Carbone, Fortunata (2011) Regulatory T cell proliferative potential as novel marker to investigate immune tolerance and clinical progression in Multiple Sclerosis. [Tesi di dottorato] (Unpublished)

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Item Type: Tesi di dottorato
Language: English
Title: Regulatory T cell proliferative potential as novel marker to investigate immune tolerance and clinical progression in Multiple Sclerosis
Creators:
CreatorsEmail
Carbone, Fortunatafortunata.carbone@alice.it
Date: 29 November 2011
Number of Pages: 53
Institution: Università degli Studi di Napoli Federico II
Department: Biologia e patologia cellullare e molecolare "L. Califano"
Doctoral School: Medicina molecolare
PHD name: Patologia e fisiopatologia molecolare
PHD cycle: 24
PHD Coordinator:
nameemail
Avvedimento, Vittorio EnricoUNSPECIFIED
Tutor:
nameemail
Matarese, Giuseppegiuseppe.matarese@cnr.it
Date: 29 November 2011
Number of Pages: 53
Uncontrolled Keywords: Treg, multiple sclerosis, immune tolerance
MIUR S.S.D.: Area 06 - Scienze mediche > MED/04 - Patologia generale
Date Deposited: 13 Dec 2011 11:30
Last Modified: 30 Apr 2014 19:47
URI: http://www.fedoa.unina.it/id/eprint/8686

Abstract

In autoimmune disorders such as Multiple Sclerosis (MS) one of the determining alteration is the breakdown of self-antigen immune-tolerance. Peripheral immune tolerance is maintained, at least in part, by Regulatory T cells (Treg). Several studies have shown that either defects in the frequency or the suppressive capacity of Treg cells can contribute to the development of break of self-tolerance, and that in animal models of autoimmunity, adoptive transfer of Treg cells was able to stop disease process. Treg cells are known to be anergic in vitro to T cell receptor-induced (TCR) stimulation and this state correlates with their in vitro suppressive capacity. It has been reported that there are differences in the number of Treg cells in MS patients when compared with healthy controls. However there is also extensive evidence indicating a defect in the suppressive function of Treg cells from MS patients. In previous studies we showed that Treg cells produce an higher amount of leptin when compared with effector T cells and that leptin acts as a negative signal for the proliferation of Treg cells. In vitro leptin neutralization results in Treg cells proliferation. Although in last few years several studies have been performed to understand the molecular mechanism leading to autoimmune disorders development, there are no surrogate markers to predict the clinical progression of autoimmune diseases and the clinical response to the classical therapeutic regimes.

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