Immunohistochemical and ultrastructural demonstration of the lymphocyte-macrophage interaction in human aortic intima
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Published on: July 1, 2011
T Shimokama1, S Haraoka, T Watanabe
1Department of Pathology, Saga Medical School, Japan.
Insights
Human arterial intima shows macrophages and T-lymphocytes interacting, even in normal areas. These cell-mediated interactions, particularly between macrophages and suppressor/cytotoxic T-lymphocytes, suggest a role in atherosclerosis pathogenesis.
Area of Science:
- Immunohistology
- Electron Microscopy
- Cellular Biology
Background:
- Atherosclerosis involves complex cellular interactions within the arterial intima.
- Understanding these interactions is crucial for elucidating disease pathogenesis.
Purpose of the Study:
- To investigate direct cellular interactions within human arterial intima.
- To examine the coexistence of macrophages and lymphocytes in normal and atherosclerotic lesions.
Main Methods:
- Immunohistologic analysis of human arterial intima.
- Electron microscopic examination of cell ultrastructure and interactions.
- Characterization of T-cell subsets (OKT4+, OKT8+) and macrophage markers (OKM1+, LeuM3+).
Main Results:
- Macrophages (OKM1+, LeuM3+) and T-lymphocytes (OKT3+) were found to intimately coexist in fatty streaks and atheromatous plaques.
- This colocalization was also observed in some grossly normal intima areas.
- Electron microscopy revealed direct apposition and rosette-like formations between macrophages and T-lymphocytes, including within lymphocytes and macrophages themselves.
- Suppressor/cytotoxic T-lymphocytes (OKT8+) outnumbered helper/inducer T-lymphocytes (OKT4+).
Conclusions:
- Direct cell-mediated interactions between macrophages and T-lymphocytes occur in human arterial intima.
- These interactions, including satellitosis-like formations, are present in both normal and atherosclerotic tissues.
- In situ cell-mediated hypersensitivity is implicated as a significant factor in human atherosclerosis pathogenesis.
Abstract:
Using immunohistologic methods coupled with electron microscopic analysis, human arterial intima such as normal areas on gross inspection, fatty streaks, and fibrous or atheromatous plaques was examined. Special emphasis was put on the possible direct interactions between the infiltrated cells of the aortic intima. In the lesions of fatty streaks and atheromatous plaques including the fibrous cap and the shoulder region, OKM1+ LeuM3+ macrophages as well as macrophage foam cells intimately coexisted with OKT3+ lymphocytes. It was worthy of note that such colocalization of macrophages and T-lymphocytes was detectable in some areas of grossly normal intima. In terms of T-cell subsets, suppressor/cytotoxic T-lymphocytes (OKT8+) outnumbered helper/inducer T-lymphocytes (OKT4+). Electron microscopic observations demonstrated the ultrastructural aspect of macrophage-T-lymphocyte interactions. The most striking finding was direct apposition of the lymphocytes to macrophages or macrophage foam cells, often forming rossette-like organizations closely resembling satellitosis. The direct cellular contact was noted not only between lymphocytes and macrophages but also among lymphocytes or macrophages themselves. These observations suggest that a specific in situ cell-mediated hypersensitivity plays an important role in the pathogenesis of human atherosclerosis.
