| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* Department of Cellular and Molecular Immunology and
Department of Hematology and Oncology, Mie University Graduate School of Medicine, Tsu, Japan;
Department of Anatomy and Developmental Neurobiology, Institute of Health Science, University of Tokushima Graduate School, Tokushima, Japan;
Central Laboratory, Effector Cell Institute, Inc., Tokyo, Japan;
¶ Department of Cancer Vaccine and
|| Department of Hepatobiliary Pancreatic Surgery, Mie University Graduate School of Medicine, Tsu, Japan; and
# Department of Microbiology, Kinki University School of Medicine, Osakasayama, Japan
Although CD4+CD25+ regulatory T (Treg) cells are known to suppress Th1 cell-mediated immune responses, their effect on Th2-type immune responses remains unclear. In this study we examined the role of Treg cells in Th2-type airway inflammation in mice. Depletion and reconstitution experiments demonstrated that the Treg cells of naive mice effectively suppressed the initiation and development of Th2-driven airway inflammation. Despite effective suppression of Th2-type airway inflammation in naive mice, adoptively transferred, allergen-specific Treg cells were unable to suppress airway inflammation in allergen-presensitized mice. Preactivated allergen-specific Treg cells, however, could suppress airway inflammation even in allergen-presensitized mice by accumulating in the lung, where they reduced the accumulation and proliferation of Th2 cells. Upon activation, allergen-specific Treg cells up-regulated CCR4, exhibited enhanced chemotactic responses to CCR4 ligands, and suppressed the proliferation of and cytokine production by polarized Th2 cells. Collectively, these results demonstrated that Treg cells are capable of suppressing Th2-driven airway inflammation even in allergen-presensitized mice in a manner dependent on their efficient migration into the inflammatory site and their regulation of Th2 cell activation and proliferation.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by grants from the Ministry of Education, Culture, Sports, Science, and Technology of Japan and the Japan Chemical Industry Association (to T.K.).
2 Address correspondence and reprint requests to Dr. Takuma Kato, Department of Cellular and Molecular Immunology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie, 514-8507, Japan. E-mail address: katotaku{at}doc.medic.mie-u.ac.jp
3 Abbreviations used in this paper: AHR, airway hyperresponsiveness; BALF, bronchoalveolar lavage fluid; BLN, bronchial lymph node; GITR, glucocorticoid-induced TNFR-related protein; i.n., intranasal(ly); PD-L1, programmed death ligand 1; TARC, thymus- and activation-regulated cytokine; Treg, regulatory T.
4 The online version of this article contains supplemental material.
This article has been cited by other articles:
|
|
 |
|
  P. B. Olkhanud, D. Baatar, M. Bodogai, F. Hakim, R. Gress, R. L. Anderson, J. Deng, M. Xu, S. Briest, and A. Biragyn Breast Cancer Lung Metastasis Requires Expression of Chemokine Receptor CCR4 and Regulatory T Cells Cancer Res., July 15, 2009; 69(14): 5996 - 6004. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
