SEARCH:   Advanced

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 (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 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. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 10, 2008 Accepted October 28, 2008 B7-H4 deficient mice display augmented neutrophil-mediated innate immunity Gefeng Zhu, Mathew M. Augustine, Takeshi Azuma, Liqun Luo, Sheng Yao, Sudarshan Anand, A. Cecilia Rietz, Jiaqiang Huang, Haiying Xu, Andrew S. Flies, Sarah J. Flies, Koji Tamada, Marco Colonna, Jan M.A. van Deursen, and Lieping Chen* Department of Dermatology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, United States Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, United States Department of Pediatrics, Mayo Clinic, Rochester, MN, United States * Corresponding author; email: lchen42{at}jhmi.edu. B7-H4 is an immunoglobulin superfamily molecule and shown to be inhibitory for T cell responses. To explore physiological 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]

	Copyright © 2008 by American Society of Hematology         Online ISSN: 1528-0020