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Cappuccio2006 - Cancer immunotherapy by interleukin-21

ABSTRACT: This model describes the effects of Il-21 on tumor eradication via natural killer cell-mediated and CD8+ T-cell-mediated lysis of tumor cells. The model demonstrates changes in growth dynamics in nonimmunogenic B16 melanoma and the immunogenic MethA and MCA205 fibrosarcomas, showing a strong dependence of the NK-cell/CD8+ T-cell balance on tumor immunogenicity.

SUBMITTER: Johannes Meyer

PROVIDER: BIOMD0000000761 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000761?filename=Cappuccio2006%20v2.0-biopax2.owl	Owl
	BIOMD0000000761?filename=Cappuccio2006%20v2.0-biopax3.owl	Owl
	BIOMD0000000761?filename=Cappuccio2006%20v2.0-matlab.m	Other
	BIOMD0000000761?filename=Cappuccio2006%20v2.0-octave.m	Other
	BIOMD0000000761?filename=Cappuccio2006%20v2.0.ode	Other

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Publications

Cancer immunotherapy by interleukin-21: potential treatment strategies evaluated in a mathematical model.

Cappuccio Antonio A Elishmereni Moran M Agur Zvia Z

Cancer research 20060701 14

The newly characterized interleukin (IL)-21 plays a central role in the transition from innate immunity to adaptive immunity and shows substantial tumor regression in mice. IL-21 is now developed as a cancer immunotherapeutic drug, but conditions for efficacious therapy, and the conflicting immunostimulatory and immunoinhibitory influence of the cytokine, are yet to be defined. We studied the effects of IL-21 on tumor eradication in a mathematical model focusing on natural killer (NK) cell-media ...[more]

PMID: 16849579

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NK cells propagate T cell immunity following in situ tumor vaccination

Project description:We report an in situ vaccination, adaptable to nearly any type of cancer, that combines radiotherapy targeting one tumor and intratumoral injection of this site with tumor-specific antibody and interleukin-2 (IL-2; 3xTx). In a phase I clinical trial, administration of 3xTx (with an immunocytokine fusion of tumor-specific antibody and IL-2, hu14.18-IL2) to subjects with metastatic melanoma increases peripheral CD8+ T cell effector polyfunctionality. This suggests the potential for 3xTx to promote antitumor immunity against metastatic tumors. In poorly immunogenic syngeneic murine melanoma or head and neck carcinoma models, 3xTx stimulates CD8+ T cell-mediated antitumor responses at targeted and non-targeted tumors. During 3xTx treatment, natural killer (NK) cells promote CTLA4+ regulatory T cell (Treg) apoptosis in non-targeted tumors. This is dependent on NK cell expression of CD86, which is upregulated downstream of KLRK1. NK cell depletion increases Treg infiltration, diminishing CD8+ T cell-dependent antitumor response. These findings demonstrate that NK cells sustain and propagate CD8+ T cell immunity following 3xTx

2023-12-21 | GSE209945 | GEO

Proteomics of immune cells from liver tumors reveals immunotherapy targets

Project description:Elucidating the mechanisms by which immune cells become dysfunctional in tumors is critical to developing next-generation immunotherapies. We profiled proteomes of cancer cells, monocyte/macrophages, CD4+ and CD8+ T cells, and NK cells isolated from tumors, liver, and blood of 48 patients with hepatocellular carcinoma. We found that tumor macrophages induce the sphingosine-1-phospate-degrading enzyme SGPL1, which dampened their inflammatory phenotype and anti-tumor function in vivo. We further discovered that the signaling scaffold protein AFAP1L2, typically only found in activated NK cells, is also upregulated in chronically stimulated CD8+ T cells in tumors. Ablation of AFAP1L2 in CD8+ T cells increased their viability upon repeated stimulation and enhanced their antitumor activity synergistically with PD-L1 blockade in mouse models. Our data revealed new targets for immunotherapy and provide a resource on immune cell proteomes in liver cancer (www.immunomics.ch/liver).

2023-04-19 | PXD040957 | Pride

A controlled trail of Autologous and umbilical cord blood cytokine-induced killer cells (U-CIKs) infusion on influence of the immune function in Advanced Cancer after Radiotherapy

Project description:Interventions: A:Autologous blood cytokine-induced killer cells;B:umbilical cord blood cytokine-induced killer cells;C:Routine treatment Primary outcome(s): NK cell population;CD4/CD8 ratio;Contents of plasma immunoglobulin Study Design: Non randomized control

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Breaking through NGF-TrkA immunosuppression in melanoma sensitizes immunotherapy for durable memory T cell protection [TCR-seq]

Project description:Melanomas are generated from melanocytes, the neural crest derivatives sharing a neuroectodermal origin with the nervous system. In investigating whether immune privilege of the nervous system might be exploited by melanoma, we found that nerve growth factor (NGF) exerts both melanoma cell-intrinsic and -extrinsic immunosuppression. In melanoma cells, autocrine NGF engages TrkA receptor to desensitize IFN-gammasignaling, leading to T and NK cell exclusion. In effector T cells, which upregulate surface TrkA expression upon T cell receptor (TCR) activation, paracrine NGF dampens TCR signaling and effector function. Targeting NGF genetically or pharmacologically with larotrectinib sensitizes melanoma responsiveness to immune checkpoint blockade (ICB) therapy for tumor eradication and induces durable protection by eliciting robust memory of low-affinity T cells. Together, these findings uncover a comprehensive mechanism through which the NGF-TrkA axis suppresses anti-tumor T cell immunity, thus providing a novel mode of action to repurpose larotrectinib for immune sensitization. Moreover, by enlisting low-affinity tumor-specific T cells, anti-NGF reduces acquired resistance to ICB therapy and prevents melanoma recurrence.

