| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Departments of
*
Immunology,
Respiratory Medicine, and
Atopy (Allergy) Research Center, Juntendo University School of Medicine, Tokyo, Japan; and
Core Research for Evolutional Science and Technology, Japan Science and Technology Cooperation, Tokyo, Japan
Lung fibrosis is an important pulmonary disease with a high mortality rate, but its pathophysiological mechanism has not been fully clarified. Various types of cells have been implicated in the development of lung fibrosis, including T cells. However, the contribution of functional molecules expressed on T cells to the development of lung fibrosis remains largely unknown. In this study, we determined whether costimulation via CD28 on T cells was crucial for the development of lung fibrosis by intratracheally administering bleomycin into CD28-deficient mice. Compared with wild-type mice, the CD28-deficient mice showed markedly impaired lung fibrosis after injection with low doses of bleomycin, as judged by histological changes and hydroxyproline content in the lungs. In addition, bleomycin-induced T cell infiltration into the airways and production of several cytokines and chemokines including IL-5 were also impaired in the CD28-deficient mice. Furthermore, adoptive transfer of CD28-positive T cells from wild-type mice recovered the impaired bleomycin-induced lung fibrosis in CD28-deficient mice. These findings suggest that the CD28-mediated T cell costimulation plays a critical role in the development of lung fibrosis, possibly by regulating the production of cytokines and chemokines in the lung. Thus, manipulation of the CD28-mediated costimulation could be a potential therapeutic strategy for the prevention of lung fibrosis.
This article has been cited by other articles:
|
|
 |
|
  T. Okazaki, A. Ni, P. Baluk, O. A. Ayeni, J. Kearley, A. J. Coyle, A. Humbles, and D. M. McDonald Capillary Defects and Exaggerated Inflammatory Response in the Airways of EphA2-Deficient Mice Am. J. Pathol., June 1, 2009; 174(6): 2388 - 2399. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. G. Luzina, N. W. Todd, A. T. Iacono, and S. P. Atamas Roles of T lymphocytes in pulmonary fibrosis J. Leukoc. Biol., February 1, 2008; 83(2): 237 - 244. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Pochetuhen, I. G. Luzina, V. Lockatell, J. Choi, N. W. Todd, and S. P. Atamas Complex Regulation of Pulmonary Inflammation and Fibrosis by CCL18 Am. J. Pathol., August 1, 2007; 171(2): 428 - 437. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. H. Kim, H. Y. Kim, S. Kim, J.-H. Chung, W. S. Park, and D. H. Chung Natural Killer T (NKT) Cells Attenuate Bleomycin-Induced Pulmonary Fibrosis by Producing Interferon-{gamma} Am. J. Pathol., November 1, 2005; 167(5): 1231 - 1241. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Singbartl, S. G.{b.}e Bockhorn, A. Zarbock, M. Schmolke, and H. Van Aken T Cells Modulate Neutrophil-Dependent Acute Renal Failure during Endotoxemia: Critical Role for CD28 J. Am. Soc. Nephrol., March 1, 2005; 16(3): 720 - 728. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Sato, M. Fujimoto, M. Hasegawa, K. Komura, K. Yanaba, I. Hayakawa, T. Matsushita, and K. Takehara Serum soluble CTLA-4 levels are increased in diffuse cutaneous systemic sclerosis Rheumatology, October 1, 2004; 43(10): 1261 - 1266. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Stambe, R. C. Atkins, G. H. Tesch, T. Masaki, G. F. Schreiner, and D. J. Nikolic-Paterson The Role of p38{alpha} Mitogen-Activated Protein Kinase Activation in Renal Fibrosis J. Am. Soc. Nephrol., February 1, 2004; 15(2): 370 - 379. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
