title: Unstable atherosclerotic plaques contain T-cells that respond to Chlamydia pneumoniae.
abstract: 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-gamma 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cardiovascular Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: O J
authors.initials: OJ
authors.lastname: de Boer
authors.forename: A C
authors.initials: AC
authors.lastname: van der Wal
authors.forename: M A
authors.initials: MA
authors.lastname: Houtkamp
authors.forename: J M
authors.initials: JM
authors.lastname: Ossewaarde
authors.forename: P
authors.initials: P
authors.lastname: Teeling
authors.forename: A E
authors.initials: AE
authors.lastname: Becker
mesh_terms: D000368:Aged; D000907:Antibodies, Bacterial / Q000276:immunology; D000918:Antibody Specificity; D000942:Antigens, Bacterial / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002340:Carotid Artery Diseases / Q000276:immunology*; D023521:Chlamydophila Infections / Q000276:immunology*; D016993:Chlamydophila pneumoniae / Q000276:immunology*; D002999:Clone Cells; D016207:Cytokines / Q000276:immunology; D006801:Humans; D007150:Immunohistochemistry; D008213:Lymphocyte Activation; D008264:Macrophages / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D016207:Cytokines