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From INSERM U589,* IFR31, Institut L. Bugnard, Toulouse, France; INSERM U545 Institut Pasteur,
Lille, France; and the Center for Molecular Medicine and Department of Medicine,
Karolinska Institute, Stockholm, Sweden
Estradiol prevents fatty streak formation in chow-fed atherosclerosis-prone apolipoprotein E (ApoE)-deficient mice. We previously reported that fatty streak development of immunodeficient ApoE//recombination activating gene 2 (RAG-2/) double-deficient mice was insensitive to estradiol. In the present work, we demonstrate that the reconstitution of ApoE//RAG-2/ with bone marrow from immunocompetent ApoE//RAG-2+/+ mice restores the protective effect of estradiol on fatty streak constitution. We extended this demonstration to the model of low-density lipoprotein receptor-deficient mice, establishing the obligatory role of mature lymphocytes in this process. We then investigated whether the protective effect of estradiol was mediated by a specific lymphocyte subpopulation by studying the hormonal effect on fatty streak constitution in recently developed models of ApoE/ mice deficient in selective T-lymphocyte subsets (either TCR
ß+, CD4+, CD8+, or TCR
+ lymphocytes) or B lymphocytes. In all these specifically immunodeficient mice, estradiol administration to ovariectomized mice conferred protection as in immunocompetent ApoE/ mice, clearly demonstrating that no single lymphocyte subpopulation was specifically required for this effect. These results point to additional lymphocyte-dependent mechanisms such as modulating the interactions among lymphocytes and between lymphocytes and endothelial and/or antigen-presenting cells.
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