CD4+ T cell phenotypes in the pathogenesis of immune thrombocytopenia

Kostić, Milica; Živković, Nikola; Cvetanovic, Ana; Marjanović, Goran

doi:10.1016/j.cellimm.2020.104096

Cited by 36 publications

(27 citation statements)

References 152 publications

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“…ITP is an autoimmune disease that is characterized by increased destruction and decreased production of platelets ( 127 ). The frequency of Th22 cells and the level of plasma IL-22 in patients with ITP were significantly higher than those in the control group ( 77 , 78 , 128 ).…”

Section: Th22 Cells In Autoimmune Diseasesmentioning

confidence: 99%

Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases

et al. 2021

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Upon antigenic stimulation, naïve CD4+T cells differentiate into different subsets and secrete various cytokines to exert biological effects. Th22 cells, a newly identified CD4+T cell subset,are distinct from the Th1, Th2 and Th17 subsets. Th22 cells secrete certain cytokines such as IL-22, IL-13 and TNF-α, but not others, such as IL-17, IL-4, or interferon-γ (IFN-γ), and they express chemokine receptors CCR4, CCR6 and CCR10. Th22 cells were initially found to play a role in skin inflammatory diseases, but recent studies have demonstrated their involvement in the development of various autoimmune diseases. Here, we review research advances in the origin, characteristics and effector mechanisms of Th22 cells, with an emphasis on the role of Th22 cells and their main effector cytokine IL-22 in the pathogenesis of autoimmune diseases. The findings presented here may facilitate the development of new therapeutic strategies for targeting these diseases.

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Section: Th22 Cells In Autoimmune Diseasesmentioning

confidence: 99%

Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases

et al. 2021

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“…T cells play an important role in regulating the immune system and its abnormal polarization (Th1/Treg cells) and associated cytokines secretion (IFN-γ and TGF-β1) play critical roles in the pathogenesis of ITP [ 6 ]. To investigate whether DMF affects T cell polarization and cytokines secretion, we collected peripheral blood mononuclear cells and plasma to measure white blood cell count, Th1/Treg cells, IFN-γ and TGF-β1 level.…”

Section: Resultsmentioning

confidence: 99%

“…On the other hand, existing studies have shown that in addition to platelet autoantibodies, cellular immune dysfunction has also been reported to play a key role in the development and pathogenesis of ITP, including T cells, B cells and antigen-presenting cells [ 3 , 5 ]. As an immune response regulating cell, the differentiation and dysfunction of T cells (Th1, Th2, Th17 cells) or related cytokines (IFN-γ, IL-4, IL-17) are closely related to ITP [ 6 , 7 ]. In addition, our previous study demonstrated that Th9 cells and IL-9 plasma level are significantly elevated in patients with ITP compared with healthy controls [ 8 ], indicating the involvement of Th9/IL-9 in the pathogenesis of ITP.…”

Section: Introductionmentioning

confidence: 99%

Dimethyl fumarate inhibits antibody-induced platelet destruction in immune thrombocytopenia mouse

Tong

Ding²,

Gui³

et al. 2021

Thrombosis J

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Background Immune thrombocytopenia (ITP) is an autoimmune disease characterized as a low platelet count resulting from immune-mediated platelet destruction. Dimethyl fumarate (DMF) is widely applied for the treatment of several autoimmune diseases with immunosuppressive effect. However, whether it ameliorates ITP is unclear. This study aims to evaluate whether DMF has a preventive effect on ITP in mice. Methods DMF (30, 60 or 90 mg/kg body weight) was intraperitoneally injected into mice followed by injection of rat anti-mouse integrin GPIIb/CD41antibody to induce ITP. Peripheral blood was isolated to measure platelet count and spleen mononuclear cells were extracted to measure Th1 and Treg cells along with detecting the levels of IFN-γ, and TGFβ-1 in plasma and CD68 expression in spleen by immuohistochemical staining. Additionally, macrophage cell line RAW264.7 was cultured and treated with DMF followed by analysis of cell apoptosis and cycle, and the expression of FcγRI, FcγRIIb and FcγRIV mRNA. Results DMF significantly inhibited antiplatelet antibody-induced platelet destruction, decreased Th1 cells and the expression of T-bet and IFN-γ, upregulated Treg cells and the expression of Foxp3 and TGF-β1 as well as reduced CD68 expression in the spleen of ITP mouse. DMF-treated RAW264.7 cells showed S-phase arrest, increased apoptosis and downregulated expression of FcγRI and FcγRIV. Meanwhile, in vitro treatment of DMF also decreased the expression of cyclin D1 and E2, reduced Bcl-2 level and increased Bax expression and caspase-3 activation. Conclusions In conclusion, DMF prevents antibody-mediated platelet destruction in ITP mice possibly through promoting apoptosis, indicating that it might be used as a new approach for the treatment of ITP.

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“…For example, some studies have found that, compared with the normal population, natural killer (NK) cells in IRH patients are reduced, and NK cells are unable to maintain the steady state of the immune system (13,14). Current research suggests that the imbalance of T lymphocyte regulation results in the abnormal function of B-lymphocytes, as well as T helper cell 17 (Th17), Th9, and Regulatory cell (Treg) cells (15). Moreover, infections caused by the invasion of pathogenic microorganisms are also important causes (16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin improves bone marrow endothelial progenitor cell function from patients with immune-related hemocytopenia

Qian¹,

Shen

Yan³

et al. 2021

Ann Transl Med

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Background: Immune-related hemocytopenia (IRH) is a type of autoimmune disease that targets bone marrow hematopoietic cells. This study investigated the influence of atorvastatin on the functional aspects of bone marrow endothelial progenitor cells (BM EPCs) in IRH patients. Methods: BM EPCs were isolated from 15 patients with IRH and 20 normal controls. The isolated BM EPCs were characterized by flow cytometry. Cell counting kit-8, flow cytometry, and Transwell migration assays were used to determine the proliferation, apoptosis, and migration of BM EPCs, respectively. Protein levels were determined by western blot assay. Results: The BM EPCs isolated from IRH patients showed reduced proliferation, increased apoptosis, and attenuated migratory ability compared to those from normal controls. Western blot analysis showed that the protein level of p-p38 was significantly increased, while that of Phosphorylated protein kinase B (p-AKT) was significantly decreased in the BM EPCs from IRH patients, compared to BM EPCs from healthy subjects. Cell proliferation and migration were significantly enhanced by atorvastatin, recombinant human thrombopoietin, and SB20358 compared to the untreated BM EPCs from IRH patients. Atorvastatin, Recombinant human thrombopoietin (TPO), and SB20358 treatment significantly suppressed the protein levels of p-p38 protein, but increased those of p-AKT in BM EPCS from IRH patients. Conclusions: In summary, atorvastatin increases the number and function of BM EPCs in IRH patients by regulating the p38 and AKT signaling pathways.

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CD4+ T cell phenotypes in the pathogenesis of immune thrombocytopenia

Cited by 36 publications

References 152 publications

Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases

Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases

Dimethyl fumarate inhibits antibody-induced platelet destruction in immune thrombocytopenia mouse

Atorvastatin improves bone marrow endothelial progenitor cell function from patients with immune-related hemocytopenia

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