dc.date.accessioned |
2019-01-22T20:57:12Z |
|
dc.date.available |
2019-01-22T20:57:12Z |
|
dc.date.issued |
2018 |
|
dc.identifier.issn |
2191-1630 |
|
dc.identifier.uri |
https://dspace.kpfu.ru/xmlui/handle/net/149586 |
|
dc.description.abstract |
© 2017, Springer Science+Business Media, LLC, part of Springer Nature. Systemic lupus erythematosus (SLE) is an autoimmune disease with a complex and largely unclear pathogenesis. Cellular phospholipid microvesicles released upon activation and/or death of a cell have been proposed to play a role in inflammatory autoimmune pathologies, including SLE. Here, circulating microvesicles of various cellular origins were marked with fluorescently labeled cell-specific antibodies and enumerated by flow cytometry in platelet-free plasma obtained from the heparinized blood of 29 SLE patients and 19 normal subjects. Significantly higher concentrations of endothelial-, monocyte-, and erythrocyte-derived microvesicles were found in the SLE patients compared to normal subjects with prevalence of microvesicles originating from endothelial cells. No significant difference was found for platelet-derived microvesicles. A correlation analysis of microvesicle counts with laboratory parameters and clinical features of SLE suggest differential implications of various cell-derived microvesicles in the pathogenesis of SLE. These data suggest that SLE is associated with functional alterations of endotheliocytes, monocytes, and erythrocytes followed by enhanced release of microvesicles that may contribute to inflammation and hypercoagulability. |
|
dc.relation.ispartofseries |
BioNanoScience |
|
dc.subject |
Flow cytometry |
|
dc.subject |
Microvesicles |
|
dc.subject |
Systemic lupus erythematosus |
|
dc.title |
Cellular Microvesicles in the Blood of Patients with Systemic Lupus Erythematosus |
|
dc.type |
Article |
|
dc.relation.ispartofseries-issue |
1 |
|
dc.relation.ispartofseries-volume |
8 |
|
dc.collection |
Публикации сотрудников КФУ |
|
dc.relation.startpage |
441 |
|
dc.source.id |
SCOPUS21911630-2018-8-1-SID85044371551 |
|