CD19 and BAFF‐R can signal to promote B‐cell survival in the absence of Syk. (28th January 2015)

• Record Type: Journal Article
• Authors: Hobeika, Elias; Levit‐Zerdoun, Ella; Anastasopoulou, Vasiliki; Pohlmeyer, Roland; Altmeier, Simon; Alsadeq, Ameera; Dobenecker, Marc‐Werner; Pelanda, Roberta; Reth, Michael
• Is Part Of: EMBO journal. Volume 34:Number 7(2015)
• Page Start: 925
• Page End: 939
• Publication Date: 2015-01-28
• Subjects: Molecular biology -- Periodicals; 572.805
• DOI: 10.15252/embj.201489732
• Languages: English
• ISSNs: 0261-4189

Abstract

<abstract abstract-type="main" id="embj201489732-abs-0001"> <title>Abstract</title> <p>The development and function of B lymphocytes is regulated by numerous signaling pathways, some emanating from the B‐cell antigen receptor (BCR). The spleen tyrosine kinase (Syk) plays a central role in the activation of the BCR, but less is known about its contribution to the survival and maintenance of mature B cells. We generated mice with an inducible and B‐cell‐specific deletion of the <italic>Syk</italic> gene and found that a considerable fraction of mature Syk‐negative B cells can survive in the periphery for an extended time. Syk‐negative B cells are defective in BCR, RP105 and CD38 signaling but still respond to an IL‐4, anti‐CD40, CpG or LPS stimulus. Our <italic>in vivo</italic> experiments show that Syk‐deficient B cells require BAFF receptor and CD19/PI3K signaling for their long‐term survival. These studies also shed a new light on the signals regulating the maintenance of the normal mature murine B‐cell pool.</p> </abstract>