Objective: Atherosclerotic lesions are characterized by an immune mediated
chronic inflammation. Seroepidemiological studies support a relationship be
tween atherosclerotic disease and infection with C. pneumoniae; an associat
ion further endorsed by immunocytochemical and DNA directed studies. Howeve
r, the question arises whether C. pneumoniae acts as a causal antigen, or i
s merely a bystander. For this reason we have analyzed the T lymphocyte pop
ulation of carotid atherosclerotic plaques of symptomatic patients for thei
r response against C. pneumoniae. Methods: T cell lines were generated from
carotid endarterectomy tissues obtained from eight patients with symptomat
ic disease. The response of these T cell lines against C. pneumoniae elemen
tary bodies was analyzed by H-3-thymidine incorporation. T cell clones were
generated by limiting dilution from the cell lines of three patients and t
ested for antigen specificity in the same manner. Furthermore, cytokine pro
files (Thl/Th0/Th2) were established by measuring the production of IFN-gam
ma and IL-4. Results: Of the eight T-cell lines five responded to C, pneumo
niae. Eighteen of 69 CD4-positive clones, generated from three patients wit
h a positive T cell Lines response, responded to C. pneumoniae also. The ma
jority (17/18, 96%) of these clones showed a Th1 cytokine profile. Conclusi
on: These results show that in a subpopulation of symptomatic patients C. p
neumoniae can activate T cells within atherosclerotic plaques suggesting th
at a C. pneumoniae enhanced proinflammatory Th1 response contributes to pla
que destabilization in these patients. (C) 2000 Elsevier Science B.V. All r
ights reserved.