Nature Communications (May 2018)
Testosterone is an endogenous regulator of BAFF and splenic B cell number
- Anna S. Wilhelmson,
- Marta Lantero Rodriguez,
- Alexandra Stubelius,
- Per Fogelstrand,
- Inger Johansson,
- Matthew B. Buechler,
- Steve Lianoglou,
- Varun N. Kapoor,
- Maria E. Johansson,
- Johan B. Fagman,
- Amanda Duhlin,
- Prabhanshu Tripathi,
- Alessandro Camponeschi,
- Bo T. Porse,
- Antonius G. Rolink,
- Hans Nissbrandt,
- Shannon J. Turley,
- Hans Carlsten,
- Inga-Lill Mårtensson,
- Mikael C. I. Karlsson,
- Åsa Tivesten
Affiliations
- Anna S. Wilhelmson
- Wallenberg Laboratory for Cardiovascular and Metabolic Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital
- Marta Lantero Rodriguez
- Wallenberg Laboratory for Cardiovascular and Metabolic Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital
- Alexandra Stubelius
- Center for Bone and Arthritis Research (CBAR), Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital
- Per Fogelstrand
- Wallenberg Laboratory for Cardiovascular and Metabolic Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital
- Inger Johansson
- Wallenberg Laboratory for Cardiovascular and Metabolic Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital
- Matthew B. Buechler
- Department of Cancer Immunology, Genentech
- Steve Lianoglou
- Department of Cancer Immunology, Genentech
- Varun N. Kapoor
- Department of Cancer Immunology, Genentech
- Maria E. Johansson
- Department of Physiology, Institute of Neuroscience and Physiology, University of Gothenburg
- Johan B. Fagman
- Sahlgrenska Cancer Center, Department of Surgery, Institute of Clinical Sciences, University of Gothenburg
- Amanda Duhlin
- Department of Microbiology, Tumor and Cell Biology, Karolinska Institute
- Prabhanshu Tripathi
- Centre for Human Microbial Ecology, Translational Health Science and Technology Institute, NCR Biotech Science Cluster
- Alessandro Camponeschi
- Department of Rheumatology and Inflammation Research, Institute of Medicine, University of Gothenburg
- Bo T. Porse
- The Finsen Laboratory, Rigshospitalet; Biotech Research and Innovation Centre (BRIC); Novo Nordisk Foundation Center for Stem Cell Biology (DanStem), Faculty of Health Sciences, University of Copenhagen
- Antonius G. Rolink
- Department of Biomedicine, Developmental and Molecular Immunology, University of Basel
- Hans Nissbrandt
- Department of Pharmacology, Institute of Neuroscience and Physiology, University of Gothenburg
- Shannon J. Turley
- Department of Cancer Immunology, Genentech
- Hans Carlsten
- Center for Bone and Arthritis Research (CBAR), Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital
- Inga-Lill Mårtensson
- Department of Rheumatology and Inflammation Research, Institute of Medicine, University of Gothenburg
- Mikael C. I. Karlsson
- Department of Microbiology, Tumor and Cell Biology, Karolinska Institute
- Åsa Tivesten
- Wallenberg Laboratory for Cardiovascular and Metabolic Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital
- DOI
- https://doi.org/10.1038/s41467-018-04408-0
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 13
Abstract
Testosterone deficiency is associated with autoimmunity and increased B cell numbers, but the underlying mechanism is unclear. Here the authors show that testosterone may modulate the production of B cell survival factor BAFF by fibroblastic reticular cells via regulation of splenic neurotransmitter levels.
