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kováImmunology Division, Department of Pediatrics, Faculty of Medicine, Université de Sherbrooke, Sherbrooke, Canada
The cysteinyl (Cys) leukotrienes (LT)C4,
LTD4, and LTE4, are lipid mediators that have
been implicated in the pathogenesis of asthma. The human
LTD4 receptor (CysLT1R) was recently cloned and
characterized. The present work was undertaken to study the potential
modulation of CysLT1R expression by the Th2 cytokines IL-13
and IL-4. In this study, we report that IL-13 up-regulates
CysLT1R mRNA levels, with consequently enhanced
CysLT1R protein expression and function in human monocytes
and monocyte-derived macrophages. CysLT1R mRNA expression
was augmented 2- to 5-fold following treatment with IL-13 and was due
to enhanced transcriptional activity. The effect was observed after
4 h, was maximal by 8 h, and maintained at 24 h. IL-4,
but not IFN-
, induced a similar pattern of CysLT1R
up-regulation. Monocytes pretreated with IL-13 or IL-4 for 24 h
showed enhanced CysLT1R protein expression, as assessed by
flow cytometry using a polyclonal anti-CysLT1R Ab. They
also showed enhanced responsiveness to LTD4, but not to
LTB4, in terms of Ca2+ mobilization, as well as
augmented chemotactic activity. Our findings suggest a possible
mechanism by which IL-13 and IL-4 can modulate CysLT1R
expression on monocytes and macrophages, and consequently their
responsiveness to LTD4, and thus contribute to the
pathogenesis of asthma and allergic diseases.
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