The role of Th17 cells in adult patients with chronic idiopathic thrombocytopenic purpura

Peking Union Medical College Hospital, Peping, Beijing, China
European Journal Of Haematology (Impact Factor: 2.41). 02/2009; 82(6):488-9. DOI: 10.1111/j.1600-0609.2009.01229.x
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    ABSTRACT: While much has been learned about the basic immunology and clinical characteristics of immune thrombocytopenia, many important questions remain with regard to pathogenesis, disease progression, identification of novel therapeutic targets and approaches, and clinical trials that rationalize and optimize use of existing therapies. The answers to these questions are likely to impact our understanding of the pathogenesis and therapeutic targets of autoimmune disease in general.
    Annals of Hematology 03/2010; 89(S1). DOI:10.1007/s00277-010-0917-1 · 2.40 Impact Factor
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    ABSTRACT: Immune thrombocytopenia (ITP) is a bleeding disorder in which both antibody and cell-mediated autoimmune responses are directed against an individual's own platelets and/or megakaryocytes, leading to either enhanced platelet destruction and/or reduced platelet production, respectively. The cause of this platelet-specific autoimmunity remains unknown, but there has been a constant stream of recent publications that suggest ITP is the result of T-cell dysregulation. In the last 18 months, a rich tapestry of studies has emerged that seems to clarify some immunopathologic issues in ITP while raising new questions related to ITP pathogenesis. The current view on the immunopathogenic mechanisms associated with ITP appears to particularly concentrate on how incompetent CD4+ T-regulatory cells (Tregs) allow autoimmune effector mechanisms to proceed and cause thrombocytopenia. There is a parallel body of recent literature focusing on molecular mimicry mechanisms, B-cell abnormalities, abnormal cytokine patterns and genetic studies in ITP. Of interest, one can recognize inter-relationships between these immune dysregulations. This article will discuss the literature from the past 18 months pertaining to these observations and will show that whereas many of the T-cell defects have been clarified, new questions have also come to light and more immunopathological research is warranted.
    Current opinion in hematology 11/2010; 17(6):590-5. DOI:10.1097/MOH.0b013e32833eaef3 · 4.05 Impact Factor
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    ABSTRACT: Previous studies evaluated Th17 cells in Immune Thrombocytopenia (ITP) patients; however contrasting results have been reported. In addition, in these studies Th17 cells were enumerated after stimulation of mononuclear cells with various molecules (phorbol myristate acetate and ionomycin) and, therefore, not under physiological conditions; moreover, these methods allowed the flow cytometry analysis of very low percentages of positive cells (around 2-3%).In the present letter, for the first time, we enumerated circulating Th17 cells in ITP patients by identifying the presence of CD4+CD161+CD196+ cells at flow cytometry, as recently described by Cosmi et al . (J Exp Med 2008). We found that Th17 cells (percentage and absolute number) were comparable between patients and controls. Thus, our results do not suggest that ITP is associated with a significant difference in the number of circulating Th17 cells as compared to healthy individuals.
    Haematologica 02/2011; 96(4):632-4. DOI:10.3324/haematol.2010.038638 · 5.87 Impact Factor