FIG. 5.

Role of the Fas/FasL-mediated death pathway in the proinflammatory effect of γδT cells. (A and B) Agonistic anti-Fas antibody was used to specifically determine if γδT cells are capable of promoting acute liver damage via the Fas-mediated death pathway. WT and γδT-cell KO mice were administered the agonistic anti-Fas antibody Jo2 (0.5 μg/g body weight; intraperitoneally), and acute liver injury (i.e., ALT levels and histology) was assessed 3.5 h later. Data are presented as means ± SEM (n = 4 to 7 mice per group; *, P ≤ 0.05 versus WT mice). Photomicrograph of H&E-stained representative liver sections depicting diffuse and severe acute liver failure (inflammation and widespread hepatocellular necrosis with numerous apoptosis) in Jo2-treated WT mice compared with patchy necrosis and reduced inflammation in a liver sections from γδT-cell KO mice administered Jo2. Original magnification, ×200. (C) C57BL/6 mice were administered vehicle or AdLacZ, and hepatic lymphoid cells were isolated from these mice 6 days after infectivity. Isolated hepatic lymphoid cells were initially stained with fluorochrome-labeled TCRγδ and CD3 MAbs to identify γδT cells and then stained with fluorochrome-labeled FasL MAb to determine FasL cell surface expression on hepatic γδT cells. A representative FACS histogram demonstrating extracellular FasL expression on γδT cells after AdLacZ administration is depicted.