title: PHA-induced IL-12R beta(2) mRNA expression in atopic and non-atopic children.
abstract: 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 signal transducing beta(2) chain of the IL-12 receptor (IL-12R beta(2)). 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-gamma production.
  
  
  OBJECTIVE
  The aim was to study the mRNA expression of the IL-12R beta(2) 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.
  
  
  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 microg/mL), which stimulates T cells through the CD2 pathway. Expression of IL-12R beta(2) mRNA was analysed by quantitative real time PCR and the cytokine production was detected with ELISA.
  
  
  RESULTS
  Atopic and non-atopic children had similar baseline expression of IL-12R beta(2) mRNA, whereas PHA-induced IL-12R beta(2) mRNA expression was 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 production and with the IFN-gamma/IL-4 ratio.
  
  
  CONCLUSIONS
  PBMC from atopic children expressed less IL-12R beta(2) 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.
authors.affiliation: Department of Health and Environment, Division of Paediatrics, Clinical Research Centre, Faculty of Health Sciences, Linköping University, Linköping, Sweden. camja@ihm.liu.se
authors.forename: C K
authors.initials: CK
authors.lastname: Janefjord
authors.forename: M C
authors.initials: MC
authors.lastname: Jenmalm
mesh_terms: D002648:Child; D002669:Child Welfare; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000097:blood / Q000235:genetics*; D007371:Interferon-gamma / Q000096:biosynthesis; D016753:Interleukin-10 / Q000378:metabolism; D018793:Interleukin-13 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D010835:Phytohemagglutinins / Q000494:pharmacology*; D012333:RNA, Messenger / Q000097:blood / Q000187:drug effects* / Q000502:physiology*; D018123:Receptors, Interleukin / Q000097:blood / Q000187:drug effects* / Q000235:genetics*; D053707:Receptors, Interleukin-12; D012882:Skin Tests; D013548:Sweden
chemical_list: D018793:Interleukin-13; D015848:Interleukin-5; D010835:Phytohemagglutinins; D012333:RNA, Messenger; D018123:Receptors, Interleukin; D053707:Receptors, Interleukin-12; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma