Modeling immunotherapy of the tumor – immune interaction

被引:10
|
作者
Denise Kirschner
John Carl Panetta
机构
[1] Department of Microbiology and Immunology,
[2] The University of Michigan Medical School,undefined
[3] Ann Arbor,undefined
[4] MI 48109-0620,undefined
[5] USA,undefined
[6] School of Science,undefined
[7] Penn State Erie,undefined
[8] The Behrend College,undefined
[9] Station Road,undefined
[10] Erie,undefined
[11] PA 16563-0203,undefined
[12] USA. e-mail: panetta@wagner.bd.psu.edu,undefined
来源
关键词
Key words: Immunotherapy; Tumor; Cytokine; Modeling; Interleukin-2; Ordinary differential equations;
D O I
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中图分类号
学科分类号
摘要
 A number of lines of evidence suggest that immunotherapy with the cytokine interleukin-2 (IL-2) may boost the immune system to fight tumors. CD4+ T cells, the cells that orchestrate the immune response, use these cytokines as signaling mechanisms for immune-response stimulation as well as lymphocyte stimulation, growth, and differentiation. Because tumor cells begin as ‘self’, the immune system may not respond in an effective way to eradicate them. Adoptive cellular immunotherapy can potentially restore or enhance these effects. We illustrate through mathematical modeling the dynamics between tumor cells, immune-effector cells, and IL-2. These efforts are able to explain both short tumor oscillations in tumor sizes as well as long-term tumor relapse. We then explore the effects of adoptive cellular immunotherapy on the model and describe under what circumstances the tumor can be eliminated.
引用
收藏
页码:235 / 252
页数:17
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