2005
DOI: 10.1074/jbc.m409752200
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Galectin-1 Sensitizes Resting Human T Lymphocytes to Fas (CD95)-mediated Cell Death via Mitochondrial Hyperpolarization, Budding, and Fission

Abstract: Galectins have emerged as a novel family of immunoregulatory proteins implicated in T cell homeostasis. Recent studies showed that galectin-1 (Gal-1) plays a key role in tumor-immune escape by killing antitumor effector T cells. Here we found that Gal-1 sensitizes human resting T cells to Fas (CD95)/caspase-8-mediated cell death. Furthermore, this protein triggers an apoptotic program involving an increase of mitochondrial membrane potential and participation of the ceramide pathway. In addition, Gal-1 induces… Show more

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Cited by 161 publications
(159 citation statements)
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“…In addition, it was shown that, although Gal-1 induces apoptosis of 2-d Con A-activated T cells, it promotes the survival of resting T cells without inducing proliferation (32). In contrast to our observations and those from other investigators, Matarrese et al (33) observed that Gal-1 sensitized human resting T lymphocytes to Fas-mediated cell death and that, at high doses, it was capable of inducing apoptosis in these primary cells. Discrepancies might reflect the different species used (human versus mouse), different protein preparations, or the method used to assess cell death, because phosphati-dylserine exposure is not necessarily associated with Gal-induced apoptosis (34).…”
Section: Discussioncontrasting
confidence: 92%
“…In addition, it was shown that, although Gal-1 induces apoptosis of 2-d Con A-activated T cells, it promotes the survival of resting T cells without inducing proliferation (32). In contrast to our observations and those from other investigators, Matarrese et al (33) observed that Gal-1 sensitized human resting T lymphocytes to Fas-mediated cell death and that, at high doses, it was capable of inducing apoptosis in these primary cells. Discrepancies might reflect the different species used (human versus mouse), different protein preparations, or the method used to assess cell death, because phosphati-dylserine exposure is not necessarily associated with Gal-induced apoptosis (34).…”
Section: Discussioncontrasting
confidence: 92%
“…Even though the signaling pathways responsible for exGal-1 driven T-cell apoptosis have largely been mapped [6,7,[36][37][38], many questions about the exact mechanism by which the cells were sensitized by inGal-1 to exGal-1 mediated apoptosis remain to be elucidated. While the anti-apoptotic effect of intracellular Gal-3 can be explained by the Bcl-2 homolog motif of the protein [39], Gal-1 does not have a homologous segment with any known apoptotic protein, and thus its function in apoptosis must stem from a yet unknown mechanism.…”
Section: Discussionmentioning
confidence: 99%
“…37 In particular, overexpression of the human fission protein hFis1, an integral protein of the outer mitochondrial membrane, triggers fission of mitochondria, Cyt c release and subsequent apoptosis. 18,38 Furthermore, Bax colocalizes at mitochondrial fission sites early in the apoptotic process, 39 linking proapoptotic members of the Bcl-2 family to the mitochondrial fission and fusion machinery. Thus, we analyzed the presence and the possible interaction of hFis1 with mitochondrial lipid microdomains.…”
Section: Discussionmentioning
confidence: 99%
“…17 Among these, h-Fis seems to play a key role. 17,18 This was described as an integral protein of the outer mitochondrial membrane participating to the membrane scission events. Members of the sphingomyelin pathway seem to have a profound influence on the apoptotic cascade, including these mitochondrial changes.…”
Section: Introductionmentioning
confidence: 99%