PubMed:23215839 JSONTXT

{"project":"Allie","denotations":[{"id":"SS1_23215839_1_0","span":{"begin":155,"end":191},"obj":"expanded"},{"id":"SS2_23215839_1_0","span":{"begin":193,"end":196},"obj":"abbr"}],"relations":[{"id":"AE1_23215839_1_0","pred":"abbreviatedTo","subj":"SS1_23215839_1_0","obj":"SS2_23215839_1_0"}],"text":"Abnormality of regulatory T-cells in remission and non-remission idiopathic thrombocytopaenic purpura patients.\nPrimer immunologic defect in patients with idiopathic thrombocytopaenic purpura (ITP) result from autoreactive B-lymphocytes secreting antiplatelet antibodies. Dysfunctional cellular immunity has also great importance in ITP pathogenesis. CD4(+)CD25(+) regulatory T-cells have immunoregulatory features and it is able to inhibit CD4(+)CD25(-) and CD8(+) responses. ITP is also an autoimmune disease; the CD4(+)CD25(+) T-cell levels of the patients decrease during the active state. According to our findings, immunosuppressive treatments increase the CD4(+)CD25(+) Treg cell levels in the non-remission ITP patients. However, this level is not enough to overcome the resistance. CD4(+)CD25(-)Foxp3(+) and CD4(+)Foxp3(+) Treg cells are responsible for the pathogenesis of the non-remission ITP patients and other factors exist, which are responsible for the resistance of ITP treatment."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":119,"end":137},"obj":"HP_0002715"},{"id":"T2","span":{"begin":184,"end":191},"obj":"HP_0000979"},{"id":"T3","span":{"begin":492,"end":510},"obj":"HP_0002960"},{"id":"T4","span":{"begin":492,"end":502},"obj":"HP_0002960"}],"text":"Abnormality of regulatory T-cells in remission and non-remission idiopathic thrombocytopaenic purpura patients.\nPrimer immunologic defect in patients with idiopathic thrombocytopaenic purpura (ITP) result from autoreactive B-lymphocytes secreting antiplatelet antibodies. Dysfunctional cellular immunity has also great importance in ITP pathogenesis. CD4(+)CD25(+) regulatory T-cells have immunoregulatory features and it is able to inhibit CD4(+)CD25(-) and CD8(+) responses. ITP is also an autoimmune disease; the CD4(+)CD25(+) T-cell levels of the patients decrease during the active state. According to our findings, immunosuppressive treatments increase the CD4(+)CD25(+) Treg cell levels in the non-remission ITP patients. However, this level is not enough to overcome the resistance. CD4(+)CD25(-)Foxp3(+) and CD4(+)Foxp3(+) Treg cells are responsible for the pathogenesis of the non-remission ITP patients and other factors exist, which are responsible for the resistance of ITP treatment."}