Aberrant expression of NLRP3, NLRC4 and NLRP6 inflammasomes in patients with primary immune thrombocytopenia

Lv, Yan; Ruan, Guangfeng; Liu, Yan; Cui, Dawei; Zhao, Yuhong; Yan, Cuilin; Lv, Mengen; Xu, Dandan; Mao, Yun; Cao, Jianping; Jin, Jie; Xie, Jue

doi:10.1016/j.thromres.2019.02.020

Cited by 9 publications

(7 citation statements)

References 10 publications

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“…12 A study reported an increase in NLRP3, NLRC4 and NLRP6-inflammasomes in patients with primary ITP. 14 The association of increased HMGB1 as an early detection marker, especially in pediatric ITP, with NLRP3-inflammasome activation has been demonstrated. 33 In a study, the polymorphisms in a number of inflammation-related genes associated with ITP were examined.…”

Section: Studies Have Shown Significant Effects Of Nlrp3inflammasome ...mentioning

confidence: 99%

“…Although the COVID-19-associated thrombocytopenia is usually mild, very severe hemorrhage has been reported in a small number of patients. 2,[12][13][14] Based on a study by Sabin et al on SARS-CoV-2induced ITP, no association was found between hemorrhage severity and COVID-19 severity. In another study, Sue Pavord et al found a sharp drop in platelets in the patients with end-stage COVID-19 due to multiple organ failure.…”

Section: Introductionmentioning

confidence: 99%

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Possible immunological mechanisms in COVID-19 patients with immune thrombocytopenic purpura

Bahadoram

Saeedi-Boroujeni

Mahmoudian-Sani

2022

Med. Jadert. (Online)

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Millions of people around the world were, or are still involved with COVID-19 due to infection with SARS-CoV-2. In addition to hallmark symptoms, thrombotic problems, lymphopenia, and thrombocytopenia have also been reported in COVID-19 patients, of which ITP is the most common and occurs in more than one-third of COVID-19 patients. Hyperinflammation, cytokine storms, and generally immune dysregulation in a percentage of patients develop the main consequences of diseases such as ALI, ARDS and multiple organ failure. Some of the important events in the immunopathogenesis of this disease are disruption of T-cell effector differentiation and the destructive role of Th17 lymphocytes, neutrophil function and inflammatory macrophages. NLRP3-inflammasome hyperactivity causes serious dysfunction of innate immune cells and, consequently, T lymphocytes in many inflammatory disorders, most notably in the COVID-19. A closer look at the immunopathogenesis of ITP and COVID-19 brings us to common ground. The purpose of this study was to review and summarize the findings of various studies on the immunopathogenesis of ITP and its possible causes in COVID-19. Finally, enhanced differentiation of Th17 and Th1, the cell death called as pyroptosis, hyperinflammation and dysfunction of inflammatory neutrophils and macrophages, and NLRP3- inflammasome hyperactivity are important factors in the development of thrombocytopenia in patients with COVID-19. Further studies are needed to better understand immunopathogenesis and effective treatments for ITP, especially in inflammatory disorders

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Section: Studies Have Shown Significant Effects Of Nlrp3inflammasome ...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Possible immunological mechanisms in COVID-19 patients with immune thrombocytopenic purpura

Bahadoram

Saeedi-Boroujeni

Mahmoudian-Sani

2022

Med. Jadert. (Online)

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“…7,8 More importantly, it can exacerbate the ITP by increasing immune cells such as neutrophils, lymphocytes, platelets, and monocytes. 9 The interaction of the immune cells spontaneously raises the levels of inflammatory and pro-inflammatory cytokines, including such as interleukin (IL-10), IL-18, interferon-alpha (IFN-α), tumor necrosis factor-alpha (TNF-α), and IL-17, which ultimately are associated with enhanced immune responses. [10][11][12] According to previous studies, one of the leading immune mechanisms of autoantibody stimulation in ITP involves the interaction of immunomodulators, including regulatory T cells (Tregs), with inflammatory cells that direct immunostimulatory effects against autoantigens.…”

Section: Introductionmentioning

confidence: 99%

“…However, research in recent decades shows the prevalence of inflammation in ITP patients is high 7,8 . More importantly, it can exacerbate the ITP by increasing immune cells such as neutrophils, lymphocytes, platelets, and monocytes 9 . The interaction of the immune cells spontaneously raises the levels of inflammatory and pro‐inflammatory cytokines, including such as interleukin (IL‐10), IL‐18, interferon‐alpha (IFN‐α), tumor necrosis factor‐alpha (TNF‐α), and IL‐17, which ultimately are associated with enhanced immune responses 10‐12 …”

Section: Introductionmentioning

confidence: 99%

Evaluation of the hematological inflammatory parameters in the patients with immune thrombocytopenic purpura: A case–control study

