The Journal of Experimental Medicine
for flow cytometry > invitrogen
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
A correction to this article has been published: Nakamura et al., J. Exp. Med. 206 (5) 1205
Published online
doi:10.1084/jem.20082179
The Journal of Experimental Medicine, Vol. 206, No. 5, 1037-1046
The Rockefeller University Press, 0022-1007 $30.00
© Nakamura et al.
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 3181K)
Right arrow PDF+supp data (5186K)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
Right arrow Related biobytes podcast
Right arrow Correction (v206,p1205)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nakamura, Y.
Right arrow Articles by Matsue, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakamura, Y.
Right arrow Articles by Matsue, H.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
*Compound via MeSH
*Substance via MeSH
*Genetics Home Reference
Hazardous Substances DB
*HISTAMINE
Medline Plus Health Information
*Hives
*Skin Conditions
Related Collections
Right arrowRelated Article
Right arrowRelated In this Issue article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

ARTICLE

 Mast cells mediate neutrophil recruitment and vascular leakage through the NLRP3 inflammasome in histamine-independent urticaria

Yuumi Nakamura1, Naotomo Kambe1, Megumu Saito2, Ryuta Nishikomori2, Yun-Gi Kim3, Makoto Murakami4, Gabriel Núñez3, and Hiroyuki Matsue1

1 Department of Dermatology, Chiba University Graduate School of Medicine, Chuo-ku, Chiba 260-8670, Japan
2 Department of Pediatrics, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8507, Japan
3 Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109
4 Biomembrane Signaling Project, The Tokyo Metropolitan Institute of Medical Science, Bunkyo-ku, Tokyo 113-8613, Japan

CORRESPONDENCE Naotomo Kambe: nkambe{at}faculty.chiba-u.jp

Urticarial rash observed in cryopyrin-associated periodic syndrome (CAPS) caused by nucleotide-binding oligomerization domain–leucine-rich repeats containing pyrin domain 3 (NLRP3) mutations is effectively suppressed by anti–interleukin (IL)-1 treatment, suggesting a pathophysiological role of IL-1β in the skin. However, the cellular mechanisms regulating IL-1β production in the skin of CAPS patients remain unclear. We identified mast cells (MCs) as the main cell population responsible for IL-1β production in the skin of CAPS patients. Unlike normal MCs that required stimulation with proinflammatory stimuli for IL-1β production, resident MCs from CAPS patients constitutively produced IL-1β. Primary MCs expressed inflammasome components and secreted IL-1β via NLRP3 and apoptosis-associated speck-like protein containing a caspase recruitment domain when stimulated with microbial stimuli known to activate caspase-1. Furthermore, MCs expressing disease-associated but not wild-type NLRP3 secreted IL-1β and induced neutrophil migration and vascular leakage, the histological hallmarks of urticarial rash, when transplanted into mouse skin. Our findings implicate MCs as IL-1β producers in the skin and mediators of histamine-independent urticaria through the NLRP3 inflammasome.

Abbreviations used: Ab, antibody; ASC, apoptosis-associated speck-like protein containing a caspase recruitment domain; BMCMC, bone marrow–derived cultured MC; CAPS, cryopyrin-associated periodic syndrome; FSMC, fetus skin–derived MC; LRR, leucine-rich repeat; MC, mast cell; MIM, Mendelian inheritance in men number; MWS, Muckle-Wells syndrome; NLRP3, NOD-LRRs containing pyrin domain 3; NOD, nucleotide-binding oligomerization domain; P2X7R, purinergic P2X, ligand-gated ion channel 7 receptor; PAMP, pathogen-associated molecular pattern.

© 2009 Nakamura et al.
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?

Related Article

Mast cells master a rash
Amy Maxmen
J. Exp. Med. 2009 206: 972-973. [Full Text] [PDF]

Related In this Issue article

Mast cells master a rash
Amy Maxmen
J. Exp. Med. 2009 206: 972-973. [Full Text] [PDF]





  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS