Background IL-12 is a strong inducer of Th1 responses. Stimulation via the
CD2 receptor increases IFN-gamma production and enhances the responsiveness
of activated T-cells to IL-12, possibly due to an up-regulation of the sig
nal transducing beta (2) chain of the IL-12 receptor (IL-12R beta (2)). Ato
pic children have a reduced Th1-like immunity and a reduced CD2 expression.
Our hypothesis is that atopic individuals have a reduced function of the C
D2 pathway, causing reduced responsiveness to IL-12 and decreased IFN-gamma
production.
Objective The aim was to study the mRNA expression of the IL-12R beta (2) c
hain, after stimulation via the CD2 pathway in peripheral blood mononuclear
cells (PBMC), of atopic and non-atopic children, and to investigate correl
ations to the production of Th1 and Th2 cytokines.
Materials and methods The study included 23 skin prick test positive, and 9
nonsensitized, 12-year-old children. PBMC were stimulated for 24 h with ph
ytohemagglutinin (PHA) (2 mug/mL), which stimulates T cells through the CD2
pathway. Expression of IL-12R beta (2) mRNA was analysed by quantitative r
eal time PCR and the cytokine production was detected with ELISA.
Results Atopic and non-atopic children had similar baseline expression of I
L-12R beta (2) mRNA, whereas PHA-induced IL-12R beta (2) mRNA expression wa
s lower in atopic than in non-atopic children. The PHA-induced IL-12R beta
(2) mRNA expression correlated well with the PHA-induced IFN-gamma producti
on and with the IFN-gamma /IL-4 ratio.
Conclusion PBMC from atopic children expressed less IL-12R beta (2) mRNA th
an non-atopic children after stimulation via the CD2 pathway (PHA). This ma
y indicate a reduced capacity to respond to Th1-inducing stimuli in atopic
children.