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Adventitial inflammation and its interaction with intimal atherosclerotic lesions.

Akhavanpoor M, Wangler S, Gleissner CA, Korosoglou G, Katus HA, Erbel C - Front Physiol (2014)

Bottom Line: These ATLOs possess similarities in development, structure and function to secondary lymphoid organs.A crosstalk between intimal atherosclerotic lesions and ATLOs has been suggested, and several studies could demonstrate a potential role for medial vascular smooth muscle cells in this process.Furthermore, we discuss the possible role of medial vascular smooth muscle cells and their interaction between plaque and ATLOs.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, University of Heidelberg Heidelberg, Germany ; DZHK (German Centre for Cardiovascular Research) Partner Site Heidelberg/Mannheim, Germany.

ABSTRACT
The presence of adventitial inflammation in correlation with atherosclerotic lesions has been recognized for decades. In the last years, several studies have investigated the relevance and impact of adventitial inflammation on atherogenesis. In the abdominal aorta of elderly Apoe(-/-) mice, adventitial inflammatory structures were characterized as organized ectopic lymphoid tissue, and therefore termed adventitial tertiary lymphoid organs (ATLOs). These ATLOs possess similarities in development, structure and function to secondary lymphoid organs. A crosstalk between intimal atherosclerotic lesions and ATLOs has been suggested, and several studies could demonstrate a potential role for medial vascular smooth muscle cells in this process. We here review the development, phenotypic characteristics, and function of ATLOs in atherosclerosis. Furthermore, we discuss the possible role of medial vascular smooth muscle cells and their interaction between plaque and ATLOs.

No MeSH data available.


Related in: MedlinePlus

Adventitial tertiary lymphoid organs (ATLOs) in atherosclerosis. The cellularity and structure of ATLOs in the diseased vessel wall is presented. ATLOs represent organized accumulation of different lymphoid cells, developed in response to the chronic inflammatory process of atherosclerosis. Stage III ATLOs show T and B cell areas. Germinal centers with follicular dendritic cells surrounded by centrocytes and B cells are present. Lymph vessels and high endothelial venules (HEV) facilitate the recruitment of lymphocytes from the blood into ATLOs. Similar to lymph nodes, ATLOs contain a mesenchymal network of conduits, connecting the lamina media with HEVs in T cell areas. Small molecular weight molecules (such as chemokines and cytokines) can be transported by these conduits. A cross-talk between the plaque and the ATLO via the medial VSMCs is postulated.
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Figure 1: Adventitial tertiary lymphoid organs (ATLOs) in atherosclerosis. The cellularity and structure of ATLOs in the diseased vessel wall is presented. ATLOs represent organized accumulation of different lymphoid cells, developed in response to the chronic inflammatory process of atherosclerosis. Stage III ATLOs show T and B cell areas. Germinal centers with follicular dendritic cells surrounded by centrocytes and B cells are present. Lymph vessels and high endothelial venules (HEV) facilitate the recruitment of lymphocytes from the blood into ATLOs. Similar to lymph nodes, ATLOs contain a mesenchymal network of conduits, connecting the lamina media with HEVs in T cell areas. Small molecular weight molecules (such as chemokines and cytokines) can be transported by these conduits. A cross-talk between the plaque and the ATLO via the medial VSMCs is postulated.

Mentions: TLOs are defined as an accumulation of lymphoid cells and develop in response to chronic inflammation, either due to infection or autoimmunity (Sansonno et al., 2004; Aloisi and Pujol-Borrell, 2006; Kendall et al., 2007; Carragher et al., 2008; Van De Pavert and Mebius, 2010). A more precise definition of TLOs was recently published by Neyt et al. (2012). In contrast to the chronic cellular compound, TLOs can be defined by the following criteria: TLOs (also known as ectopic lymphoid structures) represent highly organized lymphoid cell formations similar to secondary lymphoid organs like lymph nodes or the spleen. The structures of TLOs form a specific, well-organized network including fibroblast reticular cells in the T cell area that warrant optimal interactions of immune cells like antigen presentation, stimulation, and cell differentiation (Fletcher et al., 2010). Similar to lymph nodes, TLOs contain a mesenchymal network promoting lymphocyte homing. Lymph vessels and high endothelial venules (HEV; PNA+ or MECA79+), specialized for the recruitment of lymphocytes from blood, facilitate lymphocyte migration and are located in the T cell area. Furthermore, structured B cell compartments containing germinal centers and activation-induced cytidinedeaminase (Geurtsvankessel et al., 2009; Perros et al., 2012) as well as T cell sections co-localized with antigen-presenting cells, including follicular dendritic cells, can be found (Fletcher et al., 2010). Figure 1 demonstrates a simplified illustration of the structure of TLOs in the adventitia in correlation to atherosclerotic lesions.


