TY - JOUR
T1 - A mathematical model for immune and autoimmune response mediated by T-cells
AU - Delitala, Marcello
AU - Dianzani, Umberto
AU - Lorenzi, Tommaso
AU - Melensi, Matteo
PY - 2013/10
Y1 - 2013/10
N2 - How do we recast the effects of molecular mimicry and genetic alterations affecting the T-cell response against self and non-self antigens into a mathematical model for the development of autoimmune disorders? Bearing this question in mind, we propose a model describing the evolution of a sample composed of immune cells and cells expressing self and non-self antigens. The model is stated in terms of integro-differential equations for structured populations and ordinary differential equations for unstructured populations. A global existence result is established and computational analyses are performed to verify the consistency with experimental data, making particular reference to the autoimmune lymphoproliferative syndrome (ALPS) as the model disease. Using our model as a virtual laboratory, we test different hypothetical scenarios and come to the conclusion that, besides molecular mimicry, genetic alterations leading to an over-proliferation of the T-cells and a less effective action against non-self antigens can be driving forces of autoimmunity.
AB - How do we recast the effects of molecular mimicry and genetic alterations affecting the T-cell response against self and non-self antigens into a mathematical model for the development of autoimmune disorders? Bearing this question in mind, we propose a model describing the evolution of a sample composed of immune cells and cells expressing self and non-self antigens. The model is stated in terms of integro-differential equations for structured populations and ordinary differential equations for unstructured populations. A global existence result is established and computational analyses are performed to verify the consistency with experimental data, making particular reference to the autoimmune lymphoproliferative syndrome (ALPS) as the model disease. Using our model as a virtual laboratory, we test different hypothetical scenarios and come to the conclusion that, besides molecular mimicry, genetic alterations leading to an over-proliferation of the T-cells and a less effective action against non-self antigens can be driving forces of autoimmunity.
KW - Immunization and autoimmunization
KW - Modeling T-cell immune and autoimmune response
KW - Molecular mimicry
KW - Structured and unstructured population dynamics
UR - https://www.scopus.com/pages/publications/84883216463
U2 - 10.1016/j.camwa.2013.06.026
DO - 10.1016/j.camwa.2013.06.026
M3 - Article
SN - 0898-1221
VL - 66
SP - 1010
EP - 1023
JO - Computers and Mathematics with Applications
JF - Computers and Mathematics with Applications
IS - 6
ER -