2001
DOI: 10.1182/blood.v98.1.130
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Immunodominant epitopes on glycoprotein IIb-IIIa recognized by autoreactive T cells in patients with immune thrombocytopenic purpura

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Cited by 117 publications
(112 citation statements)
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“…20 The other enriched processes such as T-cell activation involved in immune response, positive regulation of leukocyte activation, and lymphocyte co-stimulation, further highlight the importance of T cells in this disease. This supports previous findings such as proliferation of T cells and production of cytokines in response to stimulation with whole platelets or fragments of GPIIb/IIIa and GPIIIa in ITP, [21][22][23][24][25] and that cytotoxic T cells can lyse platelets in patients with ITP. 2,[26][27][28] That both B-cell and T-cell mechanisms are important pathophysiologic mechanisms in ITP has also been shown in an elegant animal model of ITP.…”
Section: Resultssupporting
confidence: 80%
“…20 The other enriched processes such as T-cell activation involved in immune response, positive regulation of leukocyte activation, and lymphocyte co-stimulation, further highlight the importance of T cells in this disease. This supports previous findings such as proliferation of T cells and production of cytokines in response to stimulation with whole platelets or fragments of GPIIb/IIIa and GPIIIa in ITP, [21][22][23][24][25] and that cytotoxic T cells can lyse platelets in patients with ITP. 2,[26][27][28] That both B-cell and T-cell mechanisms are important pathophysiologic mechanisms in ITP has also been shown in an elegant animal model of ITP.…”
Section: Resultssupporting
confidence: 80%
“…These data appear to support previous observations in humans, showing that T helper cell abnormalities are responsible for the initiation and perpetuation of the immune effector mechanisms responsible for the human disease. [27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43] In addition, it suggests that the CD4 ϩ T cells can be examined with relation to how a relatively platelet-specific antigen (CD61) initiates their activation, which has relevance to understanding and developing platelet-derived peptide-based therapies for reducing immune responses against platelets. These types of therapies have been proposed for patients with chronic ITP and those patients with human platelet antigen-specific alloantibodies.…”
Section: Discussionmentioning
confidence: 99%
“…For example, it is well established from studies in patients with chronic ITP that the disorder is associated with several T-cell abnormalities, including abnormally activated T helper cells with a T helper type 1 cytokine bias, a deficiency of T regulatory cells that lead to autoantibody production, and, in some patients, thrombocytopenia mediated by CD8 ϩ T cells. [27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43] To date, however, there are no known animal models that mimic these T-cell abnormalities or show the severe form of chronic ITP with active bleeding. We report here the development of such a murine model that shows both antibody (CD8 T cell-depleted)-and cell (CD19-depleted)-mediated effector responses that lead to thrombocytopenia and bleeding mortality.…”
Section: Discussionmentioning
confidence: 99%
“…Abnormal antibody production in ITP appears to originate from a limited number of auto-reactive B-cell clones [44]. Furthermore, auto-reactive CD4 + T-helper cells have been shown to promote this B-cell synthesis of anti-IIb/ IIIa antibodies after exposure to the amino-terminal portions of IIba and IIIa but not to native IIb/IIIa proteins [45]. This phenomenon suggests a role for modification of the intact platelet IIb/IIIa glycoprotein by antigen-presenting cells and subsequent T-helper cell interaction.…”
Section: Introductionmentioning
confidence: 99%