Evidence indicates that erythrocytes can represent a potent atherogenic stimulus. In physiological conditions they display an immunomodulatory activity by promoting T cell survival [1] and controlling slan dendritic cell (DC) maturation [2]. To sum up we state that erythrocytes from patients with carotid atherosclerosis fail to control DC maturation. Changes in their integrity and functions, probably due to erythrocyte exposure to high oxidative stress generated by atherosclerotic risk factors such as diabetes, smoking, hypercholesterolemia, may cause the impairment of erythrocyte immunomodulatory activity, thus contributing to atherosclerotic plaque progression and destabilization. We suggest that the altered expression of CD47 at erythrocyte surface, or its loss due to vesiculation, could represent the main mechanism determining the functional impairment of patient erythrocytes in their cross-talk with DCs
Erythrocytes from patients with carotid atherosclerosis fail to control dendritic cell maturation / Profumo, E.; Buttari, B.; Genuini, I.; Salvati, Bruno; Capoano, Raffaele; Straface, E.; Malorni, V.; Cuccu, B.; Gambardella, L; Riganò, R.. - In: INTERNATIONAL JOURNAL OF CARDIOLOGY. - ISSN 0167-5273. - STAMPA. - 2:Ms. Ref. No.: IJC-D-11-03926(2012), pp. 446-448. [10.1016/j.ijcard.2011.12.068]
Erythrocytes from patients with carotid atherosclerosis fail to control dendritic cell maturation
SALVATI, Bruno;CAPOANO, Raffaele;
2012
Abstract
Evidence indicates that erythrocytes can represent a potent atherogenic stimulus. In physiological conditions they display an immunomodulatory activity by promoting T cell survival [1] and controlling slan dendritic cell (DC) maturation [2]. To sum up we state that erythrocytes from patients with carotid atherosclerosis fail to control DC maturation. Changes in their integrity and functions, probably due to erythrocyte exposure to high oxidative stress generated by atherosclerotic risk factors such as diabetes, smoking, hypercholesterolemia, may cause the impairment of erythrocyte immunomodulatory activity, thus contributing to atherosclerotic plaque progression and destabilization. We suggest that the altered expression of CD47 at erythrocyte surface, or its loss due to vesiculation, could represent the main mechanism determining the functional impairment of patient erythrocytes in their cross-talk with DCsI documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
