation and angiogenesis. lal(-/-) ECs also suppressed T cell proliferation in vitro. Interestingly, lal(-/-) Ly6G(+) cells promoted in vivo angiogenesis (including a tumor model), EC tube formation, and proliferation. Finally, the mammalian target of rapamycin (mTOR) pathway was activated in lal(-/-) ECs, and inhibition of mTOR reversed EC dysfunctions, including decreasing Ly6G(+) cell transmigration, delaying migration, and relieving suppression of T cell proliferation, which was mediated by decreasing production of reactive oxygen species. Our results indicate that LAL regulates EC functions through interaction with MDSCs and modulation of the mTOR pathway, which may provide a mechanistic basis for targeting MDSCs or mTOR to rejuvenate EC functions in LAL deficiency-related diseases.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1301941
Journal	The Journal of Immunology
Issue Number	4
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-08-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Endothelial Cells Immunology Macrophages Tor Serine-threonine Kinases Transendothelial And Transepithelial Migration Wolman Disease Animals Antigens, Cd31 Biosynthesis Genetics Antigens, Ly Apoptosis Bone Marrow Cells Cd4-positive T-lymphocytes Cell Proliferation Cells, Cultured Chemokine Ccl2 Lymphocyte Activation Mice Mice, Knockout Neovascularization, Physiologic Rna Interference Reactive Oxygen Species Metabolism Sterol Esterase Deficiency Antagonists & Inhibitors Vascular Endothelial Growth Factor Receptor-2 Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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