Qualitative dynamics of a network model of regulation of the immune system: A rationale for the IgM to IgG switch
A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond...
Ausführliche Beschreibung
Gespeichert in:
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1982 |
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| Reproduktion: |
Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 |
|---|---|
| Übergeordnetes Werk: |
in: Journal of Theoretical Biology - Amsterdam : Elsevier, 94(1982), 4, Seite 815-855 |
| Übergeordnetes Werk: |
volume:94 ; year:1982 ; number:4 ; pages:815-855 |
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| 520 | |a A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory. | ||
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(DE-627)NLEJ183164849 (DE-599)GBVNLZ183164849 DE-627 ger DE-627 rakwb eng Qualitative dynamics of a network model of regulation of the immune system: A rationale for the IgM to IgG switch 1982 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Gunther, N. oth Hoffmann, G.W. oth in Journal of Theoretical Biology Amsterdam : Elsevier 94(1982), 4, Seite 815-855 (DE-627)NLEJ176864393 (DE-600)1470953-3 0022-5193 nnns volume:94 year:1982 number:4 pages:815-855 http://dx.doi.org/10.1016/0022-5193(82)90080-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 94 1982 4 815-855 |
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(DE-627)NLEJ183164849 (DE-599)GBVNLZ183164849 DE-627 ger DE-627 rakwb eng Qualitative dynamics of a network model of regulation of the immune system: A rationale for the IgM to IgG switch 1982 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Gunther, N. oth Hoffmann, G.W. oth in Journal of Theoretical Biology Amsterdam : Elsevier 94(1982), 4, Seite 815-855 (DE-627)NLEJ176864393 (DE-600)1470953-3 0022-5193 nnns volume:94 year:1982 number:4 pages:815-855 http://dx.doi.org/10.1016/0022-5193(82)90080-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 94 1982 4 815-855 |
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(DE-627)NLEJ183164849 (DE-599)GBVNLZ183164849 DE-627 ger DE-627 rakwb eng Qualitative dynamics of a network model of regulation of the immune system: A rationale for the IgM to IgG switch 1982 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Gunther, N. oth Hoffmann, G.W. oth in Journal of Theoretical Biology Amsterdam : Elsevier 94(1982), 4, Seite 815-855 (DE-627)NLEJ176864393 (DE-600)1470953-3 0022-5193 nnns volume:94 year:1982 number:4 pages:815-855 http://dx.doi.org/10.1016/0022-5193(82)90080-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 94 1982 4 815-855 |
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(DE-627)NLEJ183164849 (DE-599)GBVNLZ183164849 DE-627 ger DE-627 rakwb eng Qualitative dynamics of a network model of regulation of the immune system: A rationale for the IgM to IgG switch 1982 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Gunther, N. oth Hoffmann, G.W. oth in Journal of Theoretical Biology Amsterdam : Elsevier 94(1982), 4, Seite 815-855 (DE-627)NLEJ176864393 (DE-600)1470953-3 0022-5193 nnns volume:94 year:1982 number:4 pages:815-855 http://dx.doi.org/10.1016/0022-5193(82)90080-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 94 1982 4 815-855 |
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(DE-627)NLEJ183164849 (DE-599)GBVNLZ183164849 DE-627 ger DE-627 rakwb eng Qualitative dynamics of a network model of regulation of the immune system: A rationale for the IgM to IgG switch 1982 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory. Elsevier Journal Backfiles on ScienceDirect 1907 - 2002 Gunther, N. oth Hoffmann, G.W. oth in Journal of Theoretical Biology Amsterdam : Elsevier 94(1982), 4, Seite 815-855 (DE-627)NLEJ176864393 (DE-600)1470953-3 0022-5193 nnns volume:94 year:1982 number:4 pages:815-855 http://dx.doi.org/10.1016/0022-5193(82)90080-7 GBV_USEFLAG_H ZDB-1-SDJ GBV_NL_ARTICLE AR 94 1982 4 815-855 |
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Qualitative dynamics of a network model of regulation of the immune system: A rationale for the IgM to IgG switch |
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A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory. |
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A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory. |
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A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ183164849</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210706194342.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070505s1982 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ183164849</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBVNLZ183164849</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Qualitative dynamics of a network model of regulation of the immune system: A rationale for the IgM to IgG switch</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1982</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">A mathematical model has been developed that simulates some of the main features of a network theory of regulation of the immune system. According to the network viewpoint, the V regions (idiotypes) on antibodies and lymphocytes are self-antigens, to which other lymphocytes of the system can respond specifically, just as they respond to foreign antigens. The resultant couplings between the lymphocytes are considered to be basic for the regulation of the system.The present mathematical model simulates the interactions between cells that recognize the antigen (''positive cells''), and ''negative cells'' that have receptors that specifically recognize the V regions of the positive cells. The mathematical model incorporates only the interactions that are postulated to be important in the four steady states of the theory, and includes neither the antigen nor any accessory (''A'') cells. The effects of both antigen-specific and anti-idiotypic T and B cells are included, as well as antigen-specific and anti-idiotypic T cell factors, and the two main classes of antibodies. The model is a first order autonomous ordinary differential equation in two variables. We describe a geometric technique that gives strong information on the model, without explicitly solving the ordinary differential equation. This technique proves to be powerful in permitting us to systematically scan the parameter space of the model. The detailed analysis leads to support for the idea that the model provides a rationale for the switch observed in the immune system from the production of one major class of antibody (IgM) to the other major class (IgG). The analysis also leads to a new, previously unsuspected possibility for the nature of the suppressed state within the context of the postulates of the symmetrical network theory.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Elsevier Journal Backfiles on ScienceDirect 1907 - 2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gunther, N.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hoffmann, G.W.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Journal of Theoretical Biology</subfield><subfield code="d">Amsterdam : Elsevier</subfield><subfield code="g">94(1982), 4, Seite 815-855</subfield><subfield code="w">(DE-627)NLEJ176864393</subfield><subfield code="w">(DE-600)1470953-3</subfield><subfield code="x">0022-5193</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:94</subfield><subfield code="g">year:1982</subfield><subfield code="g">number:4</subfield><subfield code="g">pages:815-855</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1016/0022-5193(82)90080-7</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_H</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SDJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">94</subfield><subfield code="j">1982</subfield><subfield code="e">4</subfield><subfield code="h">815-855</subfield></datafield></record></collection>
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