The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Interleukin-17 mRNA expression in blood and CSF mononuclear cells is augmented in multiple sclerosis
Abstract
Myelin-directed autoimmunity is considered to play a key role in the pathogenesis of multiple sclerosis (MS). Increased production of both pro- and anti-inflammatory cytokines is a common finding in MS. Interleukin-17 (IL-17) is a recently described cytokine produced in humans almost exclusively by activated memory T cells, which can induce the production of proinflammatory cytokines and chemokines from parenchymal cells and macrophages. In situ hybridisation with synthetic oligonucleotide probes was adopted to detect and enumerate IL-17 mRNA expressing mononuclear cells (MNC) in blood and cerebrospinal fluid (CSF) from patients with MS and control individuals. Numbers of IL-17 mRNA expressing blood MNC were higher in patients with MS and acute aseptic meningoencephalitis (AM) compared to healthy individuals. Higher numbers of IL-17 mRNA expressing blood MNC were detected in MS patients examined during clinical exacerbation compared to remission. Patients with MS had higher numbers of IL-17 mRNA expressing MNC in CSF compared to blood. This increase in numbers of IL-17 mRNA expressing MNC in CSF was not observed in patients with AM. Our results thus demonstrate increased numbers of IL-17 mRNA expressing MNC in MS with higher numbers in CSF than blood, and with the highest numbers in blood during clinical exacerbations.
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Rating neurologic impairment in multiple sclerosis: An expanded disability status scale (EDSS)
Kurtzke, J. F. (1983) · Neurology · doi:10.1212/wnl.33.11.1444 · Cited by 15,011
T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines
Fossiez, F., Djossou, O., Chomarat, P., Flores-Romo, L., Ait-Yahia, S., Maat, C., Pin, J. J., Garrone, P., Garcia, E., Saeland, S., et al. (1996) · The Journal of Experimental Medicine · doi:10.1084/jem.183.6.2593 · Cited by 1,526
Cited by
Korn, T., Bettelli, E., Oukka, M., & Kuchroo, V. K. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132710 · Cited by 4,873
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
Langrish, C. L., Chen, Y., Blumenschein, W. M., Mattson, J., Basham, B., Sedgwick, J. D., McClanahan, T., Kastelein, R. A., & Cua, D. J. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041257 · Cited by 4,099
Phenotypic and functional features of human Th17 cells
Annunziato, F., Cosmi, L., Santarlasci, V., Maggi, L., Liotta, F., Mazzinghi, B., Parente, E., Filì, L., Ferri, S., Frosali, F., et al. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070663 · Cited by 1,861
Increased expression of interleukin 17 in inflammatory bowel disease
Fujino, S., Andoh, A., Bamba, S., Ogawa, A., Hata, K., Araki, Y., Bamba, T., & Fujiyama, Y. (2003) · Gut · doi:10.1136/gut.52.1.65 · Cited by 1,713
IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis
Komiyama, Y., Nakae, S., Matsuki, T., Nambu, A., Ishigame, H., Kakuta, S., Sudo, K., & Iwakura, Y. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.1.566 · Cited by 1,536
Metadata
- Authors
- Matusevicius, D., Kivisäkk, P., He, B., Kostulas, N., Özenci, V, Fredrikson, S., & Link, H.
- Venue
- Multiple Sclerosis Journal
- Publisher
- SAGE Publications
- Published
- 1999-04
- Volume
- 5
- Issue
- 2
- Pages
- 101-104
- ISSN
- 1352-4585 (ISSN-L)
- 1477-0970
- OpenAlex
- W2113577022
- Cited by
- 751
- References
- 2
- FWCI
- 3.56
- Type
- journal article
- Language
- en
- Open access
- closed
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- Matusevicius, D., Kivisäkk, P., He, B., Kostulas, N., Özenci, V, Fredrikson, S., & Link, H. (1999). Interleukin-17 mRNA expression in blood and CSF mononuclear cells is augmented in multiple sclerosis. Multiple Sclerosis Journal. https://doi.org/10.1177/135245859900500206
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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