Immunology
- An acute phase protein ready to go therapeutic for sepsis
- 1Inflammation Research Center VIB, Ghent, Belgium
- 2Department for Biomedical Molecular Biology, Ghent University, Ghent, Belgium
- ↵* Corresponding author: Tel: +32 93313700; Email: Claude.Libert{at}irc.VIB-UGent.be
While APP are well‐known inflammation biomarkers, A2MG found in sepsis patients' sera within lipid microparticles is an essential player in the host response to sepsis and has diagnostic as well as therapeutic potentials.
- © 2014 The Authors.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
- Fas (CD95) expression in myeloid cells promotes obesity‐induced muscle insulin resistance
- Stephan Wueest1,2,
- Rouven Mueller3,
- Matthias Blüher4,
- Flurin Item1,2,
- Annie S H Chin1,2,5,
- Michael S F Wiedemann1,2,5,
- Hitoshi Takizawa3,
- Larisa Kovtonyuk3,
- Alexander V Chervonsky6,
- Eugen J Schoenle1,2,
- Markus G Manz3 and
- Daniel Konrad*,1,2,5
- 1Division of Pediatric Endocrinology and Diabetology, University Children's Hospital, Zurich, Switzerland
- 2Children's Research Centre, University Children's Hospital, Zurich, Switzerland
- 3Division of Hematology, University Hospital Zurich, Zurich, Switzerland
- 4University of Leipzig, Department of Medicine, Leipzig, Germany
- 5Zurich Centre for Integrative Human Physiology, University of Zurich, Zurich, Switzerland
- 6Department of Pathology, University of Chicago, Chicago, IL, USA
- ↵*Corresponding author: Tel: +41 44 266 7966; Fax: +41 44 266 7983; E‐mail: daniel.konrad{at}kispi.uzh.ch
Fas expression in circulating monocytes correlates with skeletal muscle insulin resistance in obese humans and loss of Fas in myeloid cells decreases the release of TNFα and thus protects mice from obesity‐induced skeletal muscle insulin resistance.
Synopsis
Fas expression in circulating monocytes correlates with skeletal muscle insulin resistance in obese humans and loss of Fas in myeloid cells decreases the release of TNFα and thus protects mice from obesity‐induced skeletal muscle insulin resistance.
Fas protein levels are increased in myeloid cells of obese and LPS‐treated mice
Mice with myeloid‐specific Fas-depletion are protected from obesity‐induced skeletal muscle insulin resistance
LPS‐induced TNFα production in myeloid cells is mediated by Fas
In humans, muscle insulin sensitivity is negatively correlated with monocytic Fas expression
- Received April 27, 2013.
- Revision received September 30, 2013.
- Accepted October 1, 2013.
- © 2013 The Authors.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
- Telomerase governs immunomodulatory properties of mesenchymal stem cells by regulating FAS ligand expression
- Chider Chen1,†,
- Kentaro Akiyama2,†,
- Takayoshi Yamaza3,
- Yong‐Ouk You1,
- Xingtian Xu1,
- Bei Li4,
- Yimin Zhao*,4 and
- Songtao Shi*,1
- 1Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA
- 2Department of Oral Rehabilitation and Regenerative Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science, Kita‐ku Okayama, Japan
- 3Department of Molecular Cell Biology and Oral Anatomy, Kyushu University Graduate School of Dental Science, Fukuoka, Japan
- 4School of Stomatology, Fourth Military Medical University, Xi'an Shanxi, China
- ↵*
Corresponding author: Tel: +1 323 442 3038; Fax: +1 323 442 2981; E‐mail: songtaos{at}usc.edu
Corresponding author: Tel: +86 29 8477 6001; Fax +86 29 8322 3047; E‐mail: zhaoym{at}fmmu.edu.cn
-
↵† These authors contributed equally to this study.
Bone marrow mesenchymal stem cells (BMMSC) have therapeutic properties in immune disorders. Telomerase function is shown to not only be critical for BMMSC stemness and osteogenic differentiation, but also to regulate BMMSC‐mediated immune therapies.
Synopsis
Bone marrow mesenchymal stem cells (BMMSC) have therapeutic properties in immune disorders. Telomerase function is shown to not only be critical for BMMSC stemness and osteogenic differentiation, but also to regulate BMMSC‐mediated immune therapies.
Telomerase governs immunomodulatory properties of BMMSCs.
TERT serves as a transcription modulator to regulate FASL expression.
Aspirin increases immunomodulation of BMMSCs through TERT activation.
EMBO Mol Med (2014) 6, 322–334
- Received May 4, 2013.
