Abstract
We studied the effects of ultraviolet B (UV-B) irradiation on cell-cell interactions using mouse lymphoma RMA cells and T cell hybridoma HTB-176.10. RMA cells act as stimulators by presenting H-2Kb surface antigens to HTB-176.10 cells, inducing IL-2 production in HTB-176.10 cells. Irradiating RMA cells with 1000J/m2 UV-B suppressed cell cluster formation between RMA and HTB-176.10 cells and reduced the level of IL-2 production in HTB-176.10 cells, although H-2Kb surface antigens of RMA cells were still expressed. Electron microscopic observations of irradiated RMA cells revealed that UV-B irradiation damaged cell structures, resulting in the disappearance of microvilli on the cell surface, destruction of mitochondria, vacuolation of cytoplasm and swelling of the perinuclear cisterna space. We found that these alterations were accompanied by polymerization of filamentous actin quantified by flow cytometry after NBD-phallacidin staining. Our results suggest that a target of UV-B-induced alterations is actin filaments, which support the cell morphology as the cytoskeleton, and that modification of filamentous actin inhibits interaction between RMA and HTB-176.10 cells. This underlying mechanism may account for the impaired interaction between antigen-presenting cells and T cells after transfusion with UV-B-irradiated allogeneic blood components.