© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Unstable atherosclerotic plaques contain T-cells that respond to Chlamydia pneumoniae
aDepartment of Cardiovascular Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
bResearch Laboratory for Infectious Diseases, National Institute for Public Health and Environment, Bilthoven, The Netherlands
* Corresponding author. Tel.: +31-20-566-5646; fax: +31-20-691-4738 m.i.schenker{at}amc.uva.nl
Objective: Atherosclerotic lesions are characterized by an immune mediated chronic inflammation. Seroepidemiological studies support a relationship between atherosclerotic disease and infection with C. pneumoniae; an association further endorsed by immunocytochemical and DNA directed studies. However, the question arises whether C. pneumoniae acts as a causal antigen, or is merely a bystander. For this reason we have analyzed the T lymphocyte population of carotid atherosclerotic plaques of symptomatic patients for their response against C. pneumoniae. Methods: T cell lines were generated from carotid endarterectomy tissues obtained from eight patients with symptomatic disease. The response of these T cell lines against C. pneumoniae elementary bodies was analyzed by 3H-thymidine incorporation. T cell clones were generated by limiting dilution from the cell lines of three patients and tested for antigen specificity in the same manner. Furthermore, cytokine profiles (Th1/Th0/Th2) were established by measuring the production of IFN-
and IL-4. Results: Of the eight T-cell lines five responded to C. pneumoniae. Eighteen of 69 CD4-positive clones, generated from three patients with a positive T cell lines response, responded to C. pneumoniae also. The majority (17/18, 96%) of these clones showed a Th1 cytokine profile. Conclusion: These results show that in a subpopulation of symptomatic patients C. pneumoniae can activate T cells within atherosclerotic plaques suggesting that a C. pneumoniae enhanced proinflammatory Th1 response contributes to plaque destabilization in these patients.
KEYWORDS Atherosclerosis; Infection/inflammation; Immunology
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  S. Schulte, G. K. Sukhova, and P. Libby Genetically Programmed Biases in Th1 and Th2 Immune Responses Modulate Atherogenesis Am. J. Pathol., June 1, 2008; 172(6): 1500 - 1508. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Loppnow, K. Werdan, and M. Buerke Invited review: Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms Innate Immunity, April 1, 2008; 14(2): 63 - 87. [Abstract] [PDF]
|
|
|
|
 |
|
 S.-J. Jiang, C.-C. Kuo, M. W. Berry, A. W. Lee, and L. A. Campbell Identification and Characterization of Chlamydia pneumoniae-Specific Proteins That Activate Tumor Necrosis Factor Alpha Production in RAW 264.7 Murine Macrophages Infect. Immun., April 1, 2008; 76(4): 1558 - 1564. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. C van der Wal Chlamydia pneumoniae inside the atherosclerotic plaque--does it affect plaque inflammation and plaque progression? Cardiovasc Res, November 1, 2002; 56(2): 178 - 180. [Full Text] [PDF]
|
|