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This model helps understandthe paradoxical outcomes of IGRPbased peptide treatment experiments. Furthermore, it predicts that slight deviations in dose or peptideaffinity can lead to treatment failure or disease progression. This will occur if the treatment increases the imbalancebetween competing IGRP206214reactive Tcell clones such thatit favors rapid takeover of highavidity clones or ii deletesall IGRP206214reactive clones, thereby creating vacuum thatpromotes the recruitment of subdominant epitopespecific Tcells and failed to prevent disease development.

Here, we mathematicallymodel competition of IGRPreactive Tcell clones during spontaneousdisease, and in response to peptide treatment.

Articles by EdelsteinKeshet, This Article Full Text FREE Full Text PDF All Versions of this Article 1871067 most recent dxl040v1 Alert me when this article is cited Alert me if correction is posted Services Email this article to friend Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Archive Download to citation manager Search for citing articles in ISI Web of Science 1 Request PermissionsGoogle Scholar Articles by Mare, Based on realisticTcell activation, proliferation and differentiation parametervalues, our model shows that progression of spontaneous diseaseis characterized by initial expansion of all IGRP206214reactiveTcell

Social Bookmarking Whats this? Antigen therapy remains promising strategy for preventionand treatment of autoimmune diseases, but translating this strategyto clinical therapy has been largely unsuccessful. Here, we mathematicallymodel competition of IGRPreactive Tcell clones during spontaneousdisease, and in response to peptide treatment. Administration of peptide analogs of IGRP206214,the dominant epitope, reduced disease incidence but only underconditions that led to selective deletion of highavidity Tcellclones.

Here, we mathematicallymodel competition of IGRPreactive Tcell clones during spontaneousdisease, and in response to peptide treatment. Social Bookmarking Whats this? Antigen therapy remains promising strategy for preventionand treatment of autoimmune diseases, but translating this strategyto clinical therapy has been largely unsuccessful. We have shownthat development of autoimmune diabetes in nonobese diabeticNOD mice involves prevalent recruitment of CD8 cells recognizingepitopes of isletspecific glucose6phosphatase catalytic subunitrelatedprotein IGRP. Articles by EdelsteinKeshet, Peptide types or doses that resulted in eliminationof all IGRP206214reactive cells, regardless of avidity,promoted the recruitment of pathogenic subdominant specificities.

Here, we mathematicallymodel competition of IGRPreactive Tcell clones during spontaneousdisease, and in response to peptide treatment. Articles by EdelsteinKeshet, Administration of peptide analogs of IGRP206214,the dominant epitope, reduced disease incidence but only underconditions that led to selective deletion of highavidity Tcellclones. This model helps understandthe paradoxical outcomes of IGRPbased peptide treatment experiments. Furthermore, it predicts that slight deviations in dose or peptideaffinity can lead to treatment failure or disease progression.
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