"Th17 cells are thought to be involved in inflammatory and autoimmune disease , . Some researchers argued that Th17 cells count did not differ between ITP patients and normal controls , . However, other groups reported up-regulation of Th17 cells in ITP patients –. "
[Show abstract][Hide abstract] ABSTRACT: Primary immune thrombocytopenia (ITP) is an autoimmune heterogeneous disorder that is characterized by decreased platelet count. Regulatory T (Treg) cells and T helper type 17 (Th17) cells are two subtypes of CD4(+) T helper (Th) cells. They play opposite roles in immune tolerance and autoimmune diseases, while they share a common differentiation pathway. The imbalance of Treg/Th17 has been demonstrated in several autoimmune diseases. In this study, we aimed to investigate the ratio of the number of Treg cells to the number of Th17 cells in ITP patients and evaluate the clinical implications of the alterations in this ratio.
Thirty adult patients with newly diagnosed ITP enrolled in this study. Twelve patients had been clinically followed up for 12 months. The percentages of CD4(+)CD25(hi)Foxp3(+) Treg cells and CD3(+)CD4(+)IL-17-producing Th17 cells in these patients and healthy controls (n = 17) were longitudinally analyzed by flow cytometry.
The percentage of Treg cells in ITP patients was significantly lower than that of healthy controls, and the percentage of Th17 cells increased significantly at disease onset. The ratio of Treg/Th17 correlated with the disease activity.
The ratio of Treg/Th17 might be relevant to the clinical diversity of ITP patients, and this Treg/Th17 ratio might have prognostic role in ITP patients.
PLoS ONE 12/2012; 7(12):e50909. DOI:10.1371/journal.pone.0050909 · 3.23 Impact Factor
[Show abstract][Hide abstract] 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 · 2.63 Impact Factor
[Show abstract][Hide abstract] 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 · 3.97 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.