کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5896860 | 1155245 | 2015 | 7 صفحه PDF | دانلود رایگان |
- IL-10, IFNλ3 and IFNβ are up-regulated in tick-borne encephalitis (TBE).
- IFNλ3 and probably IFNβ and IL10 are expressed within the central nervous system.
- High concentration of IFNλ3 correlates with a mild clinical presentation of TBE.
- Genetic polymorphisms associated with IFNλ3 expression may determine the severity of TBE.
Tick-borne encephalitis (TBE) has a wide clinical spectrum, from asymptomatic to severe encephalitis, and host-dependent factors determining the outcome remain elusive. We have measured concentrations of pro-inflammatory/Th1 interferon-γ (IFNγ), immunomodulatory/Th2 interleukin-10 (IL-10), anti-viral type I (IFNβ) and type III (IFNλ3) interferons in cerebrospinal fluid (csf) and serum of 18 TBE patients, simultaneously genotyped for polymorphisms associated with the expression of genes IFNL3 (coding IFNλ3), IL10, CD209 and CCR5. IL-10, IFNβ and IFNλ3 were up-regulated in csf, with IFNλ3 level higher in patients with the milder clinical presentation (meningitis) than in meningoencephalitis. There was an increased serum IFNβ and a tendency for increased serum IL-10 in meningitis patients. Genotype in rs12979860 locus upstream of IFNL3 was associated with IFNλ3 expression and in rs287886 (CD209) - IL-10 expression. IL-10, IFNβ and IFNλ3 are expressed and play a protective role in TBE and their expression in TBE patients is associated with genetic polymorphisms.
Journal: Cytokine - Volume 71, Issue 2, February 2015, Pages 125-131