Adventitial inflammation and its interaction with intimal atherosclerotic lesions.

Akhavanpoor M, Wangler S, Gleissner CA, Korosoglou G, Katus HA, Erbel C - Front Physiol (2014)

Adventitial tertiary lymphoid organs (ATLOs) in atherosclerosis. The cellularity and structure of ATLOs in the diseased vessel wall is presented. ATLOs represent organized accumulation of different lymphoid cells, developed in response to the chronic inflammatory process of atherosclerosis. Stage III ATLOs show T and B cell areas. Germinal centers with follicular dendritic cells surrounded by centrocytes and B cells are present. Lymph vessels and high endothelial venules (HEV) facilitate the recruitment of lymphocytes from the blood into ATLOs. Similar to lymph nodes, ATLOs contain a mesenchymal network of conduits, connecting the lamina media with HEVs in T cell areas. Small molecular weight molecules (such as chemokines and cytokines) can be transported by these conduits. A cross-talk between the plaque and the ATLO via the medial VSMCs is postulated.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4126462&req=5

Figure 1: Adventitial tertiary lymphoid organs (ATLOs) in atherosclerosis. The cellularity and structure of ATLOs in the diseased vessel wall is presented. ATLOs represent organized accumulation of different lymphoid cells, developed in response to the chronic inflammatory process of atherosclerosis. Stage III ATLOs show T and B cell areas. Germinal centers with follicular dendritic cells surrounded by centrocytes and B cells are present. Lymph vessels and high endothelial venules (HEV) facilitate the recruitment of lymphocytes from the blood into ATLOs. Similar to lymph nodes, ATLOs contain a mesenchymal network of conduits, connecting the lamina media with HEVs in T cell areas. Small molecular weight molecules (such as chemokines and cytokines) can be transported by these conduits. A cross-talk between the plaque and the ATLO via the medial VSMCs is postulated.
Mentions: TLOs are defined as an accumulation of lymphoid cells and develop in response to chronic inflammation, either due to infection or autoimmunity (Sansonno et al., 2004; Aloisi and Pujol-Borrell, 2006; Kendall et al., 2007; Carragher et al., 2008; Van De Pavert and Mebius, 2010). A more precise definition of TLOs was recently published by Neyt et al. (2012). In contrast to the chronic cellular compound, TLOs can be defined by the following criteria: TLOs (also known as ectopic lymphoid structures) represent highly organized lymphoid cell formations similar to secondary lymphoid organs like lymph nodes or the spleen. The structures of TLOs form a specific, well-organized network including fibroblast reticular cells in the T cell area that warrant optimal interactions of immune cells like antigen presentation, stimulation, and cell differentiation (Fletcher et al., 2010). Similar to lymph nodes, TLOs contain a mesenchymal network promoting lymphocyte homing. Lymph vessels and high endothelial venules (HEV; PNA+ or MECA79+), specialized for the recruitment of lymphocytes from blood, facilitate lymphocyte migration and are located in the T cell area. Furthermore, structured B cell compartments containing germinal centers and activation-induced cytidinedeaminase (Geurtsvankessel et al., 2009; Perros et al., 2012) as well as T cell sections co-localized with antigen-presenting cells, including follicular dendritic cells, can be found (Fletcher et al., 2010). Figure 1 demonstrates a simplified illustration of the structure of TLOs in the adventitia in correlation to atherosclerotic lesions.

Bottom Line: These ATLOs possess similarities in development, structure and function to secondary lymphoid organs.A crosstalk between intimal atherosclerotic lesions and ATLOs has been suggested, and several studies could demonstrate a potential role for medial vascular smooth muscle cells in this process.Furthermore, we discuss the possible role of medial vascular smooth muscle cells and their interaction between plaque and ATLOs.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, University of Heidelberg Heidelberg, Germany ; DZHK (German Centre for Cardiovascular Research) Partner Site Heidelberg/Mannheim, Germany.

ABSTRACT
The presence of adventitial inflammation in correlation with atherosclerotic lesions has been recognized for decades. In the last years, several studies have investigated the relevance and impact of adventitial inflammation on atherogenesis. In the abdominal aorta of elderly Apoe(-/-) mice, adventitial inflammatory structures were characterized as organized ectopic lymphoid tissue, and therefore termed adventitial tertiary lymphoid organs (ATLOs). These ATLOs possess similarities in development, structure and function to secondary lymphoid organs. A crosstalk between intimal atherosclerotic lesions and ATLOs has been suggested, and several studies could demonstrate a potential role for medial vascular smooth muscle cells in this process. We here review the development, phenotypic characteristics, and function of ATLOs in atherosclerosis. Furthermore, we discuss the possible role of medial vascular smooth muscle cells and their interaction between plaque and ATLOs.

No MeSH data available.


Related in: MedlinePlus