Dataset Information

Eftimie2010 - immunity to melanoma

ABSTRACT: The paper describes a model of immunity to melanoma. Created by COPASI 4.25 (Build 207) This model is described in the article: Modeling anti-tumor Th1 and Th2 immunity in the rejection of melanoma Raluca Eftimie, Jonathan L. Bramson, David J.D. Earn Journal of Theoretical Biology 265 (2010) 467–480 Abstract: Recent experiments indicate that CD4+ Th2 cells can reject skin tumors in mice, while CD4+ Th1 cells cannot (Mattes et al., 2003; Zhang et al., 2009). These results are surprising because CD4+ Th1 cells are typically considered to be capable of tumor rejection. We used mathematical models to investigate this unexpected outcome. We found that neither CD4+ Th1 nor CD4+ Th2 cells could eliminate the cancer cells when acting alone, but that tumor elimination could be induced by recruitment of eosinophils by the Th2 cells. These recruited eosinophils had unexpected indirect effects on the decay rate of type 2 cytokines and the rate at which Th2 cells are inactivated through interactions with cancer cells. Strikingly, the presence of eosinophils impacted tumor growth more significantly than the release of tumor-suppressing cytokines such as IFN-g and TNF-a. Our simulations suggest that novel strategies to enhance eosinophil recruitment into skin tumors may improve cancer immunotherapies. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

SUBMITTER: Jinghao Men

PROVIDER: BIOMD0000000768 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000768?filename=Eftimie2010.cps	Other
	BIOMD0000000768?filename=Eftimie2010.sedml	Other
	BIOMD0000000768?filename=Eftimie2010.xml	Xml

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Publications

Modeling anti-tumor Th1 and Th2 immunity in the rejection of melanoma.

Eftimie Raluca R Bramson Jonathan L JL Earn David J D DJ

Journal of theoretical biology 20100505 3

Recent experiments indicate that CD4(+) Th2 cells can reject skin tumors in mice, while CD4(+) Th1 cells cannot (Mattes et al., 2003; Zhang et al., 2009). These results are surprising because CD4(+) Th1 cells are typically considered to be capable of tumor rejection. We used mathematical models to investigate this unexpected outcome. We found that neither CD4(+) Th1 nor CD4(+) Th2 cells could eliminate the cancer cells when acting alone, but that tumor elimination could be induced by recruitment ...[more]

PMID: 20450922

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Project description:The paper describes a model of interaction of Th cells and macrophage in melanoma. Created by COPASI 4.25 (Build 207) This model is described in the article: Modelling and investigation of the CD4 T cells – Macrophages paradox in melanoma immunotherapies Raluca Eftimie, Haneen Hamam Journal of Theoretical Biology 420 (2017) 82–104 Abstract: It is generally accepted that tumour cells can be eliminated by M1 anti-tumour macrophages and CD8+ T cells. However, experimental results over the past 10–15 years have shown that B16 mouse melanoma cells can be eliminated by the CD4+ T cells alone (either Th1 or Th2 sub-types), in the absence of CD8+ T cells. In some studies, elimination of B16 melanoma was associated with a Th1 immune response (i.e., elimination occurred in the presence of cytokines produced by Th1 cells), while in other studies melanoma elimination was associated with a Th2 immune response (i.e., elimination occurred in the presence of cytokines produced by Th2 cells). Moreover, macrophages have been shown to be present inside the tumours, during both Th1 and Th2 immune responses. To investigate the possible biological mechanisms behind these apparently contradictory results, we develop a class of mathematical models for the dynamics of Th1 and Th2 cells, and M1 and M2 macrophages in the presence/absence of tumour cells. Using this mathematical model, we show that depending on the re- polarisation rates between M1 and M2 macrophages, we obtain tumour elimination in the presence of a type-I immune response (i.e., more Th1 and M1 cells, compared to the Th2 and M2 cells), or in the presence of a type- II immune response (i.e., more Th2 and M2 cells). Moreover, tumour elimination is also possible in the presence of a mixed type-I/type-II immune response. Tumour growth always occurs in the presence of a type-II immune response, as observed experimentally. Finally, tumour dormancy is the result of a delicate balance between the pro-tumour effects of M2 cells and the anti-tumour effects of M1 and Th1 cells. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.