A thermodynamic perspective of immune capabilities
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Publication:1786397
DOI10.1016/J.JTBI.2011.07.027zbMATH Open1397.92123arXiv1105.3146OpenAlexW2099308902WikidataQ51541516 ScholiaQ51541516MaRDI QIDQ1786397FDOQ1786397
Authors: Elena Agliari, Adriano Barra, Francesco Guerra, Francesco Moauro 
Publication date: 24 September 2018
Published in: Journal of Theoretical Biology (Search for Journal in Brave)
Abstract: We consider the mutual interactions, via cytokine exchanges, among helper lymphocytes, B lymphocytes and killer lymphocytes, and we model them as a unique system by means of a tripartite network. Each part includes all the different clones of the same lymphatic subpopulation, whose couplings to the others are either excitatory or inhibitory (mirroring elicitation and suppression by cytokine). First of all, we show that this system can be mapped into an associative neural network, where helper cells directly interact with each other and are able to secrete cytokines according to "strategies" learnt by the system and profitable to cope with possible antigenic stimulation; the ability of such a retrieval corresponds to a healthy reaction of the immune system. We then investigate the possible conditions for the failure of a correct retrieval and distinguish between the following outcomes: massive lymphocyte expansion/suppression (e.g. lymphoproliferative syndromes), subpopulation unbalance (e.g. HIV, EBV infections) and ageing (thought of as noise growth); the correlation of such states to auto-immune diseases is also highlighted. Lastly, we discuss how self-regulatory effects within each effector branch (i.e. B and killer lymphocytes) can be modeled in terms of a stochastic process, ultimately providing a consistent bridge between the tripartite-network approach introduced here and the immune networks developed in the last decades.
Full work available at URL: https://arxiv.org/abs/1105.3146
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Cited In (19)
- A mathematical model for immune and autoimmune response mediated by \(T\)-cells
- Can persistent Epstein-Barr virus infection induce chronic fatigue syndrome as a Pavlov reflex of the immune response?
- The role of idiotypic interactions in the adaptive immune system: a belief-propagation approach
- Nonlinear dynamics and statistical physics of models for the immune system
- Replica symmetry breaking in multi-species Sherrington-Kirkpatrick model
- Ferromagnetic models for cooperative behavior: revisiting universality in complex phenomena
- Anergy in self-directed B lymphocytes: a statistical mechanics perspective
- Complex reaction kinetics in chemistry: a unified picture suggested by mechanics in physics
- Multitasking attractor networks with neuronal threshold noise
- Statistical mechanics of clonal expansion in lymphocyte networks modelled with slow and fast variables
- The energy criterion for quality of immune defence and pathogenicity of microorganisms
- Central immune system, the self and autoimmunity
- Spontaneous replica symmetry breaking and interpolation methods for complex statistical mechanics systems
- Endogenous versus exogenous origins of diseases
- An artificial immune-memory model based on idiotypic immune networks: perspectives on antibody dynamics
- Unveiling the relation between herding and liquidity with trader lead-lag networks
- The role of the T-helper/T-suppressor ratio in the adaptive immune response: a dynamical model
- Immune networks: multitasking capabilities near saturation
- Free energies of Boltzmann machines: self-averaging, annealed and replica symmetric approximations in the thermodynamic limit
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