Despite highly developed specific immune responses, tumour cells often manage to escape recognition by the immune system, continuing to grow uncontrollably. Experimental work suggests that mature myeloid cells may be central to the activation of the specific immune response. Recognition and subsequent control of tumour growth by the cells of the specific immune response depend on the balance between immature (ImC) and mature (MmC) myeloid cells in the body. However, tumour cells produce cytokines that inhibit ImC maturation, altering the balance between ImC and MmC. Hence, the focus of this manuscript is on the study of the potential role of this inhibiting mechanism on tumour growth dynamics. A conceptual predator-prey type model that incorporates the dynamics and interactions of tumour cells, CD8+ T cells, ImC and MmC is proposed in order to address the role of this mechanism. The prey (tumour) has a defence mechanism (blocking the maturation of ImC) that prevents the predator (immune system) from recognizing it. The model, a four-dimensional nonlinear system of ordinary differential equations, is reduced to a twodimensional system using time-scale arguments that are tied to the maturation rate of ImC. Analysis shows that the model is capable of supporting biologically reasonable patterns of behaviour depending on the initial conditions.A range of parameters, where healing without external influences can occur, is identified both qualitatively and quantitatively. Â\copyright 2010 Taylor & Francis.
Cancer; Immune system; Myeloid cells; Predator-prey; Time scales
issn
17513758
correspondence_address1
Kareva, I.; Computational Modeling Sciences Center, Arizona State University, P.O. Box 871904, Tempe, AZ 85287, United States; email: ikareva@asu.edu
affiliation
Computational Modeling Sciences Center, Arizona State University, P.O. Box 871904, Tempe, AZ 85287, United States; Department of Mathematics, Howard University, Washington, DC 20895, United States; School of Human Evolution and Social Changes, Arizona State University, Tempe, AZ 85287, United States; School of Mathematics and Statistics, Arizona State University, Tempe, AZ 85287, United States; Santa Fe Institute, 1399 Hyde Park Road, Santa Fe, NM 87501, United States
%0 Journal Article
%1 Kareva2010315
%A Kareva, I.
%A Berezovskaya, F.
%A Castillo-Chavez, C.
%D 2010
%J Journal of Biological Dynamics
%K Cell Cells; Communication; Differentiation; Humans; Immunological; Models, Myeloid Neoplasms article; biological bone cell cell; communication; differentiation; human; immunology; marrow model; neoplasm; pathology,
%N 4
%P 315-327
%R http://dx.doi.org/10.1080/17513750903261281
%T Myeloid cells in tumour-immune interactions
%U http://dx.doi.org/10.1080/17513750903261281
%V 4
%X Despite highly developed specific immune responses, tumour cells often manage to escape recognition by the immune system, continuing to grow uncontrollably. Experimental work suggests that mature myeloid cells may be central to the activation of the specific immune response. Recognition and subsequent control of tumour growth by the cells of the specific immune response depend on the balance between immature (ImC) and mature (MmC) myeloid cells in the body. However, tumour cells produce cytokines that inhibit ImC maturation, altering the balance between ImC and MmC. Hence, the focus of this manuscript is on the study of the potential role of this inhibiting mechanism on tumour growth dynamics. A conceptual predator-prey type model that incorporates the dynamics and interactions of tumour cells, CD8+ T cells, ImC and MmC is proposed in order to address the role of this mechanism. The prey (tumour) has a defence mechanism (blocking the maturation of ImC) that prevents the predator (immune system) from recognizing it. The model, a four-dimensional nonlinear system of ordinary differential equations, is reduced to a twodimensional system using time-scale arguments that are tied to the maturation rate of ImC. Analysis shows that the model is capable of supporting biologically reasonable patterns of behaviour depending on the initial conditions.A range of parameters, where healing without external influences can occur, is identified both qualitatively and quantitatively. Â\copyright 2010 Taylor & Francis.
@article{Kareva2010315,
abstract = {Despite highly developed specific immune responses, tumour cells often manage to escape recognition by the immune system, continuing to grow uncontrollably. Experimental work suggests that mature myeloid cells may be central to the activation of the specific immune response. Recognition and subsequent control of tumour growth by the cells of the specific immune response depend on the balance between immature (ImC) and mature (MmC) myeloid cells in the body. However, tumour cells produce cytokines that inhibit ImC maturation, altering the balance between ImC and MmC. Hence, the focus of this manuscript is on the study of the potential role of this inhibiting mechanism on tumour growth dynamics. A conceptual predator-prey type model that incorporates the dynamics and interactions of tumour cells, CD8+ T cells, ImC and MmC is proposed in order to address the role of this mechanism. The prey (tumour) has a defence mechanism (blocking the maturation of ImC) that prevents the predator (immune system) from recognizing it. The model, a four-dimensional nonlinear system of ordinary differential equations, is reduced to a twodimensional system using time-scale arguments that are tied to the maturation rate of ImC. Analysis shows that the model is capable of supporting biologically reasonable patterns of behaviour depending on the initial conditions.A range of parameters, where healing without external influences can occur, is identified both qualitatively and quantitatively. {\^A}{\copyright} 2010 Taylor & Francis.},
added-at = {2017-11-10T22:48:29.000+0100},
affiliation = {Computational Modeling Sciences Center, Arizona State University, P.O. Box 871904, Tempe, AZ 85287, United States; Department of Mathematics, Howard University, Washington, DC 20895, United States; School of Human Evolution and Social Changes, Arizona State University, Tempe, AZ 85287, United States; School of Mathematics and Statistics, Arizona State University, Tempe, AZ 85287, United States; Santa Fe Institute, 1399 Hyde Park Road, Santa Fe, NM 87501, United States},
author = {Kareva, I. and Berezovskaya, F. and Castillo-Chavez, C.},
author_keywords = {Cancer; Immune system; Myeloid cells; Predator-prey; Time scales},
biburl = {https://www.bibsonomy.org/bibtex/29ee63fc1092c2576b53faba676a3ebd6/ccchavez},
correspondence_address1 = {Kareva, I.; Computational Modeling Sciences Center, Arizona State University, P.O. Box 871904, Tempe, AZ 85287, United States; email: ikareva@asu.edu},
date-added = {2017-11-10 21:45:26 +0000},
date-modified = {2017-11-10 21:45:26 +0000},
document_type = {Article},
doi = {http://dx.doi.org/10.1080/17513750903261281},
interhash = {a84ccc73582e01bef8df7ee1eccc25e5},
intrahash = {9ee63fc1092c2576b53faba676a3ebd6},
issn = {17513758},
journal = {Journal of Biological Dynamics},
keywords = {Cell Cells; Communication; Differentiation; Humans; Immunological; Models, Myeloid Neoplasms article; biological bone cell cell; communication; differentiation; human; immunology; marrow model; neoplasm; pathology,},
language = {English},
number = 4,
pages = {315-327},
pubmed_id = {22881128},
timestamp = {2017-11-10T22:48:29.000+0100},
title = {Myeloid cells in tumour-immune interactions},
url = {http://dx.doi.org/10.1080/17513750903261281},
volume = 4,
year = 2010
}