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Blood, 15 February 2007, Vol. 109, No. 4, pp. 1620-1626. Prepublished online as a Blood First Edition Paper on October 24, 2006; DOI 10.1182/blood-2006-03-013771. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-03-013771v1 109/4/1620    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Dzhagalov, I. Articles by He, Y.-W. Search for Related Content PubMed PubMed Citation Articles by Dzhagalov, I. Articles by He, Y.-W. Related Collections Phagocytes Apoptosis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY The antiapoptotic protein Mcl-1 is essential for the survival of neutrophils but not macrophages Ivan Dzhagalov1, Ashley St. John1, and You-Wen He1 1 Department of Immunology, Duke University Medical Center, Durham, NC The antiapoptotic protein Mcl-1, a member of the Bcl-2 family, plays critical roles in promoting the survival of lymphocytes and hematopoietic stem cells. Although previous studies have implicated Mcl-1 in regulating the survival of neutrophils and macrophages, the in vivo function of Mcl-1 in these 2 cell lineages remained unclear. To address this, we have generated mice conditionally lacking Mcl-1 expression in neutrophils and macrophages. We show that Mcl-1 conditional knockout mice had a severe defect in neutrophil survival, whereas macrophage survival was normal. The granulocyte compartment in the blood, spleen, and bone marrow of Mcl-1 conditional knockout mice exhibited an approximately 2- to 3-fold higher apoptotic rate than control cells. In contrast, resting and activated macrophages from Mcl-1–deficient mice exhibited normal survival and contained up-regulated expression of Bcl-2 and Bcl-xL. These data suggest that Mcl-1 plays a nonredundant role in promoting the survival of neutrophils but not macrophages. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: I. Dzhagalov, A. Dunkle, and Y.-W. He The Anti-Apoptotic Bcl-2 Family Member Mcl-1 Promotes T Lymphocyte Survival at Multiple Stages J. Immunol., July 1, 2008; 181(1): 521 - 528. [Abstract] [Full Text] [PDF] K.-N. Son, R. P. Becker, P. Kallio, and H. L. Lipton Theiler's Virus-Induced Intrinsic Apoptosis in M1-D Macrophages Is Bax Mediated and Restricts Virus Infectivity: a Mechanism for Persistence of a Cytolytic Virus J. Virol., May 1, 2008; 82(9): 4502 - 4510. [Abstract] [Full Text] [PDF] K. L. Lin, Y. Suzuki, H. Nakano, E. Ramsburg, and M. D. Gunn CCR2+ Monocyte-Derived Dendritic Cells and Exudate Macrophages Produce Influenza-Induced Pulmonary Immune Pathology and Mortality J. Immunol., February 15, 2008; 180(4): 2562 - 2572. [Abstract] [Full Text] [PDF]

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