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Activation of Platelet mTORC2/Akt Pathway by Anti-β2GP1 Antibody Promotes Thrombosis in Antiphospholipid Syndrome

Tang, Zihan ; Shi, Hui ; Chen, Changming ; [et al.]

Ovid Technologies (Wolters Kluwer Health) ; 2023

In: Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 43, No. 10 ( 2023-10), p. 1818-1832

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In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. 10 ( 2023-10), p. 1818-1832

Abstract: Anti-β2GP1 (β2-glycoprotein 1) antibodies are the primary pathogenic antibody to promote thrombosis in antiphospholipid syndrome (APS), yet the underlying mechanism remains obscure. We aimed to explore the intracellular pathway that mediated platelet activation. METHODS: Platelets were isolated from patients with APS and subjected to RNA sequencing. Platelet aggregation, the release of platelet granules, platelet spreading, and clot retraction were detected to evaluate platelet activation. We purified anti-β2GP1 antibodies from patients with APS and the total IgG from healthy donors to stimulate platelets with/without FcγRIIA (Fcγ receptor IIA) blocking antibody or Akt (protein kinase B) inhibitor. Platelet-specific Sin1 (stress-activated protein kinase–interacting protein) deficiency mice were established. The thrombus model of inferior vena cava flow restriction, ferric chloride–induced carotid injury model, and laser-induced vessel wall injury in cremaster arterioles model were constructed after administration of anti-β2GP1 antibodies. RESULTS: Combined RNA sequencing and bioinformatics analysis suggested that APS platelets exhibited increased levels of mRNA associated with platelet activation, which was in line with the hyperactivation of APS platelets in response to stimuli. Platelet activation in APS platelets was accompanied by upregulation of the mTORC2 (mammalian target of the rapamycin complex 2)/Akt pathway and increased levels of SIN1 phosphorylation at threonine 86. Anti-β2GP1 antibody derived from patients with APS enhanced platelet activation and upregulated the mTORC2/Akt pathway. Moreover, the Akt inhibitor weakened the potentiating effect of the anti-β2GP1 antibody on platelet activation. Notably, Sin1 deficiency suppresses anti-β2GP1 antibody–enhanced platelet activation in vitro and thrombosis in all 3 models. CONCLUSIONS: This study elucidated the novel mechanism involving the mTORC2/Akt pathway, which mediates the promotion of platelet activation and induction of thrombosis by the anti-β2GP1 antibody. The findings suggest that SIN1 may be a promising therapeutic target for the treatment of APS.

Type of Medium: Online Resource

ISSN: 1079-5642 , 1524-4636

URL: Article

DOI: 10.1161/ATVBAHA.123.318978

Language: English

Publisher: Ovid Technologies (Wolters Kluwer Health)

Publication Date: 2023

detail.hit.zdb_id: 1494427-3

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Performance of the modified Systemic Manifestation Score for systemic juvenile idiopathic arthritis in Adult-onset Still’s disease

Zhu, Dehao ; Meng, Jianfen ; Jia, Jinchao ; [et al.]

Springer Science and Business Media LLC ; 2023

In: Clinical Rheumatology Vol. 42, No. 1 ( 2023-01), p. 187-195

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In: Clinical Rheumatology, Springer Science and Business Media LLC, Vol. 42, No. 1 ( 2023-01), p. 187-195

Type of Medium: Online Resource

ISSN: 0770-3198 , 1434-9949

URL: Article

DOI: 10.1007/s10067-022-06340-7

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2023

detail.hit.zdb_id: 1480901-1

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Anti-β2GPI domain 1 antibodies stratify high risk of thrombosis and late pregnancy morbidity in a large cohort of Chinese patients with antiphospholipid syndrome

Liu, Tingting ; Gu, Jieyu ; Wan, Liyan ; [et al.]

Elsevier BV ; 2020

In: Thrombosis Research Vol. 185 ( 2020-01), p. 142-149

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In: Thrombosis Research, Elsevier BV, Vol. 185 ( 2020-01), p. 142-149

Type of Medium: Online Resource

ISSN: 0049-3848

URL: Article

DOI: 10.1016/j.thromres.2019.11.029

Language: English

Publisher: Elsevier BV

Publication Date: 2020

detail.hit.zdb_id: 1500780-7

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Table_3.docx

Sun, Yue ; Wang, Fan ; Zhou, Zhuochao ; [et al.]

