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Modelling the Control of an Immune Response
Through Cytokine Signalling
Thiago Guzella
1
, Tomaz Mota-Santos
2
,
Joaquim Uchoa
3
, and Walmir Caminhas
1
1
Electrical Engineering Dept., Federal University of Minas Gerais
Belo Horizonte (MG) 31270-010, Brazil
{
tguzella, caminhas
}
@cpdee.ufmg.br
2
Biochemistry and Immunology Dept., Federal University of Minas Gerais
Belo Horizonte (MG) 31270-010, Brazil
tomaz@icb.ufmg.br
3
Computer Science Dept., Federal University of Lavras
Lavras (MG) 37200-000, Brazil
joukim@dcc.ufla.br
Abstract.
This paper presents the computer aided simulation of a model
for the control of an immune response. This model has been developed to
investigate the proposed hypothesis that the same cytokine that amplifies
an initiated response can eventually lead to its downregulation, if it can
act on more than one cell type. The simulation environment is composed
of effector cells and regulatory cells; the former, when activated, initi-
ate an immune response, while the latter are responsible for controlling
the magnitude of the response. The signalling that coordinates this pro-
cess is modelled using stimulation and regulation cytokines. Simulation
results obtained, in accordance with the motivating idea, are presented
and discussed.
1
Introduction
The immune system is a complex aggregate of cells, antibodies and signalling
molecules. The Clonal Selection Theory [1] has been, for nearly 5 decades, the
dominating base to explain how the immune system discriminates between self
and nonself. This discrimination is extremely important, because the system
must be able to eliminate nonself components that infiltrate the body, while
remaining unresponsive to self. The Clonal Selection Theory argues that the
system's tolerance to self is accomplished through a process denominated neg-
ative selection, when self-reactive B and T lymphocytes are eliminated during
their development.
However, there's increasing evidence that some self-reactive cells eventually
escape from the clonal deletion [2]. Therefore, these lymphocytes are present
in the periphery, and could give rise to hazardous autoimmune diseases. Vari-
ous models have been proposed to explain why, most of the times, these cells
remain inactive, ignoring self antigens. These models are based on passive or re-
cessive mechanisms, such as low avidities of their receptors for self-antigens and
