When human gammadelta lymphocytes bind to tumor cells for killing, they also strip their membrane for unknown reasons. Here we investigated this topic using the model of human gammadelta lymphocytes co-incubated with anaplastic large cell lymphomas, a group of tumors with cytolytic T or null lineage. By using flow cytometry and live cell imaging, we show that as soon as both cells were in contact, the TCR-mediated activation of gammadelta lymphocytes simultaneously triggered their secretion of lytic granules and stripping of lymphoma cell membranes, and both activities continued even after their cell death.
View Article and Find Full Text PDFAlthough gammadelta T cells express clonally distributed T-cell receptors (TCRs), a hallmark of adaptive immunity, they are classically considered as innate-like effectors, owing to the high frequency of preactivated gammadelta T cells, with restricted antigen recognition repertoire in particular tissue locations. Actually, such features are shared only by a fraction of gammadelta T-cell subsets located in the skin and reproductive organ mucosa in rodents or in peripheral blood in humans. By contrast, other gammadelta subsets, e.
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