Frontiers Media SA ; 2020

In: Frontiers in Immunology Vol. 11 ( 2020-9-4)

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In: Frontiers in Immunology, Frontiers Media SA, Vol. 11 ( 2020-9-4)

Type of Medium: Online Resource

ISSN: 1664-3224

URL: Article

DOI: 10.3389/fimmu.2020.02112

DOI: 10.3389/fimmu.2020.02112.s001

DOI: 10.3389/fimmu.2020.02112.s002

DOI: 10.3389/fimmu.2020.02112.s003

DOI: 10.3389/fimmu.2020.02112.s004

Language: Unknown

Publisher: Frontiers Media SA

Publication Date: 2020

detail.hit.zdb_id: 2606827-8

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DataSheet_1.docx

Meng, Jianfen ; Ma, Yuning ; Jia, Jinchao ; [et al.]

Frontiers Media SA ; 2021

In: Frontiers in Immunology Vol. 11 ( 2021-1-19)

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In: Frontiers in Immunology, Frontiers Media SA, Vol. 11 ( 2021-1-19)

Abstract: The catastrophic outbreak of coronavirus disease 2019 (COVID-19) is currently a public emergency. Adult-onset Still’s disease (AOSD) is an autoinflammatory disease characterized by life-threatening complications. Systemic hyperinflammation and cytokine storm play a critical role in the pathogenesis of both COVID-19 and AOSD. We aimed to compare the similarities and differences focusing on ferritin and cytokine levels between severe COVID-19 and active AOSD. A literature search was performed using the databases PubMed, EMBASE, and Web of Science to collect the levels of cytokine including IL-1β, IL-6, IL-18, TNF-α, IL-10, and ferritin in severe COVID-19 patients. After extracting available data of indicators of interest, we acquired these statistics with a single-arm meta-analysis. Furthermore, a comparison was conducted between 52 patients with active AOSD in our center and severe COVID-19 patients from databases. The levels of IL-6 and IL-10 were higher in severe COVID-19 compared with those in active AOSD. There were no significant differences on the cytokine of IL-1β and TNF-α. Fold changes of IL-18 were defined as the mean expression level ratio of severe COVID-19 to healthy controls in the COVID-19 study and active AOSD to healthy controls in our study, individually. Although the fold change of IL-18 in patients with AOSD was significantly higher than patients with severe COVID-19 (fold change: 594.00 vs 2.17), there was no statistical comparability. In addition, the level of ferritin was higher in active AOSD in comparison with severe COVID-19. Our findings suggest that severe COVID-19 and active AOSD have differences in cytokine panel and ferritin level, indicating the pathogenic role of ferritin in overwhelming inflammation. And it paves the way to make efficacy therapeutic strategy targeting the hyperinflammatory process in COVID-19 according to AOSD management, especially in severe COVID-19.

Type of Medium: Online Resource

ISSN: 1664-3224

URL: Article

DOI: 10.3389/fimmu.2020.603389

DOI: 10.3389/fimmu.2020.603389.s001

Language: Unknown

Publisher: Frontiers Media SA

Publication Date: 2021

detail.hit.zdb_id: 2606827-8

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Circulating Neutrophil Extracellular Traps Signature for Identifying Organ Involvement and Response to Glucocorticoid in Adult-Onset Still’s Disease: A Machine Learning Study

Jia, Jinchao ; Wang, Mengyan ; Ma, Yuning ; [et al.]

Frontiers Media SA ; 2020

In: Frontiers in Immunology Vol. 11 ( 2020-11-9)

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In: Frontiers in Immunology, Frontiers Media SA, Vol. 11 ( 2020-11-9)

Type of Medium: Online Resource

ISSN: 1664-3224

URL: Article

DOI: 10.3389/fimmu.2020.563335

Language: Unknown

Publisher: Frontiers Media SA

Publication Date: 2020

detail.hit.zdb_id: 2606827-8

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COVID-19 vaccine affects neither prothrombotic antibody profile nor thrombosis in primary anti-phospholipid syndrome: a prospective study

Pan, Haoyu ; Tang, Zihan ; Teng, Jialin ; [et al.]

