Form of presentation | Articles in international journals and collections |
Year of publication | 2015 |
Язык | английский |
|
Beluchi Saverio , author
Lombardi Vinsent Klifford , author
Martynova Ekaterina Vladimirovna, author
Khaybullina Svetlana Francevna, author
|
Bibliographic description in the original language |
Khaiboullina S.F. CCL27: Novel Cytokine with Potential Role in Pathogenesis of Multiple Sclerosis / S.F. Khaiboullina, A.R. Gumerova, I.Khafizova, E.V. Martynova, V.C. Lombardi, S. Bellusci, A.A. Rizvanov // BioMed Research International. - Vol. 2015. - 2015. - Article ID 189638. - DOI: 10.1155/2015/189638. |
Annotation |
Multiple sclerosis (MS) is an autoimmune and neurodegenerative disease of unknown etiology. Leukocyte infiltration of brain tissue and the subsequent inflammation, demyelination, axonal damage, and formation of sclerotic plaques is a hallmark of MS. Upregulation of proinflammatory cytokines has been suggested to play an essential role in regulating lymphocyte migration in MS. Here we present data on serum cytokine expression in MS cases. Increased serum levels of IL-17 and IL-23 were observed, suggesting activation of the Th17 population of immune effector cells. Additionally, increased levels of IL-22 were observed in the serum of those with acute phase MS. Unexpectedly, we observed an upregulation of the serum chemokine CCL27 in newly diagnosed and acute MS cases. CCL27 is an inflammatory chemokine associated with homing of memory T cells to sites of inflammation. Therefore, its upregulation in association with MS suggests a potential role in disease pathogenesis. |
Keywords |
Multiple sclerosis, CCL27 |
The name of the journal |
BioMed Research International
|
URL |
http://www.hindawi.com/journals/bmri/2015/189638/ |
Please use this ID to quote from or refer to the card |
https://repository.kpfu.ru/eng/?p_id=113218&p_lang=2 |
Full metadata record |
Field DC |
Value |
Language |
dc.contributor.author |
Beluchi Saverio |
ru_RU |
dc.contributor.author |
Lombardi Vinsent Klifford |
ru_RU |
dc.contributor.author |
Martynova Ekaterina Vladimirovna |
ru_RU |
dc.contributor.author |
Khaybullina Svetlana Francevna |
ru_RU |
dc.date.accessioned |
2015-01-01T00:00:00Z |
ru_RU |
dc.date.available |
2015-01-01T00:00:00Z |
ru_RU |
dc.date.issued |
2015 |
ru_RU |
dc.identifier.citation |
Khaiboullina S.F. CCL27: Novel Cytokine with Potential Role in Pathogenesis of Multiple Sclerosis / S.F. Khaiboullina, A.R. Gumerova, I.Khafizova, E.V. Martynova, V.C. Lombardi, S. Bellusci, A.A. Rizvanov // BioMed Research International. - Vol. 2015. - 2015. - Article ID 189638. - DOI: 10.1155/2015/189638. |
ru_RU |
dc.identifier.uri |
https://repository.kpfu.ru/eng/?p_id=113218&p_lang=2 |
ru_RU |
dc.description.abstract |
BioMed Research International |
ru_RU |
dc.description.abstract |
Multiple sclerosis (MS) is an autoimmune and neurodegenerative disease of unknown etiology. Leukocyte infiltration of brain tissue and the subsequent inflammation, demyelination, axonal damage, and formation of sclerotic plaques is a hallmark of MS. Upregulation of proinflammatory cytokines has been suggested to play an essential role in regulating lymphocyte migration in MS. Here we present data on serum cytokine expression in MS cases. Increased serum levels of IL-17 and IL-23 were observed, suggesting activation of the Th17 population of immune effector cells. Additionally, increased levels of IL-22 were observed in the serum of those with acute phase MS. Unexpectedly, we observed an upregulation of the serum chemokine CCL27 in newly diagnosed and acute MS cases. CCL27 is an inflammatory chemokine associated with homing of memory T cells to sites of inflammation. Therefore, its upregulation in association with MS suggests a potential role in disease pathogenesis. |
ru_RU |
dc.language.iso |
ru |
ru_RU |
dc.subject |
Multiple sclerosis |
ru_RU |
dc.subject |
CCL27 |
ru_RU |
dc.title |
CCL27: Novel Cytokine with Potential Role in Pathogenesis of Multiple Sclerosis |
ru_RU |
dc.type |
Articles in international journals and collections |
ru_RU |
|