DNAX accessory molecule‐1 (CD226) promotes human hepatocellular carcinoma cell lysis by Vγ9Vδ2 T cells

Toutirais, Olivier; Cabillic, Florian; Friec, Gaëlle Le; Salot, Samuel; Loyer, Pascal; Gallo, Matthieu Le; Desille, Mireille; Pintière, Cécile Thomas de La; Daniel, Pascale; Bouet, Françoise; Catros, Véronique

doi:10.1002/eji.200838409

Cited by 103 publications

(96 citation statements)

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“…Membraneexpression of CD16 leaves the possibility of antibody-dependent cellular cytotoxicity. 4,27,28 Another feature of gd T cells is their immunoregulatory function. As being an important early source of pro-inflammatory cytokines such as interferon (IFN)-g, TNF and interleukin (IL)-17, gd T cells support DC, T cell, B cell and stromal cell functions.…”

Section: Gd T Cells and Cancer Immunitymentioning

confidence: 99%

Empowering gamma delta T cells with antitumor immunity by dendritic cell-based immunotherapy

Anguille

et al. 2015

OncoImmunology

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These authors equally contributed to the work.Keywords: gd T cell, cancer, DC-mediated gd T cell activation, dendritic cell, immunotherapy Abbreviations: gd, gamma delta; BCG, Bacillus Calmette-Guerin; BrHPP, bromohydrin pyrophosphate; CTL, cytotoxic T lymphocyte; DC, dendritic cell; GM-CSF, granulocyte-macrophage colony-stimulating factor; HIV, human immunodeficiency virus; HMBPP, (E)-4-hydroxy-3-methyl-but-2-enyl pyrophosphate; iDC, immature DC; IFN, interferon; IL, interleukin; IPP, isopentyl pyrophosphate; mDC, myeloid dendritic cell; MHC, major histocompatibility complex; mo-DC, monocyte-derived dendritic cell; pDC, plasmacytoid dendritic cell; PD, programmed cell death protein; TCR, T-cell receptor; Th, T-helper cell; TLR, toll-like receptor; TNF, tumor necrosis factor; Treg, regulatory T cellGamma delta (gd) T cells are the all-rounders of our immune-system with their major histocompatibility complexunrestricted cytotoxicity, capacity to secrete immunostimulatory cytokines and ability to promote the generation of tumor antigen-specific CD8 C and CD4 C T cell responses. Dendritic cell (DC)-based vaccine therapy has the prospective to harness these unique features of the gd T cells in the fight against cancer. In this review, we will discuss our current knowledge on DC-mediated gd T cell activation and related opportunities for tumor immunologists.

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Section: Gd T Cells and Cancer Immunitymentioning

confidence: 99%

Empowering gamma delta T cells with antitumor immunity by dendritic cell-based immunotherapy

Anguille

et al. 2015

OncoImmunology

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“…NKG2D contributes to the cell lysis of target cells bearing the MHC class I-related chain A/B (MICA/B), UL16-binding protein (ULBP), and DNAM-1 binds the nectin-2 (CD112) and necl-5 (CD155) ligands. 10,13 The significant lytic abilities of Vc9Vd2 T cells were shown to be mediated primarily by the perforin degranulation pathway.…”

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confidence: 99%

Sensitization of ovarian carcinoma cells with zoledronate restores the cytotoxic capacity of Vγ9Vδ2 T cells impaired by the prostaglandin E2 immunosuppressive factor: Implications for immunotherapy

Lavoué

Cabillic

Toutirais

et al. 2011

Intl Journal of Cancer

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Epithelial ovarian cancer (EOC) usually spreads into the peritoneal cavity, thereby providing an opportunity for intraperitoneal adoptive immunotherapy with Vc9Vd2 T lymphocytes, a T cell subpopulation endowed with high lytic properties against tumor cells. However, previous studies have reported that Vc9Vd2 T cells fail to expand from peripheral blood mononuclear cells in one-third of patients with cancer. Here, from a cohort of 37 patients with EOC, a multiple correspondence analysis identified three populations, one of which was not suitable for Vc9Vd2 T-cell adoptive therapy. Interestingly, the ineligible patients were identified based on the frequency of Vc9Vd2 T cells in their peripheral blood and the patients' age. The average time to tumor recurrence was also found to be significantly different between the three populations, suggesting that the innate immune response is involved in EOC prognosis. A dramatic decrease in the lytic properties of Vc9Vd2 T cells occurred following incubation with ascitic supernatant and was found to be associated with reduced perforin/granzyme degranulation. Prostaglandin E2, but not IL-6, IL-10, VEGF or TGF-b, showed immunosuppressive effects in Vc9Vd2 T cells. Interestingly, our results emphasize that pretreating ovarian tumor cells with zoledronate partially reverses the immunosuppressive effects of ovarian cancer-associated ascites and restores a high level of lytic activity. These data sustain that optimal Vc9Vd2 T-cell adoptive immunotherapy previously requires counteracting the tumor immunosuppressive microenvironment. Altogether, our findings provide a rationale for clinically evaluating Vc9Vd2 T-cell adoptive immunotherapy with intraperitoneal carcinomatosis presensitization by zoledronate in patients with EOC.Epithelial ovarian cancer (EOC) is the fifth most frequent cancer among women and the fourth most common cause of cancer-related deaths among women.1 More than 70% of patients are diagnosed when the cancer has spread beyond the ovaries, and these patients have low median survival rates.2 The prognosis is poor, with a 5-year survival rate of only 30%, and the rate is less than 10% for patients with bulky residual disease remaining after surgery and chemotherapy, which emphasizes the need for innovative treatments.3 The inflammatory microenvironment of ovarian carcinomas prevents the maturation of myeloid cells, favors regulatory T-cell development and restrains the cytotoxic activity of effector T lymphocytes, leading to the escape of the tumor from the immune system. 4 Thus, research is ongoing to develop innovative approaches aimed at stimulating the immune system. 5 The preferential spread pattern of EOC in the peritoneal cavity offers an excellent opportunity for the regional administration of adoptive T-cell therapy.2 Some pilot trials have shown the feasibility of and promising

