Lymphocyte populations in atherosclerotic lesions of ApoE -/- and LDL receptor -/- mice: Decreasing density with disease progression

Simon E. Roselaar, Paul X. Kakkanathu, Alan Daugherty

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165 Scopus citations


Lymphocytes are prominent components of human atherosclerotic lesions, but their presence in murine models of disease has not been confirmed. Lymphocyte subpopulations have been identified in apoE -/- and LDL receptor -/- mice fed a cholesterol-enriched diet for up to 3 months. ApoE - /mice had higher serum cholesterol concentrations than did LDL receptor -/- mice during most of the feeding period, primarily due to large increases in VLDL concentrations. Total area of atherosclerotic lesions was greater at all times in apoE -/- than LDL receptor -/- mice (lesion area after 3 months on cholesterol-enriched diet: apoE -/-, 993±193 and LDL receptor -/-, 560±131 μm2x103, mean±SEM, n=6 in each group). Lesions in apoE -/- mice contained larger macrophage-rich necrotic cores and more calcification than did those in LDL receptor -/- mice. Immunocytochemical analyses of tissue sections of ascending aortas performed with monoclonal antibodies to T and B lymphocytes and macrophages revealed that T lymphocytes immunoreactive for Thy 1.2, CD5, CD4, and CD8 were observed in lesions from both strains, but no B lymphocytes were detected. The density of Thy 1.2+ T lymphocytes in lesions was greatest at 1 month (apoE -/-, 98±23 and LDL receptor -/-, 201±40 lymphocytes/mm2, n=6 in each group), decreasing in apoE -/- mice to 12±3 and in LDL receptor -/- mice to 51±20 lymphocytes/mm2 at 3 months. The presence of T lymphocytes in murine atherosclerotic lesions makes these animals potentially useful for studying the involvement of the immune system in atherogenesis.

Original languageEnglish
Pages (from-to)1013-1018
Number of pages6
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Issue number8
StatePublished - 1996


  • T lymphocytes
  • atherosclerosis
  • immunohistochemistry
  • murine model

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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