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Breaking through NGF-TrkA immunosuppression in melanoma sensitizes immunotherapy for durable memory T cell protection [scRNA-Seq]

2023-11-02 | GSE236680 | GEO

Breaking through NGF-TrkA immunosuppression in melanoma sensitizes immunotherapy for durable memory T cell protection [RNA-Seq 1]

Project description:Melanomas are generated from melanocytes, the neural crest derivatives sharing a neuroectodermal origin with the nervous system. In investigating whether immune privilege of the nervous system might be exploited by melanoma, we found that nerve growth factor (NGF) exerts both melanoma cell-intrinsic and -extrinsic immunosuppression. In melanoma cells, autocrine NGF engages TrkA receptor to desensitize IFN-gamma signaling, leading to T and NK cell exclusion. In effector T cells, which upregulate surface TrkA expression upon T cell receptor (TCR) activation, paracrine NGF dampens TCR signaling and effector function. Targeting NGF genetically or pharmacologically with larotrectinib sensitizes melanoma responsiveness to immune checkpoint blockade (ICB) therapy for tumor eradication and induces durable protection by eliciting robust memory of low-affinity T cells. Together, these findings uncover a comprehensive mechanism through which the NGF-TrkA axis suppresses anti-tumor T cell immunity, thus providing a novel mode of action to repurpose larotrectinib for immune sensitization. Moreover, by enlisting low-affinity tumor-specific T cells, anti-NGF reduces acquired resistance to ICB therapy and prevents melanoma recurrence.

2023-11-02 | GSE236673 | GEO

Breaking through NGF-TrkA immunosuppression in melanoma sensitizes immunotherapy for durable memory T cell protection [RNA-Seq 2]

2023-11-02 | GSE236674 | GEO

Transcription profiling of mouse NK cells in presence/absence of activated CD8 T cells

Project description:we compare NK cells in presence of activated CD8 T cells or not. Although both natural killer (NK) cells and CD8 T cells are capable of anti-tumor responses, Recombinase Activating Gene (RAG)-deficient mice, which have a normal component of NK cells, are incapable of rejecting the P815 mastocytoma tumor. We established a model where monoclonal CD8 T cell reactivity was restricted to the tumor antigen (Ag) P1A expressed on the P815 mastocytoma. Reconstitution of the RAG-deficient mice with these (TCRP1A) T cells conferred resistance to tumor growth selectively for the P1A-expressing, but not for a P1A-negative variant of P815. Nevertheless, TCRP1A CD8 T cells were efficient and necessary to promote the NK cell dependent rejection of P1A-negative tumors when both P1A-positive and -negative tumors were present at the same site. Gene expression profiling in NK cells infiltrating the P1A-positive, as compared to the P1A-negative tumor, in mice transferred with TCRP1A CD8 T cells established their acquisition of an activated effector phenotype. Help from CD8 T cells was provided locally, as it did not induce activation of NK cells present in a P1A-negative variant at a distant site, nor the rejection of this variant. These results illustrate a mechanism by which, in the face of immunoselection / editing, the synergy between specific anti-tumor Ag T cells and NK cells can contribute to the elimination of tumor cells whether or not they express the tumor Ag. This mechanism appears ineffective, however, once tumor variants lacking the tumor Ag are separated from the wild-type tumor, as would be the case in tumor metastasis.

2007-11-01 | E-MEXP-1284 | biostudies-arrayexpress

Multi-center clincal study of umbilical cord blood cytokine-induced killer cells (U-CIKs) infusion on influence of the immune function in Advanced Cancer after Chemotherapy

Project description:Interventions: A:umbilical cord blood cytokine-induced killer cells;B:Routine radiotherapy Primary outcome(s): NK cell population;CD4/CD8 ratio;Contents of plasma immunoglobulin Study Design: Non randomized control

| 2669506 | ecrin-mdr-crc

Transcription profiling of mouse CD8 T cells in response to P1A antigen expressing tumor cells or cells not expressing 1A antigen

Project description:Activation status of CD8 T cells in response to a tumor challenge. Although both natural killer (NK) cells and CD8 T cells are capable of anti-tumor responses, Recombinase Activating Gene (RAG)-deficient mice, which have a normal component of NK cells, are incapable of rejecting the P815 mastocytoma tumor. We established a model where monoclonal CD8 T cell reactivity was restricted to the tumor antigen (Ag) P1A expressed on the P815 mastocytoma. Reconstitution of the RAG-deficient mice with these (TCRP1A) T cells conferred resistance to tumor growth selectively for the P1A-expressing, but not for a P1A-negative variant of P815. Nevertheless, TCRP1A CD8 T cells were efficient and necessary to promote the NK cell dependent rejection of P1A-negative tumors when both P1A-positive and -negative tumors were present at the same site. Gene expression profiling in NK cells infiltrating the P1A-positive, as compared to the P1A-negative tumor, in mice transferred with TCRP1A CD8 T cells established their acquisition of an activated effector phenotype. Help from CD8 T cells was provided locally, as it did not induce activation of NK cells present in a P1A-negative variant at a distant site, nor the rejection of this variant. These results illustrate a mechanism by which, in the face of immunoselection / editing, the synergy between specific anti-tumor Ag T cells and NK cells can contribute to the elimination of tumor cells whether or not they express the tumor Ag. This mechanism appears ineffective, however, once tumor variants lacking the tumor Ag are separated from the wild-type tumor, as would be the case in tumor metastasis.

2007-12-01 | E-MEXP-1285 | biostudies-arrayexpress

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