TY  - JOUR
AU  - Miljković, Đorđe
AU  - Stanojević, Zeljka S
AU  - Momčilović, Miljana
AU  - Odoardi, Francesca
AU  - Fluegel, Alexander
AU  - Mostarica-Stojković, Marija B
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1267
AB  - Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis, a chronic inflammatory and demyelinating disease of the CNS. Albino Oxford (AO) rats are resistant to the induction of EAE, while the disease can be readily induced in Dark Agouti (DA) rats. Here we investigated a potential contribution of the CNS milieu in the limitation of the encephalitogenic autoimmune response. EAE was induced by immunization of the respective rat strains with spinal cord homogenate emulsified in complete Freund's adjuvant. AO rats did not exhibit clinical signs after immunization while DA rats developed severe neurologic deficits. Infiltration of immune cells into spinal cords (SC) was evident in both strains 12-14 days after the immunization. EAE lesions of AO rats contained substantially lower numbers of CD4+ T cells and CD11b+ cells compared to those in DA rats. This went together with lower levels of interferon (IFN)-gamma and interleukin (IL)-17 in the cells isolated from SC. We found a dramatic increase of CXCL12 expression in SC tissue and microvessels of AO rats, whereas DA rats markedly decreased the expression of this chemokine within their CNS. Administration of the CXCL12 antagonist AMD3100 to a substrain of AO rats that developed a weak EAE led to earlier onset and exacerbation of the disease. These results suggest a role of CXCL12 in down-regulating autoimmune processes in AO rats during EAE. Therapeutic modulation of CXCL12 could be a promising strategy for the treatment of CNS autoimmunity. (C) 2011 Elsevier GmbH. All rights reserved.
T2  - Immunobiology
T1  - CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats
IS  - 9
VL  - 216
EP  - 987
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1267
ER  - 

@article{
author = "Miljković, Đorđe and Stanojević, Zeljka S and Momčilović, Miljana and Odoardi, Francesca and Fluegel, Alexander and Mostarica-Stojković, Marija B",
year = "2011",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis, a chronic inflammatory and demyelinating disease of the CNS. Albino Oxford (AO) rats are resistant to the induction of EAE, while the disease can be readily induced in Dark Agouti (DA) rats. Here we investigated a potential contribution of the CNS milieu in the limitation of the encephalitogenic autoimmune response. EAE was induced by immunization of the respective rat strains with spinal cord homogenate emulsified in complete Freund's adjuvant. AO rats did not exhibit clinical signs after immunization while DA rats developed severe neurologic deficits. Infiltration of immune cells into spinal cords (SC) was evident in both strains 12-14 days after the immunization. EAE lesions of AO rats contained substantially lower numbers of CD4+ T cells and CD11b+ cells compared to those in DA rats. This went together with lower levels of interferon (IFN)-gamma and interleukin (IL)-17 in the cells isolated from SC. We found a dramatic increase of CXCL12 expression in SC tissue and microvessels of AO rats, whereas DA rats markedly decreased the expression of this chemokine within their CNS. Administration of the CXCL12 antagonist AMD3100 to a substrain of AO rats that developed a weak EAE led to earlier onset and exacerbation of the disease. These results suggest a role of CXCL12 in down-regulating autoimmune processes in AO rats during EAE. Therapeutic modulation of CXCL12 could be a promising strategy for the treatment of CNS autoimmunity. (C) 2011 Elsevier GmbH. All rights reserved.",
journal = "Immunobiology",
title = "CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats",
number = "9",
volume = "216",
pages = "987",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1267"
}

Miljković, Đ., Stanojević, Z. S., Momčilović, M., Odoardi, F., Fluegel, A.,& Mostarica-Stojković, M. B.. (2011). CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats. in Immunobiology, 216(9).
https://hdl.handle.net/21.15107/rcub_ibiss_1267

Miljković Đ, Stanojević ZS, Momčilović M, Odoardi F, Fluegel A, Mostarica-Stojković MB. CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats. in Immunobiology. 2011;216(9):null-987.
https://hdl.handle.net/21.15107/rcub_ibiss_1267 .

Miljković, Đorđe, Stanojević, Zeljka S, Momčilović, Miljana, Odoardi, Francesca, Fluegel, Alexander, Mostarica-Stojković, Marija B, "CXCL12 expression within the CNS contributes to the resistance against experimental autoimmune encephalomyelitis in Albino Oxford rats" in Immunobiology, 216, no. 9 (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1267 .

