T cells in Cardiac Allograft Vasculopathy Are Skewed to Memory Th-1 Cells in the Presence of a Distinct Th-2 Population

Hagemeijer, M.C.; Oosterhout, Matthijs F.M. van; Wichen, D.F. van; Kuik, J. van; Koning, E. Siera-de; Meyling, F. H. J. Gmelig; Schipper, Marguérite E.I.; Jonge, Nicolaas de; Weger, Roel A. de

doi:10.1111/j.1600-6143.2008.02198.x

Cited by 23 publications

(25 citation statements)

References 43 publications

(59 reference statements)

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“…This study also showed a significant population of CD4+ T-cells expressing CCR3 and CCR8 (Th2 phenotype). The presence of this population in human TV may explain the proliferative response/matrix deposition/remodeling, which are also characteristic features of TV 12.…”

Section: Chemokine-cc Chemokine Receptormentioning

confidence: 97%

“…Additionally, the current immunosuppressive therapies are quite effective against acute rejection, but have failed to significantly alter the incidence and/or course of TV. There is also experimental and clinical evidence that the chemotactic mediators of mononuclear cell recruitment in acute rejection may be different from those in TV 5, 11, 12.…”

Section: Introductionmentioning

confidence: 99%

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Chemokines and Transplant Vasculopathy

Belperio

Ardehali

2008

Circulation Research

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Transplant vasculopathy (TV) remains the leading cause of late death among heart transplant recipients. TV is characterized by progressive neointimal proliferation, leading to ischemic failure of the allograft. Multiple experimental and clinical studies have shown that injury to the graft at various stages of transplantation can be a risk factor for development of TV. The hallmark of cardiac allograft injury is the infiltration of leukocytes. Recruitment of leukocytes requires intercellular communication between infiltrating cells, endothelium, parenchymal cells, and components of extra-cellular matrix. These events are mediated via the generation of adhesion molecules, cytokines, and chemokines. The chemokines, by virtue of their specific cell receptor expression, can selectively mediate the local recruitment/activation of distinct leukocytes/cells, allowing for migration across the endothelium and beyond the vascular compartment. This report will provide a comprehensive review of the chemokines that participate in the development of TV.

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Section: Chemokine-cc Chemokine Receptormentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Chemokines and Transplant Vasculopathy

Belperio

Ardehali

2008

Circulation Research

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“…Cardiac allograft vasculopathy (CAV), a typical feature of chronic rejection, involves diffuse narrowing and occlusion of graft vessels. Several investigations have demonstrated that chronic rejection is associated with up-regulation of proinflammatory cytokines such as IL-17A and interferongamma (IFN-g) in allograft (3,4). In a model of CAV, graft recipients lacking the Th1 transcription factor T-bet have exacerbated vasculopathy associated with enhanced IL-17-producing CD4 þ cells infiltration (3).…”

Section: Introductionmentioning

confidence: 99%

HMGB1 Is Involved in Chronic Rejection of Cardiac Allograft via Promoting Inflammatory-Like mDCs

Zou

Yang

Gao

et al. 2014

American Journal of Transplantation

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“…In human coronary arteries, 5-to 10-fold fewer leukocytes are detected in the media than in the intima or adventitia of specimens with transplant vasculopathy, and no lymphocyte markers are detected in the media of control specimens. 92,93 The sparse medial infiltrates in arteriosclerotic arteries are generally associated with a preservation of VSMCs in that compartment, despite evidence of cellular injury elsewhere in the vessel wall. It is therefore not unexpected that VSMCs may remain functional even in the presence of endothelial dysfunction.…”

Section: Operational and Failed Medial Immunoprivilege In Arterial DImentioning

confidence: 99%

Inflammatory and Immune Responses in the Arterial Media

Tellides

Pober

2015

Circulation Research

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Inflammatory arterial diseases differentially affect the compartments of the vessel wall. The intima and adventitia are commonly involved by the disease process, with luminal and microvascular endothelial cells playing a critical role in the recruitment and activation of leukocytes. In contrast, the avascular media is often spared by immune-mediated disorders. Surprisingly, vascular smooth muscle cells (VSMCs), the predominant and often exclusive cell type of the media, are capable of robust proinflammatory responses to diverse stressors. The multiple cytokines and chemokines produced within the media can profoundly affect macrophage and T cell function, thus amplifying and shaping innate and adaptive immune responses. On the other hand, VSMCs and the extracellular matrix that they produce also display significant anti-inflammatory properties. The balance between the pro- and anti-inflammatory effects of VSMCs and their extracellular matrix versus the strength of the inciting immunologic events determines the pattern of medial pathology. Limitations on the extent of medial infiltration and injury, defined as medial immunoprivilege, are typically seen in arteriosclerotic diseases, such as atherosclerosis and transplant vasculopathy. Conversely, breakdown of medial immunoprivilege that manifests as more intense leukocytic infiltrates, loss of VSMCs, and destruction of the extracellular matrix architecture is a general feature of certain aneurysmal diseases and vasculitides. In this review, we consider the inflammatory and immune functions of VSMCs and how they may lead to medial immunoprivilege or medial inflammation in arterial diseases.

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T cells in Cardiac Allograft Vasculopathy Are Skewed to Memory Th-1 Cells in the Presence of a Distinct Th-2 Population

Abstract: Cardiac allograft vasculopathy (CAV) in heart trans

Cited by 23 publications

References 43 publications

Chemokines and Transplant Vasculopathy

Chemokines and Transplant Vasculopathy

HMGB1 Is Involved in Chronic Rejection of Cardiac Allograft via Promoting Inflammatory-Like mDCs

Inflammatory and Immune Responses in the Arterial Media

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