Background: IL-1 has 2 receptors, type I (IL-1RI) and type II (IL-1RII), wh
ich have 2 forms each, membrane (m) and soluble (s). When IL-1 binds to mIL
-1RI, the active receptor, an inflammatory response is initiated, which doe
s not occur when IL-1 binds to mIL-1RII, the decoy receptor. Both sIL-1RT a
nd sIL-1RII function as IL-1-mopping mechanisms. We hypothesized that the r
atio of active (mIL-1RI) to inactive (mIL-1RII, sIL-1RI, and sIL-1RII) rece
ptors is important in determining the amount of inflammation produced in al
lergic reactions.
Objective: Our aim was to compare the concentrations of mIL-1RI and mIL-1RI
I on cultured PBLs and sIL-1RI, sIL-1RII, and IL-1 beta in sera and superna
tants of cultured PBMCs from atopic and nonatopic subjects.
Methods: The membrane receptors, soluble receptors, and IL-1 concentrations
were measured by ELISA with specific mAbs.
Results: Although there was no difference in the level of serum IL-1 beta b
etween the 2 groups, PBMCs from atopic persons spontaneously secreted highe
r levels of IL-1 beta than those from nonatopic donors (P < .05). PBLs from
atopic subjects compared with those from nonatopic individuals expressed h
igher mIL-1RI (P < .0001) and mIL-1RII (P < .05). Levels of both the solubl
e receptors from both serum (P < .0001) and PBMCs (P < .05) of nonatopic do
nors were higher than those found in atopic donors.
Conclusion: This augmentation of mIL-1RI concomitant with a reduction in so
luble receptors may be an important contributory factor to the inflammation
that occurs with allergen exposure.