Modulation of CD8+ T-cell activation events by monocytic and granulocytic myeloid-derived suppressor cells

Schouppe, Elio; Overmeire, Eva Van; Laoui, Damya; Keirsse, Jiri; Ginderachter, Jo A. Van

doi:10.1016/j.imbio.2013.07.003

Cited by 42 publications

(33 citation statements)

References 77 publications

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“…These observations clearly show that rapamycin not only inhibited the recruitment of CD8 þ T cells and CD4 þ T eff s to the tumor site but also enhanced the accumulation of MDSC known to inhibit the cytotoxic CD8 þ T-cell response (23), thus favoring the escape from antitumor immune responses.…”

Section: Chronic Treatment With Rapamycin Inhibits Cyaa-e7 Vaccineindmentioning

confidence: 69%

“…Rapamycin treatment also inhibits the induction of antigen-specific cytotoxic CD8 þ T-cell responses, thus completely abrogating the vaccine-induced tumor eradication. Furthermore, rapamycin favors the intratumoral recruitment of MDSC, known to inhibit cytotoxic CD8 þ T cells (23), thus further contributing to the suppression of the antitumor immune response. Therefore, we clearly establish that although rapamycin might act directly on tumor cells and inhibit their proliferation, in our experimental model, rapamycin also inhibits T-cell recruitment to the tumor site and the induction of antitumor immune response by the CyaA-E7 vaccine.…”

Section: Discussionmentioning

confidence: 99%

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Rapamycin Impairs Antitumor CD8+ T-cell Responses and Vaccine-Induced Tumor Eradication

et al. 2015

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The metabolic sensor mTOR broadly regulates cell growth and division in cancer cells, leading to a significant focus on studies of rapamycin and its analogues as candidate anticancer drugs. However, mTOR inhibitors have failed to produce useful clinical efficacy, potentially because mTOR is also critical in T cells implicated in immunosurveillance. Indeed, recent studies using rapamycin have demonstrated the important role of mTOR in differentiation and induction of the CD8 þ memory in T-cell responses associated with antitumor properties.

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Section: Chronic Treatment With Rapamycin Inhibits Cyaa-e7 Vaccineindmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Rapamycin Impairs Antitumor CD8+ T-cell Responses and Vaccine-Induced Tumor Eradication

et al. 2015

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“…We thus identified a population of CD45 + collagen type 1 + CD34 − cells that were 2.3‐fold higher in COPD, compared to controls, with a CD14 − HLA‐DR − CD15 + CD66b + phenotype that resembled adult blood‐derived MDSC‐like fibrocytes, probably mononuclear PMN‐MDSC . Myeloid‐derived suppressor cells, defined by their immunosuppressive effect on T‐cell proliferation , are heterogeneous cells that copurify with PBMCs following density gradient centrifugation and it has been shown that the CD14 − , HLA‐DR − , CD33 + CD11b + phenotype (collagen type 1 was not measured) is increased in COPD blood . Our identification is based on few markers, but we have shown in a subset of control and COPD patients (Fig.…”

Section: Discussionmentioning

confidence: 98%

Myeloid-derived suppressor cell-like fibrocytes are increased and associated with preserved lung function in chronic obstructive pulmonary disease

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Hartley

et al. 2016

Allergy

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“…The anti-apoptotic effect of IL-17 was blocked when MDSCs were treated with ERK1/2 inhibitor. Arg-1 and iNOS are both highly expressed in MDSCs derived from tumor bearing mice [37]. NO generated from iNOS can suppress T cell function and Arg-1 depletes from T cell amino acid L-arginine to inhibit T cell function.…”

Section: Discussionmentioning

confidence: 99%

IL-17A weakens the antitumor immuity by inhibiting apoptosis of MDSCs in Lewis lung carcinoma bearing mice

et al. 2016

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Myeloid-derived suppressor cells (MDSCs) weaken the antitumor immune response through the inhibition of effector T cell activity and the production of immunosuppressive factors in pathological sites. It is well established that interleukin-17A (IL-17A) has a remarkable role on the promotion of inflammation and tumor formation, and IL-17 has been implicated in the enhancement of immunosuppression of MDSCs, which consequently promotes tumor progression. A detailed study of this relationship remains elusive. In our study, we not only confirmed the promotion of IL-17 on Lewis lung carcinoma (LLC) development but also surprisingly showed that IL-17 could extend the fate and enhance the immunosuppressive effect of MDSCs through activating ERK1/2. Additionally, the effect of IL-17 on MDSCs was reversed, even in tumors by blocking ERK1/2. Interdicting the signaling molecule ERK1/2 could increase the apoptosis of MDSCs and weaken the suppressive activity of MDSCs, so that thereafter, the antitumor immunity could be restored partly. Therefore, these findings offer new insights into the importance of IL-17 and the downstream signaling factor ERK1/2 for MDSCs.

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Modulation of CD8+ T-cell activation events by monocytic and granulocytic myeloid-derived suppressor cells

Cited by 42 publications

References 77 publications

Rapamycin Impairs Antitumor CD8+ T-cell Responses and Vaccine-Induced Tumor Eradication

Rapamycin Impairs Antitumor CD8+ T-cell Responses and Vaccine-Induced Tumor Eradication

Myeloid-derived suppressor cell-like fibrocytes are increased and associated with preserved lung function in chronic obstructive pulmonary disease

IL-17A weakens the antitumor immuity by inhibiting apoptosis of MDSCs in Lewis lung carcinoma bearing mice

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