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“…Ces NKR sont également présents à la surface des cellules de l'immunité transitionnelle que sont les lymphocytes T. La molécule DNAM-1 est constitutivement exprimée par les cellules NK humaines [6] et les lymphocytes TV9V2 [24]. Elle interagit avec nectine-2 et Necl-5, et favorise ainsi la fonction cytolytique des cellules NK [25,26] (Figure 3).…”

Section: Rôle Des Nectines/nectines-like Dans Le Développement Tumoralunclassified

“…Pour les lymphocytes TV9V2, des expériences menées sur des lignées d'hépatocar-cinome ont révélé que l'engagement de DNAM-1 avec Necl-5 (mais pas avec nectine-2) participe aussi à leur capacité de reconnaissance et de lyse des cellules tumorales. L'engagement conjoint de DNAM-1 et de NKG2D potentialise la capacité lytique de ces cellules effectrices [24]. À la différence de DNAM-1, la molécule CRTAM ne s'exprime à la surface des lymphocytes T CD8, NK, NKT et TV9V2 qu'après leur activation.…”

Section: Rôle Des Nectines/nectines-like Dans Le Développement Tumoralunclassified

Les récepteurs de nectines/nectines-likeDNAM-1 et CRTAM

et al. 2014

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Historiquement, PVR (poliovirus receptor) (CD155), aujourd'hui dénommée nectine-like 5 (Necl-5), est la première molécule de la famille des nectines/nectines-like à avoir été caractérisée : c'est le récepteur d'entrée du poliovirus humain. Nectine-1 et nectine-2 ont été les premières nectines isolées, et leur rôle de récepteur dans l'internalisation des virus herpes simplex 1 et 2 a ensuite été démontré. Actuellement, quatre nectines (nectine-1 à -4) et cinq molécules apparentées aux nectines (Necl-1 à -5) ont été identifiées. Leur nomenclature est compliquée du fait que chaque nectine/nectine-like possède plusieurs appellations (voir pour revue [2]). Par exemple, nectine-1 est parfois appelée PRR1 (poliovirus receptor-related protein) ou HVEC (herpes virus entry mediator C). Il faut noter que nectine-4, aussi appelée PVLR4 (poliovirus-receptor-like 4), est éga-lement un des récepteurs d'entrée du virus de la rougeole [3]. Pour Necl-2, plusieurs appellations existent selon la situation biologique dans laquelle son expression a été recherchée : TSLC1 (tumor suppressor in lung cancer 1), IGSF4 (immunoglobulin superfamily member 4), Ra175, SglGSF (spermatogenic immunoglobulin superfamily), ou Syn-CAM1 (synaptic cell adhesion molecule 1). Toutes ces molécules ont une structure similaire ( Figure 1A). Les trois domaines de type Ig-like de la portion extracellulaire -un de type V et deux de type C2 -sont responsables des interactions homophiliques et hétérophiliques des nectines/nectines-like entre elles ou avec leurs ligands, ainsi que de leur dimérisation ( Figure 1B) Les nectines/nectines-like et leurs ligandsLes nectines et nectines-like (Necl) sont des molé-cules dont le nom vient du terme latin necto qui signifie connecter. Elles appartiennent à la superfamille des immunoglobulines (Ig) et ont été initialement décrites pour leur rôle dans les processus d'adhérence indépendants du Ca 2+ [1]. Ce sont des partenaires importants de la formation des jonctions cellulaires dans les tissus épithéliaux et elles participent éga-lement à la polarité cellulaire [2]. Leurs rôles dans la migration cellulaire, l'inhibition de contact, puis la prolifération et la différenciation ont été décrits secondairement. Récemment, la corrélation entre leur surexpression dans les tumeurs ou, au contraire, la perte de leur expression, et le pronostic de ces

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DNAX accessory molecule‐1 (CD226) promotes human hepatocellular carcinoma cell lysis by Vγ9Vδ2 T cells

Cited by 103 publications

References 30 publications

Empowering gamma delta T cells with antitumor immunity by dendritic cell-based immunotherapy

Empowering gamma delta T cells with antitumor immunity by dendritic cell-based immunotherapy

Sensitization of ovarian carcinoma cells with zoledronate restores the cytotoxic capacity of Vγ9Vδ2 T cells impaired by the prostaglandin E2 immunosuppressive factor: Implications for immunotherapy

Les récepteurs de nectines/nectines-likeDNAM-1 et CRTAM

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