It has been proposed that a down-regulation of interleukin (IL)-12 and inte
rferon (IFN)-gamma might be related to susceptibility to allergy in early l
ife. The aim of this study was to assess serum IL-12 levels in food-sensiti
zed and pollen-sensitized children and to compare these with another activa
tion marker, sCD30. Twenty children with pollen allergy and 22 food-sensiti
zed children were included. The diagnosis of immunoglobulin (Ig)-E-mediated
allergy, suggested by clinical symptoms, was based on skin-prick tests, se
rum IgE antibodies and total IgE levels. Samples from 24 non-allergic child
ren were used as controls. IL-12 and sCD30 levels were measured by ELISA. I
t was found that pollen-sensitized patients had normal IL-12 and higher sCD
30 levels than controls (114 vs. 63 U/ml, p = 0.028), but, surprisingly, fo
od-sensitized infants showed normal sCD30 and increased serum IL-12 levels
(323 vs. 118 pg/ml, p = 0.0001). No differences were found in patients suff
ering from asthma or allergic dermatitis. Levels of sCD30 and IL-12 determi
ned in May showed a strong correlation with those obtained in November. Int
erleukin-12 and IgE levels had an inverse correlation (r = -0.494, p = 0.00
01) whereas no correlation was found between sCD30 and IgE, Age had a stron
g negative influence on IL-12 levels in allergic (Z = 4.834, p < 0.0005) an
d in normal children (Z = 3.00, p < 0.002); by contrast, sCD30 levels were
not significantly age-dependent. When IL-12 levels from the food-allergy gr
oup were compared with those from normal controls younger than 4 years of a
ge, the difference remained significant (p = 0.001), ruling out an age-bias
. The conclusions made in this study were that serum IL-12 and sCD30 showed
different behaviors in children with food or pollen allergy. We found IL-1
2 and sCD30 levels in pollen-allergic patients that agree with the classica
l T-helper (Th) 1/Th2 paradigm of allergy. In contrast, serum IL-12 levels
were increased in food-sensitized children, suggesting a different immunolo
gic pathogenesis.