title: The lamina adventitia is the major site of immune cell accumulation in standard chow-fed apolipoprotein E-deficient mice.
abstract: OBJECTIVE
  Cells of adaptive immunity have been implicated in atherogenesis. Though substantial information is available on immune cells in atherosclerotic lesions of the lamina intima, cells in the lamina adventitia have received less attention.
  
  
  RESULTS
  The composition of immune cells in the innominate artery and abdominal aorta was examined in young, adult, and old apolipoprotein (apo) E(-/-) and wild-type mice on standard mouse chow. In the innominate artery of apoE(-/-) mice, adventitial T cells increased at 32, 52, and 78 weeks exceeding those of the intima by 6-, 24-, and 85-fold. Single T cells dominated in young mice, later T/B cell clusters emerged, and lymphoid-like structures reminiscent of inflammatory follicles formed preferentially in the abdominal aorta of old mice. Follicles contained organized sets of immune response-regulating cells: Interdigitating dendritic cells, T cell effectors, proliferating B cells, and plasma cells. Adventitial T cell inflammation was associated with a marked increase in transcripts of the chemokine MIP-1alpha in the aorta but not in spleen or liver.
  
  
  CONCLUSIONS
  Adventitial lymphocyte infiltration and formation of inflammatory follicle-like structures in the abdominal aorta of old apoE(-/-) mice point to the adventitia as a site of local adaptive immune reactions during atherogenesis in hyperlipidemic mice.
authors.affiliation: The Institute for Vascular Medicine, Friedrich Schiller University of Jena, Germany.
authors.forename: Michael P W
authors.initials: MP
authors.lastname: Moos
authors.forename: Nicole
authors.initials: N
authors.lastname: John
authors.forename: Rolf
authors.initials: R
authors.lastname: Gräbner
authors.forename: Silke
authors.initials: S
authors.lastname: Nossmann
authors.forename: Bernd
authors.initials: B
authors.lastname: Günther
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Vollandt
authors.forename: Colin D
authors.initials: CD
authors.lastname: Funk
authors.forename: Brigitte
authors.initials: B
authors.lastname: Kaiser
authors.forename: Andreas J R
authors.initials: AJ
authors.lastname: Habenicht
mesh_terms: D000367:Age Factors; D000821:Animal Feed; D000818:Animals; D001011:Aorta / Q000166:cytology / Q000276:immunology*; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics*; D050197:Atherosclerosis / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D001402:B-Lymphocytes / Q000276:immunology; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D003238:Connective Tissue / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D015870:Gene Expression / Q000276:immunology; D006949:Hyperlipidemias / Q000235:genetics / Q000276:immunology / Q000473:pathology; D008214:Lymphocytes / Q000276:immunology*; D008221:Lymphoid Tissue / Q000276:immunology / Q000473:pathology; D019402:Macrophage Inflammatory Proteins / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D010950:Plasma Cells / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D014657:Vasculitis / Q000235:genetics / Q000276:immunology* / Q000473:pathology
chemical_list: D001057:Apolipoproteins E; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D019402:Macrophage Inflammatory Proteins