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Deletion of apolipoprotein E gene substantially alters immune function in the mouse
Author(s) -
Moghadasian Mohammed H.,
HayGlass Kent,
Nashed Baher
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a148-b
Subject(s) - ovalbumin , immune system , apolipoprotein b , knockout mouse , apolipoprotein e , downregulation and upregulation , animal model , immunology , function (biology) , biology , endocrinology , gene , medicine , disease , microbiology and biotechnology , cholesterol , genetics
Objective The objective of this study was to investigate the role of apolipoprotein E in regulating immune function in the mouse. Material and Methods Male apolipoprotein E‐knockout (apo E‐KO, n= 7) mice and their wild type counterparts (C57BL, n= 9 ) were used. The animals were immunized with ovalbumin 5 days before sacrifice. The spleenocytes from both groups of mice were cultured and stimulated by ovalbumin (1000 μg/ml), and several pro‐ and anit‐inflammatory markers were measured. Results Our data are summarized in the following Table: Conclusions Our data suggest that apo E modifies immune system. Our present data plus previous findings of in vivo upregulation of IL‐12 production endorse that impaired immune function in apo E‐KO mice may be one of the major contributing factors for accelerated atherogenesis in this animal model.