- Author:
- pmr2.import <nobody@models.cellml.org>
- Date:
- 2006-07-09 07:33:08+12:00
- Desc:
- committing version01 of nevo_golding_neumann_schwartz_akselrod_2004
- Permanent Source URI:
- http://models.cellml.org/workspace/nevo_golding_neumann_schwartz_akselrod_2004/rawfile/60594de6740a9384f6088bb319ed0335a066fb2c/nevo_golding_neumann_schwartz_akselrod_2004.cellml
<?xml version='1.0' encoding='utf-8'?>
<!-- FILE : nevo_model_2004.xml
CREATED : 25th October 2004
LAST MODIFIED : 25th October 2004
AUTHOR : Catherine Lloyd
Bioengineering Institute
The University of Auckland
MODEL STATUS : This model conforms to the CellML 1.0 Specification released on
10th August 2001, and the 16/1/02 CellML Metadata 1.0 Specification.
DESCRIPTION : This file contains a CellML description of Nevo et al.'s 2004 mathematical model of autoimmunity.
CHANGES:
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<documentation xmlns="http://cellml.org/tmp-documentation">
<article>
<articleinfo>
<title>Modelling the Bright Side of Autoimmunity</title>
<author>
<firstname>Catherine</firstname>
<surname>Lloyd</surname>
<affiliation>
<shortaffil>Bioengineering Institute, University of Auckland</shortaffil>
</affiliation>
</author>
</articleinfo>
<section id="sec_status">
<title>Model Status</title>
<para>
This is the original unchecked version of the model imported from the previous
CellML model repository, 24-Jan-2006.
</para>
</section>
<sect1 id="sec_structure">
<title>Model Structure</title>
<para>
It is generally believed that the main function of the immune system is to protect the body from foreign pathogens such as bacteria and viruses. Another important role of the immune system is to prevent the destruction of the organism's own tissues, a phenomenon known as self-tolerance. Several theories as to how the body's immune system achieves this self-tolerance have been proposed. Some of these theories have been described by mathematical models, in an attempt to elucidate the basic mechanisms underlying the autoimmune response, and also to predict its possible consequences.
</para>
<para>
When self-tolerance breaks down, the immune system synthesises antibodies against the body's own cell and tissue components. This is known as an autoimmune response, and autoimmune responses are often associated with tissue damage (such as in multiple sclerosis and rhumatoid arthritis). However, the idea that autoimmunity always has a negative effect on an organism has recently been challenged. Following traumatic injury to the central nervous system, autoimmunity can play a protective role. This led the authors of the current study to put forward the <emphasis>comprehensive immunity</emphasis> model, where autoimmunity is thought to be a defense mechanism that fights against the potential threat of self-destructive activity within an organism. This is not dissimilar to the <emphasis>standard</emphasis> immune defense that protects the body against foreign, exogenous pathogens.
</para>
<para>
In the Nevo <emphasis>et al.</emphasis> 2004 publication described here, the authors present a mathematical model which supports the idea of autoimmunity being a protective mechanism (see <xref linkend="fig_cell_diagram"/> below). The model describes self-propagating tissue damage after a focal insult. The tissue can be lost via two routes:
</para>
<itemizedlist>
<listitem>
<para>1) Through self-perpetuating death, which is induced by the secretion of a damage-inducing factor; or</para>
</listitem>
<listitem>
<para>2) Through immune-mediated death, (an autoimmune response)</para>
</listitem>
</itemizedlist>
<para>
These two methods of tissue loss compete locally for the same resource, namely the healthy tissue. In this way, the autoimmune response can stop the progression of tissue damage by firstly shifting tissue loss from the self-perpetuating route to the immune-mediated route, and then the immune-mediated pathway will cease as the feedback, stimulating signal from the self-perpetuating pathway will be lost (again, please see <xref linkend="fig_cell_diagram"/> below to make this clearer).
</para>
<para>
The model has been described here in CellML (the raw CellML description of the Nevo <emphasis>et al.</emphasis> 2004 model can be downloaded in various formats as described in <xref linkend="sec_download_this_model"/>).
</para>
<para>
The complete original paper reference is cited below:
</para>
<para>
<ulink url="http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WMD-4BN0GPJ-2&_user=140507&_coverDate=04%2F21%2F2004&_alid=217221533&_rdoc=1&_fmt=summary&_orig=search&_qd=1&_cdi=6932&_sort=d&_docanchor=&view=c&_acct=C000011498&_version=1&_urlVersion=0&_userid=140507&md5=de446ef8edc983234217f0a4b4ae01ec">Autoimmunity as an immune defense against degenerative processes: a primary mathematical model illustrating the bright side of autoimmunity</ulink>, Uri Nevo, Ido Golding, Avidan U. Neumann, Michal Schwartz, and Solange Akselrod, 2004, <ulink url="http://www.molbiolcell.org/">
<emphasis>Journal of Theoretical Biology</emphasis>
</ulink>, 227, 583-592. (<ulink url="http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WMD-4BN0GPJ-2&_coverDate=04%2F21%2F2004&_alid=217221533&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=6932&_sort=d&view=c&_acct=C000011498&_version=1&_urlVersion=0&_userid=140507&md5=12a84054c5163f0f2808147e2003e8c5">Full text (HTML)</ulink> and <ulink url="http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6WMD-4BN0GPJ-2-2W&_cdi=6932&_orig=search&_coverDate=04%2F21%2F2004&_qd=1&_sk=997729995&view=c&wchp=dGLbVlz-zSkzS&_acct=C000011498&_version=1&_userid=140507&md5=7f378551caff25be0a089e8d18ffaec9&ie=f.pdf">PDF</ulink> versions of the article are available on the <emphasis>Journal of Theoretical Biology</emphasis> website.) <ulink url="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15038992&dopt=Abstract">PubMed ID: 15038992</ulink>
</para>
<informalfigure float="0" id="fig_cell_diagram">
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<title>cell diagram</title>
</objectinfo>
<imagedata fileref="nevo_2004.png"/>
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<caption>Schematic diagram of the mathematical model. Healthy cells (H) can be lost via two routes, 1) self-perpetuating death (H-N-D), or 2) immune-mediated loss (H-P-D).</caption>
</informalfigure>
</sect1>
</article>
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This is the CellML description of Nevo et al.'s 2004 mathematical model of autoimmunity.
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<dcterms:W3CDTF>2004-10-25</dcterms:W3CDTF>
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Autoimmunity as an immune defense against degenerative processes: a
primary mathematical model illustrating the bright side of
autoimmunity
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<dc:title>Journal of Theoretical Biology</dc:title>
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<vCard:Given>Michal</vCard:Given>
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The University of Auckland, Bioengineering Institute
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Nevo et al.'s 2004 mathematical model of autoimmunity.
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<vCard:Given>Avidan</vCard:Given>
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