Abstract:
PURPOSE:T-helper (Th) cells abnormalities are considered to be associated with the pathogenesis of Systemic lupus erythematosus (SLE). Recently, The Th22 cells have been identified and implicated in the pathogenesis of autoimmune diseases such as Rheumatoid arthritis (RA), although therir role in Systemic lupus erythematosus (SLE) remains unclear. The present study intends to investigate their roles in SLE. METHODS:Clinical data were collected in 65 SLE patients and 30 healthy controls. The patients were divided into active and inactive groups. CD4(+)IFN-γ(-)IL-17(-)IL-22(+)Tcells (Th22 cells),CD4(+) IFN-γ(-)IL-22(-)IL-17(+)T cells (Th17 cells),and CD4(+) IFN-γ(+) (Th1 cells) were assayed by flow cytometry. Serum interleukin-22 (IL-22) and IL-17 levels were measured by enzyme-linked immunosorbent assay. RESULTS:The main observation focused on increased Th22 cells in patients with sole lupus skin disease and decreased Th22 cells in patients with sole lupus nephritis. Likewise, concentrations of serum IL-22 were increased in patients with sole lupus skin disease, and decreased in patients with sole lupus nephritis. Additionally, there was a positive correlation between the percentage of Th22 cells and IL-22 production. The percentage of Th17 cells or concentration of serum IL-17 correlated positively with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). CONCLUSION:Th22 seems to be a more significant index to predict the tissue involvement of SLE than Th17, although Th17 may play a role in the activity of SLE.
journal_name
J Clin Immunoljournal_title
Journal of clinical immunologyauthors
Yang XY,Wang HY,Zhao XY,Wang LJ,Lv QH,Wang QQdoi
10.1007/s10875-013-9878-1subject
Has Abstractpub_date
2013-05-01 00:00:00pages
767-74issue
4eissn
0271-9142issn
1573-2592journal_volume
33pub_type
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journal_title:Journal of clinical immunology
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journal_title:Journal of clinical immunology
pub_type: 杂志文章
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pub_type: 杂志文章,评审
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journal_title:Journal of clinical immunology
pub_type: 杂志文章
doi:10.1007/BF00918271
更新日期:1992-01-01 00:00:00
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pub_type: 信件
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