S100 Proteins As an Important Regulator of Macrophage Inflammation

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Abstract

The S100 proteins, a family of calcium-binding cytosolic proteins, have a broad range of intracellular and extracellular functions through regulating calcium balance, cell apoptosis, migration, proliferation, differentiation, energy metabolism, and inflammation. The intracellular functions of S100 proteins involve interaction with intracellular receptors, membrane protein recruitment/transportation, transcriptional regulation and integrating with enzymes or nucleic acids, and DNA repair. The S100 proteins could also be released from the cytoplasm, induced by tissue/cell damage and cellular stress. The extracellular S100 proteins, serving as a danger signal, are crucial in regulating immune homeostasis, post-traumatic injury, and inflammation. Extracellular S100 proteins are also considered biomarkers for some specific diseases. In this review, we will discuss the multi-functional roles of S100 proteins, especially their potential roles associated with cell migration, differentiation, tissue repair, and inflammation.

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Most cited references 147

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Altered macrophage differentiation and immune dysfunction in tumor development.

Antonio Sica, Vincenzo Bronte (2007)

Tumors require a constant influx of myelomonocytic cells to support the angiogenesis and stroma remodeling needed for their growth. This is mediated by tumor-derived factors, which cause sustained myelopoiesis and the accumulation and functional differentiation of myelomonocytic cells, most of which are macrophages, at the tumor site. An important side effect of the accumulation and functional differentiation of these cells is that they can induce lymphocyte dysfunction. A complete understanding of the complex interplay between neoplastic and myelomonocytic cells might offer novel targets for therapeutic intervention aimed at depriving tumor cells of important growth support and enhancing the antitumor immune response.

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RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides.

M A Hofmann, S. Drury, C Fu … (1999)

S100/calgranulin polypeptides are present at sites of inflammation, likely released by inflammatory cells targeted to such loci by a range of environmental cues. We report here that receptor for AGE (RAGE) is a central cell surface receptor for EN-RAGE (extracellular newly identified RAGE-binding protein) and related members of the S100/calgranulin superfamily. Interaction of EN-RAGEs with cellular RAGE on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Blockade of EN-RAGE/RAGE quenches delayed-type hypersensitivity and inflammatory colitis in murine models by arresting activation of central signaling pathways and expression of inflammatory gene mediators. These data highlight a novel paradigm in inflammation and identify roles for EN-RAGEs and RAGE in chronic cellular activation and tissue injury.

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Inhibition of dendritic cell differentiation and accumulation of myeloid-derived suppressor cells in cancer is regulated by S100A9 protein

Pingyan Cheng, Cesar A. Corzo, Noreen Luetteke … (2008)

Accumulation of myeloid-derived suppressor cells (MDSCs) associated with inhibition of dendritic cell (DC) differentiation is one of the major immunological abnormalities in cancer and leads to suppression of antitumor immune responses. The molecular mechanism of this phenomenon remains unclear. We report here that STAT3-inducible up-regulation of the myeloid-related protein S100A9 enhances MDSC production in cancer. Mice lacking this protein mounted potent antitumor immune responses and rejected implanted tumors. This effect was reversed by administration of wild-type MDSCs from tumor-bearing mice to S100A9-null mice. Overexpression of S100A9 in cultured embryonic stem cells or transgenic mice inhibited the differentiation of DCs and macrophages and induced accumulation of MDSCs. This study demonstrates that tumor-induced up-regulation of S100A9 protein is critically important for accumulation of MDSCs and reveals a novel molecular mechanism of immunological abnormalities in cancer.

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Author and article information

Contributors

Zachary Braunstein: URI : http://frontiersin.org/people/u/469864

Jixin Zhong: URI : http://frontiersin.org/people/u/200046

Xiaoquan Rao: URI : http://frontiersin.org/people/u/398941

Journal

Journal ID (nlm-ta): Front Immunol

Journal ID (iso-abbrev): Front Immunol

Journal ID (publisher-id): Front. Immunol.

Title: Frontiers in Immunology

Publisher: Frontiers Media S.A.

ISSN (Electronic): 1664-3224

Publication date (Electronic): 05 January 2018

Publication date Collection: 2017

Volume: 8

Electronic Location Identifier: 1908

Affiliations

[1] ¹College of Health Science and Nursing, Wuhan Polytechnic University , Wuhan, China

[2] ²Cardiovascular Research Institute, Case Western Reserve University , Cleveland, OH, United States

[3] ³Boonshoft School of Medicine, Wright State University , Dayton, OH, United States

[4] ⁴Department of Health Sciences, University of Missouri , Columbia, MO, United States

Author notes

Edited by: Leticia A. Carneiro, Universidade Federal do Rio de Janeiro, Brazil

Reviewed by: Charles E. McCall, Wake Forest Baptist Medical Center, United States; Penghua Yang, University of Maryland, Baltimore, United States

*Correspondence: Jixin Zhong, jixin.zhong@ 123456case.edu ; Xiaoquan Rao, jannet18@ 123456163.com

Specialty section: This article was submitted to Molecular Innate Immunity, a section of the journal Frontiers in Immunology

Article

DOI: 10.3389/fimmu.2017.01908

PMC ID: 5770888

PubMed ID: 29379499

SO-VID: afd8d08e-87b6-4c07-a079-6c62186b32d8

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

History

Date received : 06 October 2017

Date accepted : 14 December 2017

Page count

Figures: 1, Tables: 0, Equations: 0, References: 167, Pages: 11, Words: 10183

Funding

Funded by: National Institutes of Health 10.13039/100000002

Award ID: K99ES026241, K01DK105108

Funded by: American Heart Association 10.13039/100000968

Award ID: 17GRNT33670485

Funded by: National Natural Science Foundation of China 10.13039/501100001809

Award ID: 81101247, 81670431

Funded by: Natural Science Foundation of Zhejiang Province 10.13039/501100004731

S100 Proteins As an Important Regulator of Macrophage Inflammation

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Abstract

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Gamma Delta T cells

Most cited references 147

Altered macrophage differentiation and immune dysfunction in tumor development.

RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides.

Inhibition of dendritic cell differentiation and accumulation of myeloid-derived suppressor cells in cancer is regulated by S100A9 protein

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