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Testosterone is an endogenous regulator of BAFF and splenic B cell number

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  • 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
Vis graf over relationer

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.

OriginalsprogEngelsk
TidsskriftNature Communications
Vol/bind9
Udgave nummer1
Sider (fra-til)2067
ISSN2041-1723
DOI
StatusUdgivet - 25 maj 2018

ID: 54443482