Universität zu Köln

Lebrun, Astrid, Lo Re, Sandra, Chantry, Mathilde, Carerra, Xavier Izquierdo, Uwambayinema, Francine, Ricci, Doriana, Devosse, Raynal, Ibouraadaten, Saloua, Brombin, Lisa, Palmai-Pallag, Mihaly, Yakoub, Yousof, Pasparakis, Manolis ORCID: 0000-0002-9870-0966, Lison, Dominique ORCID: 0000-0001-6557-2518 and Huaux, Francois (2017). CCR2(+) monocytic myeloid-derived suppressor cells (M-MDSCs) inhibit collagen degradation and promote lung fibrosis by producing transforming growth factor-1. J. Pathol., 243 (3). S. 320 - 331. HOBOKEN: WILEY. ISSN 1096-9896

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Abstract

Monocytes infiltrating scar tissue are predominantly viewed as progenitor cells. Here, we show that tissue CCR2(+) monocytes have specific immunosuppressive and profibrotic functions. CCR2(+) monocytic cells are acutely recruited to the lung before the onset of silica-induced fibrosis in mice. These tissue monocytes are defined as monocytic myeloid-derived suppressor cells (M-MDSCs) because they significantly suppress T-lymphocyte proliferation in vitro. M-MDSCs collected from silica-treated mice also express transforming growth factor (TGF)-1, which stimulates lung fibroblasts to release tissue inhibitor of metalloproteinase (TIMP)-1, an inhibitor of metalloproteinase collagenolytic activity. By using LysMCreCCR2(loxP/loxP) mice, we show that limiting CCR2(+) M-MDSC accumulation reduces the pulmonary contents of TGF-1, TIMP-1 and collagen after silica treatment. M-MDSCs do not differentiate into lung macrophages, granulocytes or fibrocytes during pulmonary fibrogenesis. Collectively, our data indicate that M-MDSCs contribute to lung fibrosis by specifically promoting a non-degrading collagen microenvironment. Copyright (C) 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Lebrun, Astrid UNSPECIFIED UNSPECIFIED UNSPECIFIED Lo Re, Sandra UNSPECIFIED UNSPECIFIED UNSPECIFIED Chantry, Mathilde UNSPECIFIED UNSPECIFIED UNSPECIFIED Carerra, Xavier Izquierdo UNSPECIFIED UNSPECIFIED UNSPECIFIED Uwambayinema, Francine UNSPECIFIED UNSPECIFIED UNSPECIFIED Ricci, Doriana UNSPECIFIED UNSPECIFIED UNSPECIFIED Devosse, Raynal UNSPECIFIED UNSPECIFIED UNSPECIFIED Ibouraadaten, Saloua UNSPECIFIED UNSPECIFIED UNSPECIFIED Brombin, Lisa UNSPECIFIED UNSPECIFIED UNSPECIFIED Palmai-Pallag, Mihaly UNSPECIFIED UNSPECIFIED UNSPECIFIED Yakoub, Yousof UNSPECIFIED UNSPECIFIED UNSPECIFIED Pasparakis, Manolis UNSPECIFIED orcid.org/0000-0002-9870-0966 UNSPECIFIED Lison, Dominique UNSPECIFIED orcid.org/0000-0001-6557-2518 UNSPECIFIED Huaux, Francois UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-213501
DOI:	10.1002/path.4956
Journal or Publication Title:	J. Pathol.
Volume:	243
Number:	3
Page Range:	S. 320 - 331
Date:	2017
Publisher:	WILEY
Place of Publication:	HOBOKEN
ISSN:	1096-9896
Language:	English
Faculty:	Faculty of Mathematics and Natural Sciences
Divisions:	Faculty of Mathematics and Natural Sciences > Department of Biology > Institute for Genetics
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language PULMONARY-FIBROSIS; T-CELL; INTERSTITIAL COMPARTMENTS; MONONUCLEAR PHAGOCYTES; LY6C(HI) MONOCYTES; MOUSE MODEL; MACROPHAGES; ALVEOLAR; DIFFERENTIATION; INFLAMMATION Multiple languages Oncology; Pathology Multiple languages
Refereed:	Yes
URI:	http://kups.ub.uni-koeln.de/id/eprint/21350