Thematic review series: The Immune System and Atherogenesis. The unusual suspects:an overview ofthe minor leukocyte populations in atherosclerosis

VanderLaan, Paul A.; Reardon, Catherine A.

doi:10.1194/jlr.r500003-jlr200

Cited by 94 publications

(72 citation statements)

References 128 publications

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“…Although many of the recruited cells differentiate into macrophages and lipid-laden foam cells, a portion may differentiate into cells with a dendritic cell appearance (116). Dendritic cells have been identified in atherosclerotic plaques and have been implicated in the pathogenesis of the disease (117). Results from a recent study suggested that differentiation into dendritic cells may constitute a pathway for monocyte emigration leading to lesion regression (118).…”

Section: Fate Of the Recruited Monocytesmentioning

confidence: 99%

Thematic Review Series: The Immune System and Atherogenesis. Molecular mechanisms regulating monocyte recruitment in atherosclerosis

Quehenberger

2005

Journal of Lipid Research

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Section: Fate Of the Recruited Monocytesmentioning

confidence: 99%

Thematic Review Series: The Immune System and Atherogenesis. Molecular mechanisms regulating monocyte recruitment in atherosclerosis

Quehenberger

2005

Journal of Lipid Research

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“…[5][6][7] In AAA, inflammatory cells (polymorphonuclear neutrophils, T cells, B cells, macrophages, mast cells, NK cells, etc) percolate through the luminal thrombus and all layers of the wall. 8,9 These infiltrating cells secrete various humoral inflammatory factors, including cytokines, chemokines, leukotrienes, reactive oxygen species, and immunoglobulins. The vessels of the vasa vasorum form the pathways by which inflammatory cells access the aortic intima and media.…”

mentioning

confidence: 99%

Inflammation and Cellular Immune Responses in Abdominal Aortic Aneurysms

Shimizu

Mitchell

Libby

2006

ATVB

567

478

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Abstract-Expansion and rupture of abdominal aortic aneurysms (AAA) result in high morbidity and mortality rates. Like stenotic atherosclerotic lesions, AAA accumulate inflammatory cells, but usually exhibit much more extensive medial damage. Leukocyte recruitment and expression of pro-inflammatory Th1 cytokines typically characterize early atherogenesis of any kind, and modulation of inflammatory mediators mutes atheroma formation in mice. 1 However, the mechanistic differences between stenotic and aneurysmal manifestations of atherosclerosis remain unexplained. We recently showed that aortic allografts deficient in interferon-␥ (IFN-␥) signaling developed AAA correlating with skewed Th2 cytokine environments, suggesting important regulatory roles for Th1/Th2 cytokine balance in modulating matrix remodeling and important implications for the pathophysiology of aortic aneurysm and atherosclerosis. Key Words: aortic aneurysm Ⅲ atherosclerosis Ⅲ cytokine Ⅲ pathogenesis Ⅲ T-lymphocytes Ⅲ transplantation A ortic aneurysms are permanent and localized aortic dilations defined as having diameters 1.5-times greater than normal (ie, Ͼ3 cm diameter for abdominal aortic aneurysms [AAA]). In comparison, the term aortic ectasia describes localized aortic enlargement Ͻ1.5-times normal diameter. 2 Although most aneurysms remain asymptomatic and undiagnosed, risk of rupture increases dramatically when diameters exceed 5.5 cm. Despite surgical advances, the prognosis of ruptured AAA remains poor, and the overall mortality remains high (80% to 90%). 3 Although surgical or endovascular repair constitutes the major therapeutic options for AAA Ͼ5.5 cm, such invasive procedures provide no therapeutic advantage for AAA Ͻ5.5 cm diameter.Most AAA develop below the renal arteries and end above the bifurcation of the iliac arteries; they typically exhibit a fusiform morphology, with symmetrical circumferential enlargement involving all layers of the aortic wall. Less frequently, aneurysms have a saccular form, with aneurysmal degeneration affecting only part of the aortic circumference. The AAA wall usually becomes laminated with thrombus and its intraluminal diameter often appears relatively normal by angiography. Important histological features of aneurysms include chronic adventitial and medial inflammatory cell infiltration, elastin fragmentation and degeneration, and medial attenuation. Collagen (especially types I and III) in the media and adventitia provides tensile strength to the aortic wall. Collagen synthesis increases during the early stages of aneurysm formation, suggesting a repair process. 4 However, in later stages, collagen degradation exceeds its synthesis (accompanied by excessive degradation of other extracellular matrix macromolecules, notably elastin), ultimately favoring AAA rupture. Indeed, AAA exhibit increased local production of enzymes capable of degrading collagen and elastin extracellular matrix proteins. [5][6][7] In AAA, inflammatory cells (polymorphonuclear neutrophils, T cells, B cells, macrophages, mast c...

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“…Experiments spanning the entire life until old age may help to delineate age-related mechanisms of atherogenesis. 21,22 Most studies related to adaptive immunity of atherosclerosis focused on characterization of intima lesions though adventitial inflammation may participate in arterial wall pathology 3,7,23,24 and a role of the adventitia in atherogenesis has also received attention. [25][26][27] However, little information is available on adventitia inflammation and immunity in hyperlipidemic mice as a function of age.…”

mentioning

confidence: 99%

The Lamina Adventitia Is the Major Site of Immune Cell Accumulation in Standard Chow-Fed Apolipoprotein E–Deficient Mice

Moos

John²,

Gräbner³

et al. 2005

ATVB

197

215

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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. Methods and Results-The composition of immune cells in the innominate artery and abdominal aorta was examined in young, adult, and old apolipoprotein (apo) E Ϫ/Ϫ and wild-type mice on standard mouse chow. In the innominate artery of apoE Ϫ/Ϫ 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.

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Thematic review series: The Immune System and Atherogenesis. The unusual suspects:an overview ofthe minor leukocyte populations in atherosclerosis

Cited by 94 publications

References 128 publications

Thematic Review Series: The Immune System and Atherogenesis. Molecular mechanisms regulating monocyte recruitment in atherosclerosis

Thematic Review Series: The Immune System and Atherogenesis. Molecular mechanisms regulating monocyte recruitment in atherosclerosis

Inflammation and Cellular Immune Responses in Abdominal Aortic Aneurysms

The Lamina Adventitia Is the Major Site of Immune Cell Accumulation in Standard Chow-Fed Apolipoprotein E–Deficient Mice

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