A5070026057- Sirtuins and Resveratrol in Medicine
- RNA regulation and disease
- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
- RNA modifications and cancer
- Cancer-related molecular mechanisms research
- Erythrocyte Function and Pathophysiology
- Cytomegalovirus and herpesvirus research
- Autophagy in Disease and Therapy
- Adenosine and Purinergic Signaling
- Cytokine Signaling Pathways and Interactions
- Cancer Cells and Metastasis
- Endoplasmic Reticulum Stress and Disease
- Heat shock proteins research
- Blood properties and coagulation
- Immunotherapy and Immune Responses
- Hippo pathway signaling and YAP/TAZ
- PI3K/AKT/mTOR signaling in cancer
- Histone Deacetylase Inhibitors Research
- interferon and immune responses
- Protein Tyrosine Phosphatases
- CAR-T cell therapy research
- Caveolin-1 and cellular processes
- Neuroinflammation and Neurodegeneration Mechanisms
- Immune cells in cancer
Beijing Normal University
2020-2024
Dendritic cells (DCs) play an important role in anti-tumor immunity by inducing T cell differentiation. Herein, we found that the DC mechanical sensor Piezo1 stimulated stiffness or inflammatory signals directs reciprocal differentiation of TH1 and regulatory (Treg) cancer. Genetic deletion DCs inhibited generation while driving development Treg promoting cancer growth mice. Mechanistically, Piezo1-deficient regulated secretion polarizing cytokines TGFβ1 IL-12, leading to increased...
Follicular helper T (TFH) cells are essential for inducing germinal center (GC) reactions to mediate humoral adaptive immunity in tumors; however, the mechanisms underlying TFH-cell differentiation remain unclear. In this study, we found that metabolism sensor sirtuin 3 (SIRT3) is critical and GC formation during tumor development viral infection. SIRT3 deficiency CD4+ intrinsically enhanced Mechanistically, damaged oxidative phosphorylation (OXPHOS) compensatively triggered NAD+-glycolysis...
The therapeutic effects of glucocorticoids on colitis and colitis-associated cancer are unclear. In this study, we investigated the roles in acute experimental ulcerative mice their immunoregulatory mechanisms. Murine was induced by dextran sulfate sodium (DSS) treated with dexamethasone (Dex) at different doses. Dex significantly exacerbated onset severity DSS-induced potentiated mucosal inflammatory macrophage neutrophil infiltration, as well cytokine production. Furthermore, under...
Follicular helper T (TFH ) cells are essential for inducing germinal centre (GC) reactions to mediate humoral adaptive immunity and antiviral effects, but the mechanisms of TFH cell differentiation remain unclear. Here, we found that hippo kinase MST1 is critical differentiation, GC formation, antibody production under steady-state conditions viral infection. deficiency intrinsically enhanced in vivo vitro. Mechanistically, mTOR HIF1α signalling involved glucose metabolism increased...
Protein tyrosine phosphatase (PTPase) is critically involved in the regulation of hematopoietic stem cell development and differentiation. Roles novel isolated receptor PTPase PTPRO from bone marrow cells granulopoiesis have not been investigated. expression correlated with granulocytic differentiation, Ptpro-/- mice developed neutrophilia, an expanded compartment resulting a cell-autonomous increase number granulocyte progenitors under steady-state potentiated innate immune responses...
<div>Abstract<p>Follicular helper T (T<sub>FH</sub>) cells are essential for inducing germinal center (GC) reactions to mediate humoral adaptive immunity in tumors; however, the mechanisms underlying T<sub>FH</sub>-cell differentiation remain unclear. In this study, we found that metabolism sensor sirtuin 3 (SIRT3) is critical and GC formation during tumor development viral infection. SIRT3 deficiency CD4<sup>+</sup> intrinsically enhanced...
<p>Fig.S10. SIRT3 is required for promoting T<sub>FH</sub> differentiation and GC responses <i>in vivo</i>.</p>
<p>Fig.S19. SIRT3 deficiency promotes T<sub>FH</sub> differentiation through mTOR and NAD<sup>+</sup> pathway.</p>
<p>Fig.S14. Oxidative phosphorylation is required for T<sub>FH</sub> differentiation induced by <i>Sirt3</i><sup><i>∆CD4</i></sup>.</p>
<p>Fig.S11. SIRT3 negatively affects efficient GC responses after immunization via antigen-specific mechanisms.</p>
<p>Fig. S15. SIRT3 deficiency upregulates the expression of Glut1 and p-S6 in T<sub>FH</sub> cells tumor.</p>
<p>Fig. S13. NAD<sup>+</sup> levels are crucial for T<sub>FH</sub> cell differentiation induced by <i>Sirt3</i><sup><i>∆CD4</i></sup> in tumor.</p>
<p>Fig. S18. SIRT3 deficiency promotes T<sub>FH</sub> differentiation through mTOR-HIF1α coupled with NAD<sup>+</sup>-dependent glucose metabolism pathway.</p>
<p>Fig. S16. SIRT3 deficiency upregulates the expressions of HIF1α</p>
<p>Fig.S12. SIRT3 deficiency enhances T<sub>FH</sub> cell differentiation <i>in vitro</i>.</p>
<p>Fig.S17. SIRT3 deficiency promotes T<sub>FH</sub> cell differentiation through mTOR-HIF1α coupled with the NAD<sup>+</sup>-dependent glucose metabolism pathway in mice.</p>