Abstract
Among various environmental factors associated with triggering or exacerbating autoimmune response, an important role is played by infections. A breakdown of immune tolerance as a byproduct of immune response against these infections is one of the major causes of autoimmune disease. In this paper we analyse the dynamics of immune response with particular emphasis on the role of time delays characterising the infection and the immune response, as well as on interactions between different types of T cells and cytokines that mediate their behaviour. Stability analysis of the model provides insights into how different model parameters affect the dynamics. Numerical stability analysis and simulations are performed to identify basins of attraction of different dynamical states, and to illustrate the behaviour of the model in different regimes.
Highlights
The main role of the immune system is to effectively protect its host against pathogens by identifying and destroying pathogen-infected cells
A number of pathogens have been identified that appear to be very strongly associated with specific autoimmune diseases, such as Epstein-Barr virus associated with rheumatoid arthritis, multiple sclerosis (MS), autoimmune thyroid disease, and systemic lupus erythematosus (SLE) [9, 10], the Coxsackie viruses associated with type-1 diabetes [11, 12], and HSV-1 virus associated with autoimmune stromal keratitis [13, 14]
Cells are not included in the model, we consider a situation where that IL-2 is only produced by cytotoxic T lymphocytes (CTLs), but it regulates the proliferation of both CTLs, and regulatory T cells
Summary
The main role of the immune system is to effectively protect its host against pathogens by identifying and destroying pathogen-infected cells. Focusing on molecular mimicry as the primary mechanism of virus-induced autoimmune response, Blyuss and Nicholson [81, 82] have developed a mathematical model that explicitly includes both a viral population, and two types of T cells with different activation thresholds. This model allows for a possibility of viral infection and autoimmune response occurring in different organs of the host.
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