Low-dose UVB radiation perturbs the functional expression of @entity12750 co-stimulatory molecules on XXXX Langerhans cells.

@entity1 @entity2937 @entity12750 @entity7938 @entity4386 @entity1412 @entity1361
In previous studies, we have shown that ultraviolet (UV) B radiation perturbs the @entity1412 function of Langerhans cells (LC) by interfering with as-yet unidentified co-stimulatory signals. Recently, @entity12750 on @entity1412 were shown to deliver important co-stimulatory signals through interaction with their counter receptors @entity1361 and @entity4386 on T cells. To determine whether UVB affects the functional expression of @entity7938 or @entity2937 on LC, @entity12750 expression was studied on @entity1 LC by multiparameter flow cytometry. Little, if any, @entity7938 or @entity2937 was detected on LC freshly isolated from skin. However, following 48 h of tissue culture, expression of both @entity12750 were markedly up-regulated. To test whether these molecules were functional, primary mixed epidermal cell leukocyte reactions (MECLR) were performed. Blocking monoclonal antibody (mAb) to @entity7938 or @entity2937 both inhibited the MECLR, with anti- @entity2937 being much more effective than anti- @entity7938 . UVB radiation dose-dependently (100-200 J/m2) suppressed the culture-induced up-regulation of @entity7938 and @entity2937 on LC. Since LC exposed to the same UVB flux (UVB-LC) failed to stimulate alloreactive T cells in a MECLR, we questioned whether this was related to their inability to provide B7 co-stimulation. Indeed, when effective B7- @entity1361 signaling was ascertained by adding submitogenic doses of exogenous anti- @entity1361 mAb to UVB-LC, the proliferative response of alloreactive T cells was restored. We conclude that the suppressive effects of low-dose UVB radiation on the @entity1412 function of LC are, at least in part, due to an inhibition of functional @entity12750 expression.
