FAS FAS LIGAND INTERACTIONS ARE INVOLVED IN ULTRAVIOLET-B-INDUCED HUMAN LYMPHOCYTE APOPTOSIS/

We wondered whether the apoptosis known to occur after UV-B irradiatio n might involve the Fas/Fas ligand (FasL) signaling pathway. We expose d PBLs from normal individuals, and also the Jurkat (E6-1) and U937 ce ll lines, to graded doses of UV-B irradiation and observed a prompt an d marked increase in Fas expression at doses as low as 0.5 mJ/cm(2). I ncreased Fas expression did not require new protein synthesis, since c ycloheximide-treated cells also showed an increase in Fas after UV-B. UV-B-irradiated cells cultured in the presence of zinc showed inhibiti on of apoptosis coincident with a marked increase in Fas(+) cells, app arently indicating the accumulation of Fas-bearing cells unable to und ergo apoptosis, After UV-B irradiation, PBLs showed increased expressi on of Fas ligand; the E6-1 lymphocytic cell line also released soluble Fast. UV-B induced apoptosis could be partially blocked by neutralizi ng Fast Abs, and a Fast-resistant variant of E6-1 cell line showed red uced apoptosis after UV-B irradiation, implying that the increase in F as expression signified a role for Fas in UV-induced apoptosis, UV-ind uced Fas expression may serve to target stress-injured cells for remov al by Fast-bearing cells or by Fast produced by the cells themselves i n response to the stimuli, and may represent a general function of the Fas/FasL pathway in facilitating the apoptosis and elimination of und esirable or harmful cells.