Modelling the Impact of NETosis During the Initial Stage of Systemic Lupus Erythematosus
Vladimira Suvandjieva, Ivanka Tsacheva, Marlene Santos, Georgios Kararigas, Peter Rashkov
TL;DR
This paper presents a mathematical model to study how NETosis contributes to the early development of Systemic Lupus Erythematosus.
Contribution
The novelty lies in modeling the role of NETosis in establishing persistent autoantigen production during early SLE stages.
Findings
NETosis is hypothesized to contribute to autoimmunogenicity in SLE.
The model analyzes steady states and asymptotic dynamics to understand autoantigen persistence.
Numerical experiments reveal insights into immune response dynamics during early SLE.
Abstract
The development of autoimmune diseases often takes years before clinical symptoms become detectable. We propose a mathematical model for the immune response during the initial stage of Systemic Lupus Erythematosus which models the process of aberrant apoptosis and activation of macrophages and neutrophils. NETosis is a type of cell death characterised by the release of neutrophil extracellular traps, or NETs, containing material from the neutrophil’s nucleus, in response to a pathogenic stimulus. This process is hypothesised to contribute to the development of autoimmunogenicity in SLE. The aim of this work is to study how NETosis contributes to the establishment of persistent autoantigen production by analysing the steady states and the asymptotic dynamics of the model by numerical experiment. The online version contains supplementary material available at 10.1007/s11538-024-01291-3.
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Taxonomy
TopicsNeutrophil, Myeloperoxidase and Oxidative Mechanisms · Cell Adhesion Molecules Research · Immune cells in cancer