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 and Åsa Tivesten ()
Additional contact information
Anna S. Wilhelmson: Sahlgrenska University Hospital
Marta Lantero Rodriguez: Sahlgrenska University Hospital
Alexandra Stubelius: Sahlgrenska University Hospital
Per Fogelstrand: Sahlgrenska University Hospital
Inger Johansson: Sahlgrenska University Hospital
Matthew B. Buechler: Genentech
Steve Lianoglou: Genentech
Varun N. Kapoor: Genentech
Maria E. Johansson: University of Gothenburg
Johan B. Fagman: University of Gothenburg
Amanda Duhlin: Karolinska Institute
Prabhanshu Tripathi: NCR Biotech Science Cluster
Alessandro Camponeschi: University of Gothenburg
Bo T. Porse: University of Copenhagen
Antonius G. Rolink: University of Basel
Hans Nissbrandt: University of Gothenburg
Shannon J. Turley: Genentech
Hans Carlsten: Sahlgrenska University Hospital
Inga-Lill Mårtensson: University of Gothenburg
Mikael C. I. Karlsson: Karolinska Institute
Åsa Tivesten: Sahlgrenska University Hospital

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract Testosterone deficiency in men is associated with increased risk for autoimmunity and increased B cell numbers through unknown mechanisms. Here we show that testosterone regulates the cytokine BAFF, an essential survival factor for B cells. Male mice lacking the androgen receptor have increased splenic B cell numbers, serum BAFF levels and splenic Baff mRNA. Testosterone deficiency by castration causes expansion of BAFF-producing fibroblastic reticular cells (FRCs) in spleen, which may be coupled to lower splenic noradrenaline levels in castrated males, as an α-adrenergic agonist decreases splenic FRC number in vitro. Antibody-mediated blockade of the BAFF receptor or treatment with the neurotoxin 6-hydroxydopamine revert the increased splenic B cell numbers induced by castration. Among healthy men, serum BAFF levels are higher in men with low testosterone. Our study uncovers a previously unrecognized regulation of BAFF by testosterone and raises important questions about BAFF in testosterone-mediated protection against autoimmunity.

Date: 2018
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DOI: 10.1038/s41467-018-04408-0

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