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1.
Blood Res ; 49(2): 132-4, 2014 Jun.
Article in English | MEDLINE | ID: mdl-25025017
2.
J Korean Med Sci ; 21(6): 1070-4, 2006 Dec.
Article in English | MEDLINE | ID: mdl-17179689

ABSTRACT

Interleukin (IL)-12 activates T helper (Th) 1 cells to produce interferon (IFN)-gamma which inhibits atopic inflammation. IL-12 acts through interaction with its receptor, especially beta(2) subunit. In several studies, the low production of IFN-gamma in peripheral mononuclear cells of atopic patients on response to IL-12 stimulation has been reported. Therefore we investigated the IL-12 receptor beta(2) (IL-12R beta(2)) mRNA expression and RNA editing, nucleotide 2451 C-to-U conversion, to find the cause of low responsiveness to IL-12 in atopy. Quantitative real time PCR for mRNA expression and sequence analysis for RNA editing were performed in 80 atopic patients and 54 healthy controls. The expression of IL-12R beta(2) mRNA was significantly lower in atopic patients than healthy controls (p<0.05). In sequence analysis, RNA editing on nucleotide 2451 was not found from either atopic patients or healthy controls. In additional evaluation, there was no relationship between expression of IL-12R beta(2) mRNA and serum total IgE or blood eosinophil count. Reduced IL-12R beta(2) mRNA expression in atopic patients indicate the reduced capacity to respond to IL-12 which induce IFN-gamma production and this may contribute to Th2-skewed immune response in atopy.


Subject(s)
Hypersensitivity, Immediate/epidemiology , Hypersensitivity, Immediate/genetics , RNA, Messenger/genetics , RNA, Messenger/metabolism , Receptors, Interleukin-12/genetics , Risk Assessment/methods , Adult , Biomarkers/metabolism , Female , Genetic Predisposition to Disease/epidemiology , Genetic Predisposition to Disease/genetics , Humans , Hypersensitivity, Immediate/metabolism , Korea/epidemiology , Male , RNA Editing/genetics , Receptors, Interleukin-12/metabolism , Reproducibility of Results , Risk Factors , Sensitivity and Specificity
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