PHA-induced IL-12Rb2 mRNA expression in atopic and non-atopic children
2001 (English)In: Clinical and Experimental Allergy, ISSN 0954-7894, Vol. 31, no 10, 1493-1500 p.Article in journal (Refereed) Published
IL-12 is a strong inducer of Th1 responses. Stimulation via the CD2 receptor increases IFN-γ production and enhances the responsiveness of activated T-cells to IL-12, possibly due to an up-regulation of the signal transducing β2 chain of the IL-12 receptor (IL-12Rβ2). Atopic children have a reduced Th1-like immunity and a reduced CD2 expression. Our hypothesis is that atopic individuals have a reduced function of the CD2 pathway, causing reduced responsiveness to IL-12 and decreased IFN-γ production.
The aim was to study the mRNA expression of the IL-12Rβ2 chain, after stimulation via the CD2 pathway in peripheral blood mononuclear cells (PBMC), of atopic and non-atopic children, and to investigate correlations to the production of Th1 and Th2 cytokines.
Materials and methods
The study included 23 skin prick test positive, and 9 non-sensitized, 12-year-old children. PBMC were stimulated for 24 h with phytohemagglutinin (PHA) (2 µg/mL), which stimulates T cells through the CD2 pathway. Expression of IL-12Rβ2 mRNA was analysed by quantitative real time PCR and the cytokine production was detected with ELISA.
Atopic and non-atopic children had similar baseline expression of IL-12Rβ2 mRNA, whereas PHA-induced IL-12Rβ2 mRNA expression was lower in atopic than in non-atopic children. The PHA-induced IL-12Rβ2 mRNA expression correlated well with the PHA-induced IFN-γ production and with the IFN-γ/IL-4 ratio.
PBMC from atopic children expressed less IL-12Rβ2 mRNA than non-atopic children after stimulation via the CD2 pathway (PHA). This may indicate a reduced capacity to respond to Th1-inducing stimuli in atopic children.
Place, publisher, year, edition, pages
2001. Vol. 31, no 10, 1493-1500 p.
CD2, PHA, IL-12Rβ2, Quantitative Real Time PCR, ELISA, cytokine, atopic children
National CategoryMedical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-13844DOI: 10.1046/j.1365-2222.2001.01206.xOAI: oai:DiVA.org:liu-13844DiVA: diva2:21852