FAILED ANTIGEN PRESENTATION AFTER UVB RADIATION CORRELATES WITH MODIFICATIONS OF LANGERHANS CELL CYTOSKELETON

Acute low-dose ultraviolet B radiation (UVR) impairs contact hypersens itivity (CH) induction in genetically defined strains of mice by a mec hanism triggered by cis-urocanic acid (UCA) and dependent upon tumor n ecrosis factor-alpha (TNF-alpha), UVR, TNF-alpha, and cis-UCA cause si milar morphologic changes among Langerhans cells, which spawns the spe culation that UVR impairs CH induction in part by altering the Langerh ans cell cytoskeleton, To examine this speculation, we studied the exp ression of vimentin in Langerhans cells after treatment with UVR, TNF- alpha, and cis-UCA, All treatments caused a reduction in expression of vimentin within the cytoplasm of Langerhans cells, Because partial lo ss of detectable vimentin may correlate with cytoskeletal disruption, we evaluated the effects of vinblastine, an agent that disrupts the cy toskeleton by disassembling microtubules, on Langerhans cell density a nd morphology, Epicutaneous treatment with vinblastine caused a reduct ion in Langerhans cell density, a loss of dendrites, and a reduction i n vimentin expression, When dinitrofluorobenzene was painted on vinbla stine-treated skin of BALB/c or C3H/HeN mice, only feeble CH was induc ed, Consequently, we propose that UVR prevents CH induction in suscept ible mice by disrupting the cytoskeleton of Langerhans cells, thereby preventing them from carrying out their crucial role as antigen-presen ting cells.