Oxford University Press (OUP) ; 2023

In: Rheumatology Vol. 62, No. 2 ( 2023-02-01), p. 829-834

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In: Rheumatology, Oxford University Press (OUP), Vol. 62, No. 2 ( 2023-02-01), p. 829-834

Abstract: To explore whether inactivated coronavirus disease 2019 vaccine influences the profile of prothrombotic autoantibodies and induces thrombotic events in primary APS patients. Methods We enrolled 39 primary APS patients who received two doses of inactivated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine (BBIBPCorV, Sinopharm, Beijing, China) voluntarily in this prospective cohort. Prothrombotic autoantibodies were determined before vaccination and 4 weeks after the second dose of vaccination. Thrombotic disorders were evaluated via hospital site visits and assessments. Results There was no significant difference in the presence of all 11 autoantibodies detected before and 4 weeks after vaccination: for aCL, IgG (14 vs 16, P = 0.64), IgM (13 vs 19, P = 0.34), IgA (2 vs 3, P = 0.64); anti-β2GP1, IgG (12 vs 12, P = 1.00), IgM (5 vs 8, P = 0.36), IgA (4 vs 3, P = 0.69); anti-PS/PT IgG (13 vs 16, P = 0.48), IgM (17 vs 22, P = 0.26); LAC (22 vs 28, P = 0.16); aPF4-heparin (0 vs 0, P = 1.00) and ANA (23 vs 26, P = 0.48). Notably, the distribution of the aPL profile in the pre- and post-vaccination cohorts was not affected by SARS-CoV-2 vaccination: for patients with a low-risk aPL profile (11 vs 10, P = 0.799) and patients with a high-risk aPL profile (28 vs 29, P = 0.799), respectively. Furthermore, no case exhibited symptoms of the thrombotic disorder during a minimum follow-up period of 12 weeks. There was no adjustment to the ongoing treatment regimens following SARS-CoV-2 vaccination. Conclusion Inactivated SARS-CoV-2 vaccine does not influence the profile of anti-phospholipid antibodies and anti-PF4-heparin antibodies nor induces thrombotic events in primary APS patients.

Type of Medium: Online Resource

ISSN: 1462-0324 , 1462-0332

URL: Article

DOI: 10.1093/rheumatology/keac400

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2023

detail.hit.zdb_id: 1474143-X

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Image_6.tif

Zhou, Zhuochao ; You, Yijun ; Wang, Fan ; [et al.]

Frontiers Media SA ; 2021

In: Frontiers in Immunology Vol. 12 ( 2021-8-19)

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In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-8-19)

Abstract: Antiphospholipid syndrome (APS) is a multisystem disorder characterized by thrombosis and/or recurrent fetal loss. This clinical phenotype heterogeneity may result in differences in response to treatment and prognosis. In this study, we aimed to identify primary thrombotic APS (TAPS) from primary obstetric APS (OAPS) using urine proteomics as a non-invasive method. Only patients with primary APS were enrolled in this study from 2016 to 2018 at a single clinical center in Shanghai. Urine samples from 15 patients with TAPS, 9 patients with OAPS, and 15 healthy controls (HCs) were collected and analyzed using isobaric tags for relative and absolute quantification (iTRAQ) labeling combined with liquid chromatography-tandem mass spectrometry analysis to identify differentially expressed proteins. Cluster analysis of urine proteomics identified differentiated proteins among the TAPS, OAPS, and HC groups. Urinary proteins were enriched in cytokine and cytokine receptor pathways. Representative secreted cytokines screened out (fold change & gt;1.20, or & lt;0.83, p & lt;0.05) in these differentiated proteins were measured by enzyme-linked immunosorbent assay in a validation cohort. The results showed that the levels of C-X-C motif chemokine ligand 12 (CXCL12) were higher in the urine of patients with TAPS than in those with OAPS ( p =0.035), while the levels of platelet-derived growth factor subunit B (PDGFB) were lower in patients with TAPS than in those with OAPS ( p =0.041). In addition, correlation analysis showed that CXCL12 levels were positively correlated with immunoglobulin G anti-β2-glycoprotein I antibody ( r =0.617, p =0.016). Our results demonstrated that urinary CXCL12 and PDGFB might serve as potential non-invasive markers to differentiate primary TAPS from primary OAPS.

Type of Medium: Online Resource

ISSN: 1664-3224

URL: Article

DOI: 10.3389/fimmu.2021.702425

DOI: 10.3389/fimmu.2021.702425.s001

DOI: 10.3389/fimmu.2021.702425.s002

DOI: 10.3389/fimmu.2021.702425.s003

DOI: 10.3389/fimmu.2021.702425.s004

DOI: 10.3389/fimmu.2021.702425.s005

DOI: 10.3389/fimmu.2021.702425.s006

DOI: 10.3389/fimmu.2021.702425.s007

Language: Unknown

Publisher: Frontiers Media SA

Publication Date: 2021

detail.hit.zdb_id: 2606827-8

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Neutrophil-derived lipocalin-2 in adult-onset Still’s disease: a novel biomarker of disease activity and liver damage

Jia, Jinchao ; Yang, Luyu ; Cao, Zhujun ; [et al.]

