Korean J Intern Med.
2000 Jul;15(2):117-121.
Prevalence of foam cells and helper-T cells in atherosclerotic plaques of Korean patients with carotid atheroma
- Affiliations
-
- 1Center for Clinical Research, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea.
- 2Department of Diagnostic Pathology,, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong, Kangnam-ku, Seoul 135-710 Korea.
- 3Division of Vascular Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong, Kangnam-ku, Seoul 135-710 Korea.
- 4Cardiology Division, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong, Kangnam-ku, Seoul 135-710 Korea.
Abstract
- BACKGROUND
Inflammation and activation of immune cells have important roles in
the pathogenesis of atherosclerosis. We analyzed the involvement of various
immune cells in the pathogenesis of atherosclerosis. METHODS: We investigated
the presence of foam cells, lymphocytes and killer cells in 11 atherosclerotic
plaque specimens removed from Korean patients who underwent carotid
endoarterectomy. Atherosclerotic plaques were analyzed by immunohistochemistry
using monoclonal antibody specific to foam cells (anti-CD68), pan-T cells
(anti-CD3), helper-T cells (anti-CD4), cytotoxic T cells (anti-CD8), granular
component of killer cells (anti-TIA-1) and pan-B cells (anti-CD20). RESULTS:
Analysis revealed a general infiltration of immune cells not only in
atherosclerotic plaques but also in the vascular wall adjacent to the plaque.
Heavy infiltration of CD68 macrophage was observed in all cases. In addition,
significant infiltration of CD3 T-lymphocytes was observed in all cases, while
CD20 B-cells were observed in only a few cases. Majority of the CD3 cells was
found to be CD4 helper-T cells. CD8 cytotoxic T cells and TIA-1 cells were
less prominent. CONCLUSION: Analysis of the human atherosclerotic plaques
suggested that helper-T cells and foam cells had a major role in the plaque
development.