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10.1038/s41467-018-04408-0

http://scihub22266oqcxt.onion/10.1038/s41467-018-04408-0
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C5970247!5970247!29802242
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suck abstract from ncbi


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pmid29802242      Nat+Commun 2018 ; 9 (ä): ä
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  • Testosterone is an endogenous regulator of BAFF and splenic B cell number #MMPMID29802242
  • Wilhelmson AS; Lantero Rodriguez M; Stubelius A; Fogelstrand P; Johansson I; Buechler MB; Lianoglou S; Kapoor VN; Johansson ME; Fagman JB; Duhlin A; Tripathi P; Camponeschi A; Porse BT; Rolink AG; Nissbrandt H; Turley SJ; Carlsten H; Mårtensson IL; Karlsson MCI; Tivesten Å
  • Nat Commun 2018[]; 9 (ä): ä PMID29802242show ga
  • 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 ?-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.
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