BioModels

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.

• Modeling anti-tumor Th1 and Th2 immunity in the rejection of melanoma.
• Eftimie R, Bramson JL, Earn DJ
• Journal of theoretical biology , 8/ 2010 , Volume 265 , Issue 3 , pages: 467-480 , PubMed ID: 20450922
Affiliation: Department of Mathematics and Statistics, McMaster University, Hamilton, ON, Canada L8S 4K1. reftimie@math.mcmaster.ca
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-gamma and TNF-alpha. Our simulations suggest that novel strategies to enhance eosinophil recruitment into skin tumors may improve cancer immunotherapies.