Ahmadi,

Maleknia,

Khoshbakht

et al. 2024

Health Science Reports

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Background and AimsInflammation is one of the immune thrombocytopenic purpura (ITP)'s aggravating elements due to inflammatory cells' function. This study aims to identify and evaluate hematological inflammatory parameters, including neutrophil‐to‐lymphocyte ratio (NLR), platelet‐to‐lymphocyte ratio (PLR), and hemoglobin‐to‐platelet ratio (HPR), in patients with ITP compared to the control group.MethodsWe retrospectively analyzed the profile of 190 ITP patients from August 2019 to January 2021 at Imam Reza Hospital of Mashhad, Iran, along with 100 healthy individuals who had no ITP‐related clinical or laboratory symptoms. Immune cell counts, NLR, PLR, and HPR were calculated using the complete blood count at the time of diagnosis and after the treatment. The results were analyzed through MedCalc, SPSS software, and the receiver operating characteristic curve.ResultsThe result showed that white blood cell (WBC) and neutrophil counts were higher in ITP patients (WBC: p: 0.001, neutrophil: p: 0.001), and conversely, platelet and lymphocyte counts were higher in the control group compared to ITP patients (platelets: p: 0.001, lymphocytes: p: 0.001). The indices analysis between the two groups revealed that NLR was significantly increased in ITP patients (p: 0.001), but PLR was significantly reduced in ITP patients (with the mean platelet count of 23.44 ± 35.26 × 109/L) compared to the control group (with the mean platelet count of 234.04 ± 55.88 × 109/L). The HPR index also significantly increased in ITP patients (p: 0.001).ConclusionAn increase in NLR, PLR, and a decrease in HPR can be considered a valuable diagnostic algorithm in patients with ITP.

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“…The typical symptom of ITP is thrombocytopenia, which may be manifested by purpura of the skin and bleeding of the mucosa, or no signs of bleeding. ITP is the most common acquired hemorrhagic disease caused by autoimmune dysfunction, with an adult prevalence of about 3.3-3.9 per 100,000 individuals, and the prevalence is increasing year by year [1,2]. Evidence has shown that cellular immune abnormalities play an important role in the occurrence and development of ITP [3].…”

Section: Introductionmentioning

confidence: 99%

Decreasing lncRNA PVT1 causes Treg/Th17 imbalance via NOTCH signaling in immune thrombocytopenia

Yu¹,

Zhang²,

Jiang

et al. 2021

Hematology

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Objectives: Immune thrombocytopenia (ITP) is an autoimmune disease. T helper cell 17 (Th17) cells are increased in peripheral blood of ITP patients. NOTCH signaling is involved in Th17 cell differentiation and function. Besides, lncRNA Plasmacytoma variant translocation 1 (PVT1) was decreased in experimental autoimmune encephalomyelitis, and overexpressing PVT1 inhibited Th17 cell differentiation. Here, we aimed to investigate the effect of lncRNA PVT1 on ITP and its related mechanism. Methods: The number of Th17 cells and Treg cells was carried out using flow cytometry. PVT1 levels were detected by quantitative real-time PCR. Interleukin-17 (IL-17) levels and transforming growth factor-β (TGF-β) levels were detected by enzyme-linked immunosorbent assay. Protein levels of retinoid acid-related orphan receptor γ t (RORγt), forkhead box P3 (Foxp3), and NOTCH1 were carried out by western blot. NOTCH1 ubiquitylation was detected by ubiquitination assay. Results: PVT1 was down-regulated and Th17 cells were up-regulated in ITP patients. Overexpression of PVT1 decreased the number of Th17 cells, and also decreased the levels of IL-17, RORγt, and NOTCH1. Besides, PVT1 could bind to NOTCH1 and mediated NOTCH1 degradation by increasing its ubiquitination. Additionally, excessive expression of PVT1 could increase the levels of PVT1, reduce the amount of Th17 cells, as well as the levels of IL-17, RORγt, and NOTCH1, while co-overexpressing NOTCH1 reversed the results. Conclusion: PVT1 was down-regulated in ITP patients. Overexpressing PVT1 might reduce Th17 cell differentiation by down-regulating NOTCH1, and further alleviated the development of ITP.

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Aberrant expression of NLRP3, NLRC4 and NLRP6 inflammasomes in patients with primary immune thrombocytopenia

Cited by 9 publications

References 10 publications

Possible immunological mechanisms in COVID-19 patients with immune thrombocytopenic purpura

Possible immunological mechanisms in COVID-19 patients with immune thrombocytopenic purpura

Evaluation of the hematological inflammatory parameters in the patients with immune thrombocytopenic purpura: A case–control study

Decreasing lncRNA PVT1 causes Treg/Th17 imbalance via NOTCH signaling in immune thrombocytopenia

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