TY  - JOUR
AU  - Bartholomaus, Ingo
AU  - Kawakami, Naoto
AU  - Odoardi, Francesca
AU  - Schlager, Christian
AU  - Miljković, Đorđe
AU  - Ellwart, Joachim
AU  - Klinkert, Wolfgang
AU  - Flugel Koch, Cassandra
AU  - Issekutz, Thomas
AU  - Wekerle, Hartmut
AU  - Flugel, Alexander
PY  - 2009
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6023
AB  - The tissues of the central nervous system are effectively shielded from the blood circulation by specialized vessels that are impermeable not only to cells, but also to most macromolecules circulating in the blood. Despite this seemingly absolute seclusion, central nervous system tissues are subject to immune surveillance and are vulnerable to autoimmune attacks. Using intravital two-photon imaging in a Lewis rat model of experimental autoimmune encephalomyelitis, here we present in real-time the interactive processes between effector T cells and cerebral structures from their first arrival to manifest autoimmune disease. We observed that incoming effector T cells successively scanned three planes. The T cells got arrested to leptomeningeal vessels and immediately monitored the luminal surface, crawling preferentially against the blood flow. After diapedesis, the cells continued their scan on the abluminal vascular surface and the underlying leptomeningeal (pial) membrane. There, the T cells encountered phagocytes that effectively present antigens, foreign as well as myelin proteins. These contacts stimulated the effector T cells to produce pro-inflammatory mediators, and provided a trigger to tissue invasion and the formation of inflammatory infiltrations.
PB  - Macmillan Publishers Limited
T2  - Nature
T1  - Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions
IS  - 7269
VL  - 462
DO  - 10.1038/nature08478
SP  - 94
EP  - 98
ER  - 

@article{
author = "Bartholomaus, Ingo and Kawakami, Naoto and Odoardi, Francesca and Schlager, Christian and Miljković, Đorđe and Ellwart, Joachim and Klinkert, Wolfgang and Flugel Koch, Cassandra and Issekutz, Thomas and Wekerle, Hartmut and Flugel, Alexander",
year = "2009",
abstract = "The tissues of the central nervous system are effectively shielded from the blood circulation by specialized vessels that are impermeable not only to cells, but also to most macromolecules circulating in the blood. Despite this seemingly absolute seclusion, central nervous system tissues are subject to immune surveillance and are vulnerable to autoimmune attacks. Using intravital two-photon imaging in a Lewis rat model of experimental autoimmune encephalomyelitis, here we present in real-time the interactive processes between effector T cells and cerebral structures from their first arrival to manifest autoimmune disease. We observed that incoming effector T cells successively scanned three planes. The T cells got arrested to leptomeningeal vessels and immediately monitored the luminal surface, crawling preferentially against the blood flow. After diapedesis, the cells continued their scan on the abluminal vascular surface and the underlying leptomeningeal (pial) membrane. There, the T cells encountered phagocytes that effectively present antigens, foreign as well as myelin proteins. These contacts stimulated the effector T cells to produce pro-inflammatory mediators, and provided a trigger to tissue invasion and the formation of inflammatory infiltrations.",
publisher = "Macmillan Publishers Limited",
journal = "Nature",
title = "Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions",
number = "7269",
volume = "462",
doi = "10.1038/nature08478",
pages = "94-98"
}

Bartholomaus, I., Kawakami, N., Odoardi, F., Schlager, C., Miljković, Đ., Ellwart, J., Klinkert, W., Flugel Koch, C., Issekutz, T., Wekerle, H.,& Flugel, A.. (2009). Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions. in Nature
Macmillan Publishers Limited., 462(7269), 94-98.
https://doi.org/10.1038/nature08478

Bartholomaus I, Kawakami N, Odoardi F, Schlager C, Miljković Đ, Ellwart J, Klinkert W, Flugel Koch C, Issekutz T, Wekerle H, Flugel A. Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions. in Nature. 2009;462(7269):94-98.
doi:10.1038/nature08478 .

Bartholomaus, Ingo, Kawakami, Naoto, Odoardi, Francesca, Schlager, Christian, Miljković, Đorđe, Ellwart, Joachim, Klinkert, Wolfgang, Flugel Koch, Cassandra, Issekutz, Thomas, Wekerle, Hartmut, Flugel, Alexander, "Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions" in Nature, 462, no. 7269 (2009):94-98,
https://doi.org/10.1038/nature08478 . .