TY - JOUR
T1 - Myeloid cells in tumour-immune interactions
AU - Kareva, Irina
AU - Berezovskaya, Faina
AU - Castillo-Chavez, Carlos
N1 - Funding Information:
The work is based on a technical report, written at the Mathematical and Theoretical Biology Institute during summer 2006: [D., Chowell, Kareva, I., Torre, R., Mubayi, A., Berezovsky, F., Castillo-Chavez, C. The Role of Myleoid Cells in Cancer–Immune System Interactions, MTBI Technical Reports, Arizona State University, 2006]. The authors would like to thank John Nagy, Yang Kuang, Baojun Song for their invaluable discussions and comments. This project has been partially supported by grants from the National Science Foundation (NSF-Grant DMS-0502349), the National Security Agency (NSA-Grant H98230-06-1-0097), the Alfred T. Sloan Foundation and the Office of the Provost of Arizona State University.
PY - 2010/7
Y1 - 2010/7
N2 - 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.
AB - 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.
KW - Cancer
KW - Immune system
KW - Myeloid cells
KW - Predator-prey
KW - Time scales
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U2 - 10.1080/17513750903261281
DO - 10.1080/17513750903261281
M3 - Article
C2 - 22881128
AN - SCOPUS:79960524726
SN - 1751-3758
VL - 4
SP - 315
EP - 327
JO - Journal of Biological Dynamics
JF - Journal of Biological Dynamics
IS - 4
ER -