Wodarz2003 - Cytotoxic T lymphocyte cross-priming

  public model
Model Identifier
BIOMD0000000685
Short description

This a model from the article:
A dynamical perspective of CTL cross-priming and regulation: implications for cancer immunology.
Wodarz D, Jansen VA. Immunol Lett 2003 May 1;86(3):213-27 12706524 ,
Abstract:
Cytotoxic T lymphocytes (CTL) responses are required to fight many diseases such as viral infections and tumors. At the same time, they can cause disease when induced inappropriately. Which factors regulate CTL and decide whether they should remain silent or react is open to debate. The phenomenon called cross-priming has received attention in this respect. That is, CTL expansion occurs if antigen is recognized on the surface of professional antigen presenting cells (APCs). This is in contrast to direct presentation where antigen is seen on the surface of the target cells (e.g. infected cells or tumor cells). Here we introduce a mathematical model, which takes the phenomenon of cross-priming into account. We propose a new mechanism of regulation which is implicit in the dynamics of the CTL: According to the model, the ability of a CTL response to become established depends on the ratio of cross-presentation to direct presentation of the antigen. If this ratio is relatively high, CTL responses are likely to become established. If this ratio is relatively low, tolerance is the likely outcome. The behavior of the model includes a parameter region where the outcome depends on the initial conditions. We discuss our results with respect to the idea of self/non-self discrimination and the danger signal hypothesis. We apply the model to study the role of CTL in cancer initiation, cancer evolution/progression, and therapeutic vaccination against cancers.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Wodarz D, Jansen VA. (2003) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland

This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..

To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

Format
SBML (L2V4)
Related Publication
  • A dynamical perspective of CTL cross-priming and regulation: implications for cancer immunology.
  • Wodarz D, Jansen VA
  • Immunology letters , 5/ 2003 , Volume 86 , Issue 3 , pages: 213-227 , PubMed ID: 12706524
  • Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, MP-665 Seattle, WA 98109, USA. wodarz@fhcrc.org
  • Cytotoxic T lymphocytes (CTL) responses are required to fight many diseases such as viral infections and tumors. At the same time, they can cause disease when induced inappropriately. Which factors regulate CTL and decide whether they should remain silent or react is open to debate. The phenomenon called cross-priming has received attention in this respect. That is, CTL expansion occurs if antigen is recognized on the surface of professional antigen presenting cells (APCs). This is in contrast to direct presentation where antigen is seen on the surface of the target cells (e.g. infected cells or tumor cells). Here we introduce a mathematical model, which takes the phenomenon of cross-priming into account. We propose a new mechanism of regulation which is implicit in the dynamics of the CTL: According to the model, the ability of a CTL response to become established depends on the ratio of cross-presentation to direct presentation of the antigen. If this ratio is relatively high, CTL responses are likely to become established. If this ratio is relatively low, tolerance is the likely outcome. The behavior of the model includes a parameter region where the outcome depends on the initial conditions. We discuss our results with respect to the idea of self/non-self discrimination and the danger signal hypothesis. We apply the model to study the role of CTL in cancer initiation, cancer evolution/progression, and therapeutic vaccination against cancers.
Contributors
Submitter of the first revision: Camille Laibe
Submitter of this revision: administrator
Modellers: administrator, Camille Laibe

Metadata information

is (2 statements)
BioModels Database MODEL1006230094
BioModels Database BIOMD0000000685

isDescribedBy (2 statements)
PubMed 12706524
PubMed 12706524

hasTaxon (1 statement)
Taxonomy Homo sapiens

isVersionOf (1 statement)
Gene Ontology adaptive immune response

hasPart (2 statements)
Brenda Tissue Ontology cytotoxic T-lymphocyte
Cell Type Ontology professional antigen presenting cell


Curation status
Curated

Tags

Connected external resources

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Model files

BIOMD0000000685_url.xml SBML L2V4 representation of Wodarz2003 - Cytotoxic T lymphocyte cross-priming 36.88 KB Preview | Download

Additional files

BIOMD0000000685-biopax2.owl Auto-generated BioPAX (Level 2) 4.22 KB Preview | Download
BIOMD0000000685-biopax3.owl Auto-generated BioPAX (Level 3) 4.32 KB Preview | Download
BIOMD0000000685.m Auto-generated Octave file 3.99 KB Preview | Download
BIOMD0000000685.pdf Auto-generated PDF file 131.72 KB Preview | Download
BIOMD0000000685.png Auto-generated Reaction graph (PNG) 4.27 KB Preview | Download
BIOMD0000000685.sci Auto-generated Scilab file 1.59 KB Preview | Download
BIOMD0000000685.svg Auto-generated Reaction graph (SVG) 845.00 Bytes Preview | Download
BIOMD0000000685.vcml Auto-generated VCML file 900.00 Bytes Preview | Download
BIOMD0000000685.xpp Auto-generated XPP file 2.13 KB Preview | Download
BIOMD0000000685_urn.xml Auto-generated SBML file with URNs 36.85 KB Preview | Download
MODEL1006230094.cps Curated and annotated COPASI file. 46.57 KB Preview | Download
MODEL1006230094.sedml SED-ML file with initial conditions and parameter values set to produce figure 4B of the reference publication. 2.15 KB Preview | Download

  • Model originally submitted by : Camille Laibe
  • Submitted: Jun 23, 2010 10:12:36 AM
  • Last Modified: Mar 14, 2018 9:11:12 AM
Revisions
  • Version: 3 public model Download this version
    • Submitted on: Mar 14, 2018 9:11:12 AM
    • Submitted by: administrator
    • With comment: Model name updated using online editor.
  • Version: 2 public model Download this version
    • Submitted on: Jun 25, 2010 2:46:40 PM
    • Submitted by: Camille Laibe
    • With comment: Current version of Wodarz2003_CTLcrosspriming
  • Version: 1 public model Download this version
    • Submitted on: Jun 23, 2010 10:12:36 AM
    • Submitted by: Camille Laibe
    • With comment: Original import of Wodarz2003_CTLcrosspriming

(*) You might be seeing discontinuous revisions as only public revisions are displayed here. Any private revisions unpublished model revision of this model will only be shown to the submitter and their collaborators.

Curator's comment:
(added: 09 Mar 2018, 11:36:22, updated: 09 Mar 2018, 11:36:22)
The curated model produces similar results for figures 4A, 4B and 4C of the reference publication. The figures illustrate target cell (black curve corresponding to left axis) and cytotoxic T-lymphocye (blue curve corresponding to right axis) dynamics for: r=0.13, low initial C (4A) ; r=1.0, increased C (4B) and r=1.0, low C (4C). The model is very sensitive to initial conditions. 4A: T(0) = 0.1, A(0)=0.1. A*(0) = 0.1, C(0)=0.01. 4B: T(0) = 0.1, A(0)=2. A*(0) = 2, C(0)=0.01. 4A: T(0) = 0.1, A(0)=2. A*(0) = 2, C(0)=0.3.