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mRNA Expression and RNA Editing (2451 C-to-U) of IL-12 Receptor β(2) in Adult Atopic Patients

Interleukin (IL)-12 activates T helper (Th) 1 cells to produce interferon (IFN)-γ which inhibits atopic inflammation. IL-12 acts through interaction with its receptor, especially β(2) subunit. In several studies, the low production of IFN-γ in peripheral mononuclear cells of atopic patients on respo...

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Detalles Bibliográficos
Autores principales: Kim, Eun Jin, Lee, Won Mok, Ha, Jung Sook, Ryoo, Nam Hee, Jeon, Dong Suk, Kim, Jae Ryong
Formato: Texto
Lenguaje:English
Publicado: The Korean Academy of Medical Sciences 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721931/
https://www.ncbi.nlm.nih.gov/pubmed/17179689
http://dx.doi.org/10.3346/jkms.2006.21.6.1070
Descripción
Sumario:Interleukin (IL)-12 activates T helper (Th) 1 cells to produce interferon (IFN)-γ which inhibits atopic inflammation. IL-12 acts through interaction with its receptor, especially β(2) subunit. In several studies, the low production of IFN-γ in peripheral mononuclear cells of atopic patients on response to IL-12 stimulation has been reported. Therefore we investigated the IL-12 receptor β(2) (IL-12Rβ(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-12Rβ(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-12Rβ(2) mRNA and serum total IgE or blood eosinophil count. Reduced IL-12Rβ(2) mRNA expression in atopic patients indicate the reduced capacity to respond to IL-12 which induce IFN-γ production and this may contribute to Th2-skewed immune response in atopy.