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CD 19 and BAFF ‐R can signal to promote B ‐cell survival in the absence of Syk
Author(s) -
Hobeika Elias,
LevitZerdoun Ella,
Anastasopoulou Vasiliki,
Pohlmeyer Roland,
Altmeier Simon,
Alsadeq Ameera,
Dobenecker MarcWerner,
Pelanda Roberta,
Reth Michael
Publication year - 2015
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201489732
Subject(s) - syk , biology , b cell , b cell activating factor , cd19 , b cell receptor , breakpoint cluster region , microbiology and biotechnology , lyn , signal transduction , cd38 , receptor , flow cytometry , tyrosine kinase , immunology , stem cell , antibody , cd34 , biochemistry
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 Syk 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 , RP 105 and CD 38 signaling but still respond to an IL ‐4, anti‐ CD 40, CpG or LPS stimulus. Our in vivo experiments show that Syk‐deficient B cells require BAFF receptor and CD 19/ PI 3K 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.