IL-6 dysregulation originates in dendritic cells and mediates graft-versus-host disease via classical signaling

Author:

Wilkinson Andrew N.12ORCID,Chang Karshing1,Kuns Rachel D.1,Henden Andrea S.123ORCID,Minnie Simone A.12,Ensbey Kathleen S.1,Clouston Andrew D.4,Zhang Ping1ORCID,Koyama Motoko15,Hidalgo Juan67ORCID,Rose-John Stefan8ORCID,Varelias Antiopi12ORCID,Vuckovic Slavica12,Gartlan Kate H.125ORCID,Hill Geoffrey R.1359

Affiliation:

1. QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia;

2. Faculty of Medicine, University of Queensland, Brisbane, QLD, Australia;

3. Royal Brisbane and Women’s Hospital, Brisbane, QLD, Australia;

4. Envoi Specialist Pathologists, Brisbane, QLD, Australia;

5. Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA;

6. Animal Physiology Unit, Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, and

7. Institute of Neurosciences, Universitat Autònoma de Barcelona, Bellaterra, Spain;

8. Institute of Biochemistry, Christian-Albrechts-Universität zu Kiel, Kiel, Germany; and

9. Division of Medical Oncology, University of Washington, Seattle, WA

Abstract

Key Points DCs are the principal source of IL-6 dysregulation after alloSCT. IL-6–dependent GVHD is driven by classical signaling of IL-6R on donor T cells but is regulated by trans signaling.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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