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Division of Dermatology, Sunnybrook Health Science Center, University of Toronto, Toronto, Ontario, Canada
The migration of epidermal Langerhans cells (LC) to lymph nodes
(LN) is critical in the initiation of contact hypersensitivity (CHS)
responses. Studies suggest that contact allergen-induced epidermal
proinflammatory cytokines, including IL-1 and TNF-
, play important
roles in promoting LC migration. Contact allergens also induce
epidermal anti-inflammatory cytokines such as IL-10. Since IL-10
down-regulates proinflammatory cytokine production and inhibits CHS, we
hypothesized that IL-10 might inhibit LC migration. To test this
hypothesis, IL-10 knockout (KO) mice were epicutaneously sensitized
with the hapten, FITC, and 24 h later hapten-bearing cells in the
draining LN were examined. The number of hapten-bearing cells in the LN
was significantly greater in IL-10 KO mice than in wild-type mice. The
mutant mice also had an exaggerated CHS to FITC. Pretreatment with
anti-TNF- Ab or IL-1R antagonist significantly reduced the
number of hapten-bearing cells in the LN, suggesting that IL-10
modulation of LC migration involves IL-1 and TNF-. Moreover, IL-10
KO mice demonstrated a greater increase in TNF-, IL-1, and
IL-1ß mRNAs in the allergen-exposed epidermis, and keratinocytes
derived from the mutant mice were able to produce higher amounts of
TNF- and IL-1 protein. These data suggest that IL-10 plays an
inhibitory role in LC migration and that this effect may occur via the
down-regulation of TNF- and IL-1 production.
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