Journal of Leukocyte Biology Crossref.org
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wang, B.
Right arrow Articles by Sauder, D. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, B.
Right arrow Articles by Sauder, D. N.
(Journal of Leukocyte Biology. 2001;70:185-191.)
© 2001 by Society for Leukocyte Biology

Insights into molecular mechanisms of contact hypersensitivity gained from gene knockout studies

Binghe Wang*, Claudio Feliciani{dagger}, Irwin Freed*, Qinchao Cai* and Daniel N. Sauder*

* Division of Dermatology, Sunnybrook and Women’s College Health Science Centre, University of Toronto, Ontario, Canada M4N 3M5, and
{dagger} Department of Dermatology, University "G.d’Annunzio", Via dei Vestini Chieti, Italy

Correspondence: Dr. Daniel N. Sauder, Professor and Chairman, Johns Hopkins University, Suite 1002, 550 N. Broadway, Baltimore, MD 21205. E-mail: dsauder{at}jhmi.edu

Contact hypersensitivity (CHS), a dendritic-cell (DC)-dependent, T-cell-mediated skin immune response to reactive haptens, has been a subject of intense research for many years. The molecular mechanisms underlying CHS are complicated and are not fully understood. During the past few years, varieties of gene-targeted knockout mice have been used in the study of CHS. Such studies have contributed significantly to our understanding of the mechanisms responsible for the initiation of CHS. This review focuses on insights into molecular requirements for CHS gained from knockout studies.

Key Words: dendritic cell • hapten • CHS • mouse • targeted mutation




This article has been cited by other articles:


Home page
 J. Exp. Med.Home page
M. Nagamachi, D. Sakata, K. Kabashima, T. Furuyashiki, T. Murata, E. Segi-Nishida, K. Soontrapa, T. Matsuoka, Y. Miyachi, and S. Narumiya
Facilitation of Th1-mediated immune response by prostaglandin E receptor EP1
J. Exp. Med., November 26, 2007; 204(12): 2865 - 2874.
[Abstract] [Full Text] [PDF]

Home page
 ANN INTERN MEDHome page
W. J. Pichler
Delayed Drug Hypersensitivity Reactions
Ann Intern Med, October 21, 2003; 139(8): 683 - 693.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
B. Wang, C. Feliciani, B. G. Howell, I. Freed, Q. Cai, H. Watanabe, and D. N. Sauder
Contribution of Langerhans Cell-Derived IL-18 to Contact Hypersensitivity
J. Immunol., April 1, 2002; 168(7): 3303 - 3308.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
H. Akiba, J. Kehren, M.-T. Ducluzeau, M. Krasteva, F. Horand, D. Kaiserlian, F. Kaneko, and J.-F. Nicolas
Skin Inflammation During Contact Hypersensitivity Is Mediated by Early Recruitment of CD8+ T Cytotoxic 1 Cells Inducing Keratinocyte Apoptosis
J. Immunol., March 15, 2002; 168(6): 3079 - 3087.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2001 by the Society for Leukocyte Biology.