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 Blood, 4 June 2009, Vol. 113, No. 23, pp. 5857-5867.
Prepublished online as a Blood First Edition Paper on March 27, 2009; DOI 10.1182/blood-2008-11-188888.

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IMMUNOBIOLOGY

Transcription factor Zfx controls BCR-induced proliferation and survival of B lymphocytes

Teresita L. Arenzana1, Matthew R. Smith-Raska1, and Boris Reizis1

1 Department of Microbiology, Columbia University Medical Center, New York, NY

The development, homeostasis, and function of B lymphocytes involve multiple rounds of B-cell receptor (BCR)–controlled proliferation and prolonged maintenance. We analyzed the role of transcription factor Zfx, a recently identified regulator of hematopoietic stem cell maintenance, in B-cell development and homeostasis. Panhematopoietic or B cell–specific deletion of Zfx in the bone marrow blocked B-cell development at the pre-BCR selection checkpoint. Zfx deficiency in peripheral B cells caused accelerated B-cell turnover, depletion of mature recirculating B cells, and delayed T-dependent antibody responses. In addition, the numbers and function of B-1 cell lineage were reduced. Zfx-deficient B cells showed normal proximal BCR signaling, but impaired BCR-induced proliferation and survival in vitro. This was accompanied by aberrantly enhanced and prolonged integrated stress response and by delayed induction of cyclin D2 and Bcl-xL proteins. Thus, Zfx restrains the stress response and couples antigen receptor signaling to cell expansion and maintenance during B-cell development and peripheral homeostasis. These results identify a novel transcriptional regulator of the B-cell lineage and highlight the common genetic control of stem cell maintenance and lymphocyte homeostasis.


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