TY  - JOUR
AU  - Trajković, Vladimir S
AU  - Vucković, Olivera
AU  - Stošić-Grujičić, Stanislava
AU  - Miljković, Đorđe
AU  - Popadić, Dušan M.
AU  - Marković, Miloš
AU  - Bumbaširević, Vesna D
AU  - Backović, Aleksandar
AU  - Stojanović, Ivana D.
AU  - Harhaji-Trajković, Ljubica
AU  - Ramić, Zorica D.
AU  - Mostarica-Stojković, Marija
PY  - 2004
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1682
AB  - Although astrocytes presumably participate in maintaining the immune privilege of the central nervous system (CNS), the mechanisms behind their immunoregulatory properties are still largely undefined. In this study, we describe the development of regulatory T cells upon contact with astrocytes. Rat T cells pre-incubated with astrocytes completely lost the ability to proliferate in response to mitogenic stimuli. The cells were blocked in G0/G1 phase of the cell cycle, expressed less IL-2R, and produced significantly lower amounts of interferon-gamma (IFN-gamma), but not interleukin-2 (IL-2), IL-10, or tumor necrosis factor (TNF). These anergic cells completely prevented mitogen-induced growth of normal T lymphocytes, as well as CNS antigen-driven proliferation of autoreactive T cells. The suppressive activity resided in both CD4(+) and CD8(+) T-cell compartments. Heat-sensitive soluble T-cell factors, not including transforming growth factor-beta (TGF-beta) or IL-10, were solely responsible for the observed suppression, as well as for the transfer of suppressive activity to normal T cells. The administration of astrocyte-induced regulatory T cells markedly alleviated CNS inflammation and clinical symptoms of CNS autoimmunity in rats with experimental allergic encephalomyelitis. Finally, the cells with suppressive properties were readily generated from human lymphocytes after contact with astrocytes. Taken together, these data indicate that astrocyte-induced regulatory T cells might represent an important mechanism for self-limitation of excessive inflammation in the brain. (C) 2004 Wiley-Liss, Inc.
T2  - Glia
T1  - Astrocyte-induced regulatory T cells mitigate CNS autoimmunity
IS  - 2
VL  - 47
DO  - 10.1002/glia.20046
SP  - 168
EP  - 179
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1682
ER  - 

@article{
author = "Trajković, Vladimir S and Vucković, Olivera and Stošić-Grujičić, Stanislava and Miljković, Đorđe and Popadić, Dušan M. and Marković, Miloš and Bumbaširević, Vesna D and Backović, Aleksandar and Stojanović, Ivana D. and Harhaji-Trajković, Ljubica and Ramić, Zorica D. and Mostarica-Stojković, Marija",
year = "2004",
abstract = "Although astrocytes presumably participate in maintaining the immune privilege of the central nervous system (CNS), the mechanisms behind their immunoregulatory properties are still largely undefined. In this study, we describe the development of regulatory T cells upon contact with astrocytes. Rat T cells pre-incubated with astrocytes completely lost the ability to proliferate in response to mitogenic stimuli. The cells were blocked in G0/G1 phase of the cell cycle, expressed less IL-2R, and produced significantly lower amounts of interferon-gamma (IFN-gamma), but not interleukin-2 (IL-2), IL-10, or tumor necrosis factor (TNF). These anergic cells completely prevented mitogen-induced growth of normal T lymphocytes, as well as CNS antigen-driven proliferation of autoreactive T cells. The suppressive activity resided in both CD4(+) and CD8(+) T-cell compartments. Heat-sensitive soluble T-cell factors, not including transforming growth factor-beta (TGF-beta) or IL-10, were solely responsible for the observed suppression, as well as for the transfer of suppressive activity to normal T cells. The administration of astrocyte-induced regulatory T cells markedly alleviated CNS inflammation and clinical symptoms of CNS autoimmunity in rats with experimental allergic encephalomyelitis. Finally, the cells with suppressive properties were readily generated from human lymphocytes after contact with astrocytes. Taken together, these data indicate that astrocyte-induced regulatory T cells might represent an important mechanism for self-limitation of excessive inflammation in the brain. (C) 2004 Wiley-Liss, Inc.",
journal = "Glia",
title = "Astrocyte-induced regulatory T cells mitigate CNS autoimmunity",
number = "2",
volume = "47",
doi = "10.1002/glia.20046",
pages = "168-179",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1682"
}

Trajković, V. S., Vucković, O., Stošić-Grujičić, S., Miljković, Đ., Popadić, D. M., Marković, M., Bumbaširević, V. D., Backović, A., Stojanović, I. D., Harhaji-Trajković, L., Ramić, Z. D.,& Mostarica-Stojković, M.. (2004). Astrocyte-induced regulatory T cells mitigate CNS autoimmunity. in Glia, 47(2), 168-179.
https://doi.org/10.1002/glia.20046
https://hdl.handle.net/21.15107/rcub_ibiss_1682

Trajković VS, Vucković O, Stošić-Grujičić S, Miljković Đ, Popadić DM, Marković M, Bumbaširević VD, Backović A, Stojanović ID, Harhaji-Trajković L, Ramić ZD, Mostarica-Stojković M. Astrocyte-induced regulatory T cells mitigate CNS autoimmunity. in Glia. 2004;47(2):168-179.
doi:10.1002/glia.20046
https://hdl.handle.net/21.15107/rcub_ibiss_1682 .

Trajković, Vladimir S, Vucković, Olivera, Stošić-Grujičić, Stanislava, Miljković, Đorđe, Popadić, Dušan M., Marković, Miloš, Bumbaširević, Vesna D, Backović, Aleksandar, Stojanović, Ivana D., Harhaji-Trajković, Ljubica, Ramić, Zorica D., Mostarica-Stojković, Marija, "Astrocyte-induced regulatory T cells mitigate CNS autoimmunity" in Glia, 47, no. 2 (2004):168-179,
https://doi.org/10.1002/glia.20046 .,
https://hdl.handle.net/21.15107/rcub_ibiss_1682 .