Oxford University Press (OUP) ; 2021

In: Rheumatology Vol. 60, No. 1 ( 2021-01-05), p. 304-315

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In: Rheumatology, Oxford University Press (OUP), Vol. 60, No. 1 ( 2021-01-05), p. 304-315

Abstract: Liver damage is a common manifestation and can be life-threatening in adult-onset Still’s disease (AOSD), an autoinflammatory disease. The hallmark of AOSD is activation of neutrophils, whose infiltration in liver is suspected to promote tissue injury. Here we aimed to identify a candidate biomarker and to validate its association with liver damage in AOSD. Methods Transcriptome analysis of neutrophils from treatment-naïve active AOSD patients and healthy donors was performed. Lipocalin-2 (LCN2) expression was assessed in neutrophils, plasma and liver biopsies of AOSD. The correlations of LCN2 with different variables and its ability to identify liver damage from AOSD patients were analysed. Results LCN2, a novel biomarker in hepatic inflammation, was found to be upregulated in AOSD neutrophils by RNA sequencing and confirmed at the mRNA and protein levels. Plasma levels of LCN2 were significantly higher in AOSD patients than healthy controls, RA and SLE patients. Plasma LCN2 levels were closely correlated with inflammatory markers, systemic score, HScore and cytokines. Moreover, LCN2 levels were increased in active AOSD with liver involvement and independently associated with liver dysfunction. Enhanced expression of LCN2 was detected in liver biopsies from three patients with ongoing liver injury. Furthermore, the area under the curve value of LCN2 for identifying AOSD with liver injury from other liver diseases was 0.9694. Conclusion Our results reveal that neutrophils-derived LCN2 is higher in plasma and liver tissue in AOSD patients than in healthy controls, and it could serve as a potent biomarker for identifying AOSD with systemic inflammation, especially liver damage caused by hyperinflammation.

Type of Medium: Online Resource

ISSN: 1462-0324 , 1462-0332

URL: Article

DOI: 10.1093/rheumatology/keaa368

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2021

detail.hit.zdb_id: 1474143-X

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The landscape of innate and adaptive immune cell subsets in patients with adult-onset Still’s disease

Chi, Huihui ; Hong, Xinyue ; Dai, Ningqi ; [et al.]

Oxford University Press (OUP) ; 2023

In: Rheumatology ( 2023-09-26)

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In: Rheumatology, Oxford University Press (OUP), ( 2023-09-26)

Abstract: Adult-onset Still’s disease (AOSD) is a systemic autoinflammatory disorder. The understanding of the changes in adaptive immune cells and the crosstalk between innate and adaptive immune systems in AOSD is limited. This study aimed to examine the peripheral immune cell composition and inflammatory protein levels in AOSD patients. Methods Twenty-nine active AOSD patients were enrolled. Flow cytometry was used to analyze the cell populations in peripheral blood. Antibody chips were utilized to detect the protein expression profile in serum. Results In active AOSD patients, there was an increase in the percentage of classical and non-classical monocytes among peripheral blood mononuclear cells. The proportion of natural killer (NK) cells decreased, with an increase in CD56dim NK1 cells and a decrease in CD56bright NK2 cells compared with healthy controls (HC). The percentage of naïve central memory T cells was decreased, while the percentage of effector and effector memory T cells was increased among adaptive lymphocytes. The proportion of naïve B and memory B cells was decreased, while plasma cells were increased in AOSD patients, indicating activation of the adaptive immune system. Additionally, the serum levels of 40 proteins were elevated in AOSD patients, primarily involved in cytokine-cytokine receptor interaction, inflammatory response, and regulation of MAPK cascade. Conclusion Our findings showed the activation of the innate and adaptive immune system in AOSD. The protein-protein interaction analysis suggested potential communication between innate and adaptive cell subsets. These findings provide new insights into the pathogenesis of the disease and the development of targeted therapies.

Type of Medium: Online Resource

ISSN: 1462-0324 , 1462-0332

URL: Article

DOI: 10.1093/rheumatology/kead507

Language: English

Publisher: Oxford University Press (OUP)

Publication Date: 2023

detail.hit.zdb_id: 1474143-X

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