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Blood, 15 April 2008, Vol. 111, No. 8, pp. 4184-4192. Prepublished online as a Blood First Edition Paper on January 24, 2008; DOI 10.1182/blood-2007-08-108936. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2007-08-108936v1 111/8/4184    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Rajakariar, R. Articles by Gilroy, D. W. Search for Related Content PubMed PubMed Citation Articles by Rajakariar, R. Articles by Gilroy, D. W. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Novel biphasic role for lymphocytes revealed during resolving inflammation Ravindra Rajakariar1, Toby Lawrence2, Jonas Bystrom3, Mark Hilliard4, Paul Colville-Nash5, Geoff Bellingan6, Desmond Fitzgerald4, Muhammad M. Yaqoob1, and Derek W. Gilroy3 1 Department of Experimental Medicine and Translational Therapeutics, William Harvey Research Institute, London, United Kingdom; 2 Institute of Cancer, Centre for Translational Oncology, London, United Kingdom; 3 Centre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London, United Kingdom; 4 Conway Institute, University College Dublin, Dublin, Ireland; 5 SW Thames Institute for Renal Research, St Helier Hospital, Carshalton, United Kingdom; and 6 Critical Care, University College London Hospitals National Health Service Foundation Trust, London, United Kingdom Acute inflammation is traditionally described as the influx of polymorphonuclear leukocytes (PMNs) followed by monocyte-derived macrophages, leading to resolution. This is a classic view, and despite subpopulations of lymphocytes possessing innate immune-regulatory properties, seldom is their role in acute inflammation and its resolution discussed. To redress this we show, using lymphocyte-deficient RAG1–/– mice, that peritoneal T/B lymphocytes control PMN trafficking by regulating cytokine synthesis. Once inflammation ensues in normal mice, lymphocytes disappear in response to DP1 receptor activation by prostaglandin D2. However, upon resolution, lymphocytes repopulate the cavity comprising B1, natural killer (NK), / T, CD4+/CD25+, and B2 cells. Repopulating lymphocytes are dispensable for resolution, as inflammation in RAG1–/– and wild-type mice resolve uniformly. However, repopulating lymphocytes are critical for modulating responses to superinfection. Thus, in chronic granulomatous disease using gp91phox–/– mice, not only is resolution delayed compared with wild-type, but there is a failure of lymphocyte re-appearance predisposing to exaggerated immune responses upon secondary challenge that is rescued by resolution-phase lymphocytes. In conclusion, as lymphocyte repopulation is also evident in human peritonitis, we hereby describe a transition in T/B cells from acute inflammation to resolution, with a central role in modulating the severity of early onset and orchestrating responses to secondary infection. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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