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Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
Adhesion of Langerhans cells (LC) to keratinocytes is mediated by
E-cadherin. IL-1, TNF-
, and LPS mobilize LC from epidermis and
presumably attenuate LC-keratinocyte adhesion. To determine whether
these mediators modulated LC E-cadherin-dependent adhesion directly, we
characterized their effects on LC-like dendritic cells expanded from
murine fetal skin (FSDDC). FSDDC were propagated from day 16 C57BL/6
fetal skin and isolated as aggregates (FSDDC-A) in which homophilic
adhesion was mediated by E-cadherin. IL-1, TNF-, and LPS induced
dissociation of FSDDC-A that began within 4 to 8 h and was
complete within 20 h. Anti-IL-1RI mAb inhibited disaggregation
caused by IL-1 and IL-1ß, but not that induced by TNF- or LPS.
Anti-TNF- mAb inhibited the effect of TNF- and LPS, but not that
caused by IL-1 or IL-1ß. Flow cytometry of FSDDC-A revealed that
IL-1, TNF-, and LPS induced increased expression of MHC class II,
CD40, and CD86 and decreased E-cadherin expression that was temporally
related to dissociation of aggregates. IL-1 and TNF- caused a rapid
reduction in FSDDC E-cadherin mRNA levels that preceded the decrease in
E-cadherin surface expression. These results demonstrate that cytokines
that induce LC emigration in vivo act directly on LC-like cells in
vitro, reduce E-cadherin mRNA levels, down-regulate E-cadherin surface
expression, and induce a loss of E-cadherin-mediated adhesion.
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