Involvement of the intrinsic and extrinsic cell‐death pathways in the induction of apoptosis of mature lymphocytes by the Escherichia coli heat‐labile enterotoxin |
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| Authors: | Esther Tamayo Jorge Postigo Giuseppe Del Giudice Rino Rappuoli Adalberto Benito Hideo Yagita Ramón Merino Jesús Merino |
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| Affiliation: | 1. Department of Molecular Biology, University of Cantabria, Santander, Spain;2. Novartis Vaccines and Diagnostics, Siena, Italy;3. Research Unit and Nephrology, IFIMAV, Hospital Universitario Marqués de Valdecilla, Santander, Spain;4. Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan;5. Instituto de Biomedicina y Biotecnología de Cantabria, Consejo Superior de Investigaciones Científicas‐Universidad de Cantabria‐IDICAN, Santander, Spain |
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| Abstract: | Escherichia coli heat‐labile enterotoxin (LT) exhibits a broad range of immunomodulatory activities, including the induction of lymphocyte‐programmed cell death. In previous studies, we have demonstrated that in vivo LT promotes apoptosis of immature T and B cells through the stimulation of endogenous glucocorticoids. In the present study, we show that the extrinsic cell‐death pathway as well as the apoptosis‐inducing factor do not participate in the LT‐induced elimination of thymocytes. In contrast to developing lymphocytes, LT promotes the death of mature lymphocytes by both glucocorticoid‐ and Fas death receptor/Fas ligand‐dependent mechanisms. However, the dependency of these mechanisms in the LT‐induced cell‐death activity seems to be different among CD4+ and CD8+ T cells. Altogether, our study shows that the same bacterial toxin can induce apoptosis of lymphoid cells through several mechanisms depending on the status of differentiation of these cells. |
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| Keywords: | Apoptosis Bcl‐2 Escherichia coli heat‐labile enterotoxin Fas Glucocorticoids |
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