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Blood, 15 June 2007, Vol. 109, No. 12, pp. 5363-5370. Prepublished online as a Blood First Edition Paper on February 27, 2007; DOI 10.1182/blood-2006-08-039131. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-08-039131v1 109/12/5363    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 Waskow, C. Articles by Rodewald, H.-R. Search for Related Content PubMed PubMed Citation Articles by Waskow, C. Articles by Rodewald, H.-R. Related Collections Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Kit is essential for PMA-inflammation–induced mast-cell accumulation in the skin Claudia Waskow1, Susanne Bartels1, Susan M. Schlenner1, Celine Costa1, and Hans-Reimer Rodewald1 1 Institute for Immunology, University of Ulm, Ulm, Germany Cutaneous mast cells have important pathogenic roles in skin inflammation, but the signals regulating mast-cell numbers in healthy and inflamed skin are not fully understood. Mast-cell development depends on the receptor tyrosine kinase Kit as shown by a greater than 95% reduction of mast-cell numbers in hypomorphic (KitW/Wv) mutant mice that are widely used as a mast-cell deficiency model. Mast-cell numbers are normally very low in KitW/Wv mice, but numbers can strongly increase under inflammatory conditions. It remains elusive whether this inflammation-driven mast-cell accumulation is mediated by signals transmitted via the KitWv receptor or by other, Kit-independent stimuli. We show here, using viable Kit- null mice (KitW/W), that Kit is essential for mast-cell accumulation in phorbol-12-myristate-13-acetate (PMA)–treated, chronically inflamed skin. This increase in mast- cell numbers is strongly attenuated in KitW/Wv mice lacking mature lymphocytes (T, B, and natural killer [NK] cells). These data, together with reconstitution experiments, point at a role for lymphocytes in the regulation of mast-cell compartments under limiting Kit signaling. We conclude that inflammation-induced cutaneous mast-cell accumulation is dependent on Kit signaling strength, and, under limiting Kit signals, on cells of the adaptive immune system. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Ding, J. G. Nedrud, B. Wershil, R. W. Redline, T. G. Blanchard, and S. J. Czinn Partial Protection against Helicobacter pylori in the Absence of Mast Cells in Mice Infect. Immun., December 1, 2009; 77(12): 5543 - 5550. [Abstract] [Full Text] [PDF] F. Paulhe, M. Wehrle-Haller, M.-C. Jacquier, B. A. Imhof, S. Tabone-Eglinger, and B. Wehrle-Haller Dimerization of Kit-ligand and efficient cell-surface presentation requires a conserved Ser-Gly-Gly-Tyr motif in its transmembrane domain FASEB J, September 1, 2009; 23(9): 3037 - 3048. [Abstract] [Full Text] [PDF]

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