Activated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cells

Activated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cells

Graft-vs.-host disease is a complication of allogenic hematopoietic stem cell transplantation, and is associated with endothelial dysfunction. Here the authors show that activated protein C signals via PAR2/PAR3 to expand Treg cells, mitigating the disease in mice.

Bibliographic Details
Main Authors: Satish Ranjan, Alexander Goihl, Shrey Kohli, Ihsan Gadi, Mandy Pierau, Khurrum Shahzad, Dheerendra Gupta, Fabian Bock, Hongjie Wang, Haroon Shaikh, Thilo Kähne, Dirk Reinhold, Ute Bank, Ana C. Zenclussen, Jana Niemz, Tina M. Schnöder, Monika Brunner-Weinzierl, Thomas Fischer, Thomas Kalinski, Burkhart Schraven, Thomas Luft, Jochen Huehn, Michael Naumann, Florian H. Heidel, Berend Isermann
Format: Article
Language:English
Published: Nature Publishing Group 2017-08-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-017-00169-4
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spelling doaj-17c58ccb118041e9a3a369a75450a6692021-01-31T12:27:26ZengNature Publishing GroupNature Communications2041-17232017-08-018111610.1038/s41467-017-00169-4Activated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cellsSatish Ranjan0Alexander Goihl1Shrey Kohli2Ihsan Gadi3Mandy Pierau4Khurrum Shahzad5Dheerendra Gupta6Fabian Bock7Hongjie Wang8Haroon Shaikh9Thilo Kähne10Dirk Reinhold11Ute Bank12Ana C. Zenclussen13Jana Niemz14Tina M. Schnöder15Monika Brunner-Weinzierl16Thomas Fischer17Thomas Kalinski18Burkhart Schraven19Thomas Luft20Jochen Huehn21Michael Naumann22Florian H. Heidel23Berend Isermann24Institute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke- University MagdeburgInstitute of Molecular and Clinical Immunology, Otto-von-Guericke-University MagdeburgInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke- University MagdeburgInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke- University MagdeburgDepartment of Experimental Pediatrics, Otto-von-Guericke-University MagdeburgInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke- University MagdeburgInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke- University MagdeburgInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke- University MagdeburgInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke- University MagdeburgInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke- University MagdeburgInstitute of Experimental Internal Medicine, Center of Internal Medicine, Otto-von-Guericke University MagdeburgInstitute of Molecular and Clinical Immunology, Otto-von-Guericke-University MagdeburgInstitute of Molecular and Clinical Immunology, Otto-von-Guericke-University MagdeburgExperimental Obstetrics and Gynecology, Medical Faculty, Otto-von-Guericke UniversityDepartment of Experimental Immunology, Helmholtz Centre for Infection Research (HZI)Internal Medicine II, Hematology and Oncology, University Hospital JenaDepartment of Experimental Pediatrics, Otto-von-Guericke-University MagdeburgDepartment of Hematology and Oncology, Center of Internal Medicine, Otto-von-Guericke University MagdeburgInstitute for Pathology, Otto-von-Guericke University MagdeburgInstitute of Molecular and Clinical Immunology, Otto-von-Guericke-University MagdeburgDepartment of Medicine V, University of HeidelbergDepartment of Experimental Immunology, Helmholtz Centre for Infection Research (HZI)Institute of Experimental Internal Medicine, Center of Internal Medicine, Otto-von-Guericke University MagdeburgInternal Medicine II, Hematology and Oncology, University Hospital JenaInstitute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke- University MagdeburgGraft-vs.-host disease is a complication of allogenic hematopoietic stem cell transplantation, and is associated with endothelial dysfunction. Here the authors show that activated protein C signals via PAR2/PAR3 to expand Treg cells, mitigating the disease in mice.https://doi.org/10.1038/s41467-017-00169-4
collection DOAJ
language English
format Article
sources DOAJ
author Satish Ranjan
Alexander Goihl
Shrey Kohli
Ihsan Gadi
Mandy Pierau
Khurrum Shahzad
Dheerendra Gupta
Fabian Bock
Hongjie Wang
Haroon Shaikh
Thilo Kähne
Dirk Reinhold
Ute Bank
Ana C. Zenclussen
Jana Niemz
Tina M. Schnöder
Monika Brunner-Weinzierl
Thomas Fischer
Thomas Kalinski
Burkhart Schraven
Thomas Luft
Jochen Huehn
Michael Naumann
Florian H. Heidel
Berend Isermann
spellingShingle Satish Ranjan
Alexander Goihl
Shrey Kohli
Ihsan Gadi
Mandy Pierau
Khurrum Shahzad
Dheerendra Gupta
Fabian Bock
Hongjie Wang
Haroon Shaikh
Thilo Kähne
Dirk Reinhold
Ute Bank
Ana C. Zenclussen
Jana Niemz
Tina M. Schnöder
Monika Brunner-Weinzierl
Thomas Fischer
Thomas Kalinski
Burkhart Schraven
Thomas Luft
Jochen Huehn
Michael Naumann
Florian H. Heidel
Berend Isermann
Activated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cells
Nature Communications
author_facet Satish Ranjan
Alexander Goihl
Shrey Kohli
Ihsan Gadi
Mandy Pierau
Khurrum Shahzad
Dheerendra Gupta
Fabian Bock
Hongjie Wang
Haroon Shaikh
Thilo Kähne
Dirk Reinhold
Ute Bank
Ana C. Zenclussen
Jana Niemz
Tina M. Schnöder
Monika Brunner-Weinzierl
Thomas Fischer
Thomas Kalinski
Burkhart Schraven
Thomas Luft
Jochen Huehn
Michael Naumann
Florian H. Heidel
Berend Isermann
author_sort Satish Ranjan
title Activated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cells
title_short Activated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cells
title_full Activated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cells
title_fullStr Activated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cells
title_full_unstemmed Activated protein C protects from GvHD via PAR2/PAR3 signalling in regulatory T-cells
title_sort activated protein c protects from gvhd via par2/par3 signalling in regulatory t-cells
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2017-08-01
description Graft-vs.-host disease is a complication of allogenic hematopoietic stem cell transplantation, and is associated with endothelial dysfunction. Here the authors show that activated protein C signals via PAR2/PAR3 to expand Treg cells, mitigating the disease in mice.
url https://doi.org/10.1038/s41467-017-00169-4
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