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(American Journal of Pathology. 2005;167:267-274.)
© 2005 American Society for Investigative Pathology

The Atheroprotective Effect of 17ß-Estradiol Depends on Complex Interactions in Adaptive Immunity

Rima Elhage*, Pierre Gourdy*, Jacek Jawien{dagger}, Laurent Brouchet*, Caroine Castano*, Catherine Fievet{ddagger}, Göran K. Hansson{dagger}, Jean-François Arnal* and Francis Bayard*

From INSERM U589,* IFR31, Institut L. Bugnard, Toulouse, France; INSERM U545 Institut Pasteur,{ddagger} Lille, France; and the Center for Molecular Medicine and Department of Medicine,{dagger} 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{alpha}ß+, CD4+, CD8+, or TCR{gamma}{delta}+ 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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