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Blood, 19 February 2009, Vol. 113, No. 8, pp. 1759-1767. Prepublished online as a Blood First Edition Paper on December 24, 2008; DOI 10.1182/blood-2008-01-133223. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2008-01-133223v1 113/8/1759    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 Zhu, G. Articles by Chen, L. Search for Related Content PubMed PubMed Citation Articles by Zhu, G. Articles by Chen, L. Related Collections Immunobiology Phagocytes, Granulocytes, and Myelopoiesis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PHAGOCYTES, GRANULOCYTES, AND MYELOPOIESIS B7-H4–deficient mice display augmented neutrophil-mediated innate immunity Gefeng Zhu1, Mathew M. Augustine1, Takeshi Azuma1, Liqun Luo1, Sheng Yao1, Sudarshan Anand1, A. Cecilia Rietz1, Jiaqiang Huang1, Haiying Xu1, Andrew S. Flies1, Sarah J. Flies1, Koji Tamada1, Marco Colonna2, Jan M. A. van Deursen3, and Lieping Chen1 1 Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD; 2 Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO; and 3 Department of Pediatrics, Mayo Clinic, Rochester, MN B7-H4 is an immunoglobulin superfamily molecule and shown to be inhibitory for T-cell responses. To explore physiologic roles of B7-H4, we created B7-H4–deficient (KO) mice by genetic targeting. B7-H4KO mice are healthy and their T- and B-cell responses to polyclonal antigens are in normal range. However, B7-H4KO mice are more resistant to infection by Listeria monocytogenes than their littermates. Within 3 days after infection, bacterial colonies in livers and spleens are significantly lower than the controls, suggesting a role of B7-H4 in enhancing innate immunity. Further studies demonstrate that neutrophils increase in peripheral organs of B7-H4KO mice more so than their littermates but their bactericidal functions remain unchanged. Augmented innate resistance is completely dependent on neutrophils, even in the absence of adaptive immunity. In vitro B7-H4 inhibits the growth of bone marrow–derived neutrophil progenitors, suggesting an inhibitory function of B7-H4 in neutrophil expansion. Our results identify B7-H4 as a negative regulator of the neutrophil response to infection and provide a new target for manipulation of innate immunity. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Rodriguez, A. Chora, B. Goumnerov, C. Mumaw, W. S. Goebel, L. Fernandez, H. Baydoun, H. HogenEsch, D. M. Dombkowski, C. A. Karlewicz, et al. Dysfunctional expansion of hematopoietic stem cells and block of myeloid differentiation in lethal sepsis Blood, November 5, 2009; 114(19): 4064 - 4076. [Abstract] [Full Text] [PDF]

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