The JI
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
Right arrow Citation Map
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Han, X.
Right arrow Articles by Yang, X.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Han, X.
Right arrow Articles by Yang, X.
The Journal of Immunology, 2006, 176: 5232-5239.
Copyright © 2006 by The American Association of Immunologists

Chlamydia Infection Induces ICOS Ligand-Expressing and IL-10-Producing Dendritic Cells That Can Inhibit Airway Inflammation and Mucus Overproduction Elicited by Allergen Challenge in BALB/c Mice1

Xiaobing Han, Shuhe Wang, Yijun Fan, Jie Yang, Lei Jiao, Hongyu Qiu and Xi Yang1,2

Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

Our previous study has shown that the adoptive transfer of dendritic cells (DCs) freshly isolated from Chlamydia-infected mice (iIDCs), unlike those from control naive mice (iNDCs), can inhibit systemic and cutaneous eosinophilia induced by OVA exposure. In the present study, we examined the mechanism by which iIDC inhibits allergen-specific Th2 cell differentiation in vitro and in vivo. The study revealed that iIDCs exhibited higher surface expression of CD8{alpha} and the ICOS ligand (ICOS-L), as well as higher IL-10 and IL-12 production than iNDCs. In vitro DC:CD4+ T cell coculture experiments showed that iIDCs could inhibit allergen-specific Th2 cell differentiation and that the inhibitory effect could be abolished by the blockage of IL-10 or IL-12 activity. More interestingly, the coblockade of IL-10 and the ICOS-L showed synergistic effect in enhancing allergen-driven Th2 cytokine production. Furthermore, adoptive transfer of iIDCs, but not iNDCs, to OVA sensitized mice significantly inhibited airway eosinophilia and mucus overproduction following intranasal challenge with OVA. Overall, the data demonstrate a critical role played by ICOS-L-expressing and IL-10-producing DCs from Chlamydia-infected mice in the infection-mediated inhibition of allergic responses.




This article has been cited by other articles:


Home page
 J. Immunol.Home page
K. N. Couper, D. G. Blount, and E. M. Riley
IL-10: The Master Regulator of Immunity to Infection
J. Immunol., May 1, 2008; 180(9): 5771 - 5777.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
X. Han, Y. Fan, S. Wang, L. Jiao, H. Qiu, and X. Yang
NK Cells Contribute to Intracellular Bacterial Infection-Mediated Inhibition of Allergic Responses
J. Immunol., April 1, 2008; 180(7): 4621 - 4628.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
E. Marks, M. Verolin, A. Stensson, and N. Lycke
Differential CD28 and Inducible Costimulatory Molecule Signaling Requirements for Protective CD4+ T-Cell-Mediated Immunity against Genital Tract Chlamydia trachomatis Infection
Infect. Immun., September 1, 2007; 75(9): 4638 - 4647.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2006 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2006 by The American Association of Immunologists, Inc. All rights reserved.