- Revision received November 10, 2013.
- Accepted November 12, 2013.
- © 2014 The Authors.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
- Inhibition of the immunoproteasome ameliorates experimental autoimmune encephalomyelitis
- Michael Basler*,1,2,†,
- Sarah Mundt2,†,
- Tony Muchamuel3,†,
- Carlo Moll4,
- Jing Jiang3,
- Marcus Groettrup*,1,2 and
- Christopher J. Kirk*,3
- 1Biotechnology Institute Thurgau (BITg) at the University of Konstanz, Kreuzlingen, Switzerland
- 2Division of Immunology, Department of Biology, University of Konstanz, Konstanz, Germany
- 3Onyx Pharmaceuticals, South San Francisco, CA, USA
- 4Institute of Pathology, Cantonal Hospital Muensterlingen, Muensterlingen, Switzerland
- ↵*
Corresponding author. Tel: +49 7531 882258; Fax: +49 7531 883102; E‐mail: Michael.Basler{at}uni-konstanz.de or
Corresponding author. Tel: +49 7531 882130; Fax: +49 7531 883102; E‐mail: Marcus.Groettrup{at}uni-konstanz.de
Corresponding author. Tel: +1 650‐266‐2660; Fax: +1 866‐778‐9068; E‐mail: ckirk{at}onyx.com
-
↵† These authors contributed equally to this work.
The immunoproteasome is found implicated in the development of experimental autoimmune encephalomyelitis and LMP7 inhibitors shown promising for the treatment of multiple sclerosis and other autoimmune diseases that rely on Th1/Th17 response.
Synopsis
The immunoproteasome is found implicated in the development of experimental autoimmune encephalomyelitis and LMP7 inhibitors shown promising for the treatment of multiple sclerosis and other autoimmune diseases that rely on Th1/Th17 response.
Immunoproteasome inhibition reduces clinical symptoms in two different animal model for multiple sclerosis
Immunoproteasome inhibition impedes Th1 and Th17 cell differentiation in experimental autoimmune encephalomyelitis
Immunoproteaome inhibition reduces cellular infiltration into the CNS in experimental autoimmune encephalomyelitis
Immunoproteasome inhibitors are promising targets for the treatment of multiple sclerosis
- Received October 3, 2013.
- Revision received November 4, 2013.
- Accepted November 5, 2013.
- © 2014 The Authors.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
- Microparticle alpha‐2‐macroglobulin enhances pro‐resolving responses and promotes survival in sepsis
- Jesmond Dalli14,
- Lucy V Norling1,
- Trinidad Montero‐Melendez1,
- Donata Federici Canova1,
- Hazem Lashin1,
- Anton M Pavlov2,
- Gleb B Sukhorukov2,
- Charles J Hinds1,3 and
- Mauro Perretti*,1
- 1Centre for Biochemical Pharmacology, The William Harvey Research Institute, Barts and The London School of Medicine Queen Mary University of London, London, UK
- 2School of Engineering & Materials Science Queen Mary University of London, London, UK
- 3Intensive Care Unit, St. Bartholomew's Hospital Barts Health, London, UK
- 4 Center for Experimental Therapeutics and Reperfusion Injury, Harvard Institute of Medicine Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA
- ↵*Corresponding author. Tel: +44 207 8828782; Fax: +44 207 8826076; E‐mail: m.perretti{at}qmul.ac.uk
A specific subset of microparticles enriched in Alpha‐2‐macroglobulin (A2MG) previously found increased in the plasma of sepsis patients, are now shown to protect septic mice from dying and improve the containment and clearance of bacteria.
Synopsis
A specific subset of microparticles enriched in Alpha‐2‐macroglobulin (A2MG) previously found increased in the plasma of sepsis patients, are now shown to protect septic mice from dying and improve the containment and clearance of bacteria.
Lethality in experiment sepsis is prevented by administration of human neutrophil microparticles enriched in alpha2‐macroglobluin (A2MG), an effect associated with higher pro‐resolving mediator levels in infectious exudates.
A2MG enriched microparticles promote bacterial clearance by mouse and human leukocytes.
A2MG is transferred by microparticles onto endothelial cells to then promote neutrophil adhesion.
Addition of A2MG to human neutrophil preserved chemotactic responses.
A2MG/CD66b+ve microparticles are elevated in the plasma of septic patients who survived commonly acquired pneumonia.
- Received September 18, 2013.
- Revision received October 2, 2013.
- Accepted October 4, 2013.
- © 2013 The Authors.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Pages
