Immunologically Motivated Simulations of Cellular Automata (original) (raw)

The antibody response: A model based on antagonistic actions of antigen

Journal of Theoretical Biology, 1963

A molecular model of antibody production is presented which is based solely on selective induction. According to this model the potential to make the various antibodies is distributed randomly among immature lymphoid cells, each cell being precommitted to a limited number of antibodies. The reaction of antigen with these immature cells has two separate and antagonistic actions mediated through two separate molecular bridges between antigen and DNA. A specific stimulus occurs following a reaction of antigen with strategically located preformed antibody and results in the passage of messenger RNA from the nucleus into the cytoplasm. The net effect of the specific stimulus is maturation of the cell, with temporary production of antibody but loss of the immature cell on which specitic antibody-forming potential depends. A specific stimulus unaccompanied by a non-specific stimulus leads to acquired immunologic tolerance. However, the non-specific stimulus, which occurs through an aggregation of antibody on the surface of the antigen, results in increased multiplication of the immature cell with specific antibody-forming potential. This counterbalances the effect of maturation and leads to increased antibody-forming potential as well as to temporary production of antibody against the antigen injected.

The transition between immune and disease states in a cellular automaton model of clonal immune response

Physica A-statistical Mechanics and Its Applications, 1997

In this paper we extend the Celada-Seiden (CS) model of the humoral immune response to include infectious virus and cytotoxic T lymphocytes (cellular response). The response of the system to virus involves a competition between the ability of the virus to kill the host cells and the host's ability to eliminate the virus. We find two basins of attraction in the dynamics of this system, one is identified with disease and the other with the immune state. There is also an oscillating state that exists on the border of these two stable states.

Deterministic Mathematical Model of Cell Mediated Immune Responses

2019

Aspects of an organism’s defense to infections are the main problems of practical immunology. Understanding the regularities in immune response provide the researchers and clinicians new powerful tools for the simulation of immune system in order to increase its efficiency in the struggle against antigen invasion. Such general regularities are revealed, as a rule, on the basis of analysis of the main components of an organism’s vital activities along with the system of immune defense. In this connection the construction of models of immune response to an antigen irritant seems to be a right tactic in the cognition of above regularities, that is why this monograph is dedicated to the analysis of the facts accumulated in immunology as a united system on the basis of logical concepts and mathematical models. Immune response to an infection by a pathogen is supported by different populations of cells (macrophages, B cells, CD4 T cells, CD8 T cells. . .). Among the many pathogen type, we...

A computer model of cellular interactions in the immune system

Immunology Today, 1992

The power of modern computers allows the modeling and simulation of complex biological systems. The last decade has seen the emergence of a growing number of simulations of the immune system. In this article, Franco Celada and Philip Selden present a model that, they suggest, is rich enough to allow computer experiments to be used as practical adjuncts to the usual biological experiments, at a saving of cost and time.

Probabilistic cellular automaton describing a biological immune system

Physical Review E, 1996

We have analyzed. a probabilistic cellular automaton to describe the T-helper cells response under parasitic infections. The evolution rules are of totalistic type and possess "up-down" symmetry. The automaton displays a dynamical phase transition, from a disordered state to an ordered one, which takes place through a spontaneous symmetry breaking. In the ordered phase, one type of T-helper cells predominates over the others. The phase transition was studied both by a pair approximation and by Monte Carlo simulations. In addition, we were able to obtain some exact results for the densities of T-helper cells.

A dynamical modeling to study the adaptive immune system and the influence of antibodies in the immune memory

arXiv (Cornell University), 2017

Immunological systems have been an abundant inspiration to contemporary computer scientists. Problem solving strategies, stemming from known immune system phenomena, have been successfully applied to challenging problems of modern computing (MONROY, SAAB, GODÍNEZ, 2004). Simulation systems and mathematical modeling are also beginning use to answer more complex immunological questions as immune memory process and duration of vaccines, where the regulation mechanisms are not still known sufficiently (LUNDEGAARD, LUND, KESMIR, BRUNAK, NIELSEN, 2007).In this article we studied in machina a approach to simulate the process of antigenic mutation and its implications for the process of memory. Our results have suggested that the durability of the immune memory is affected by the process of antigenic mutation and by populations of soluble antibodies in the blood. The results also strongly suggest that the decrease of the production of antibodies favors the global maintenance of immune memory.

A model of auto immune response

BMC immunology, 2017

In this work, we develop a theoretical model of an auto immune response. This is based on modifications of standard second messenger trigger models using both signalling pathways and diffusion and a macro level dynamic systems approximation to the response of a triggering agent such as a virus, bacteria or environmental toxin. We show that there, in general, will be self damage effects whenever the triggering agent's effect on the host can be separated into two distinct classes of cell populations. In each population, the trigger acts differently and this behavior is mediated by the nonlinear interactions between two signalling agents. If these interactions satisfy certain critical assumptions this will lead to collateral damage. If the initial triggering agent's action involves any critical host cell population whose loss can lead to serious host health issues, then there is a much increased probability of host death. Our model also shows that if the nonlinear interaction a...

A Brief Background on the Immune System

This document is intended to provide some background on the basic functions of the human immune system. Please note that this information is by no means comprehensive, and that many of these terms are de ned only in their broadest and least technical sense. Terms in italics are important to understanding the structure of the immune system, and those interested should take the time to look them up in a dictionary of medicine or immunology. (See for example, [CL95]. ) The main function of the immune system is to deal with foreign invaders, whether these are particles or living organisms. Hence the key to the immune system's successful functioning is its ability to distinguish between \self" and \non-self. " Once a foreign agent is identi ed, the body is then able to mount a response to it. An antigen is, generally speaking, any foreign agent that the can be rec-ognized by the body's immune system. If the immune system is then able to mount an active response to it,...

A computerized model for the self-nonself discrimination at the level of the T-helper (Th genesis). II. The behavior of the system upon encounter with nonself antigens. Int Immunol 15:593

International Immunology

The ability of the immune system to respond by ridding a pathogen without debilitating the host depends upon the ability of the effector T h (eT h ) to make a discrimination between`self' and`nonself' antigens. This ability is somatically learned and involves the sorting of the somatically generated random repertoire of initial state T h (iT h ) into two classes of speci®city: one, anti-self, the functional expression of which must be inactivated; the other, anti-non-self, the functional expression of which must be activated. We propose a model for the origin of a suf®ciency of eT h anti-non-self and an insuf®ciency of eT h anti-self based on two postulates. (i) An antigenindependent pathway to a priming level of eT h anti-non-self under conditions where iT h anti-self are effectively deleted by interaction with self. This state is established during a window of fetal development and maintained throughout life because self is persistent. (ii) Associative recognition of antigen (peptide±MHC class II) on an antigen-presenting cell between iT h and`primer' eT h that results in the rapid induction of an effective level of helper activity to non-self antigen. A computer simulation is provided that enables evaluation of this model. ² It is with great sadness that we report the death of Dr Rodney E.