Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
746
result(s) for
"Lu, Liwei"
Sort by:
The Roles of Immune Cells in the Pathogenesis of Fibrosis
Tissue injury and inflammatory response trigger the development of fibrosis in various diseases. It has been recognized that both innate and adaptive immune cells are important players with multifaceted functions in fibrogenesis. The activated immune cells produce various cytokines, modulate the differentiation and functions of myofibroblasts via diverse molecular mechanisms, and regulate fibrotic development. The immune cells exhibit differential functions during different stages of fibrotic diseases. In this review, we summarized recent advances in understanding the roles of immune cells in regulating fibrotic development and immune-based therapies in different disorders and discuss the underlying molecular mechanisms with a focus on mTOR and JAK-STAT signaling pathways.
Journal Article
Integration of InSAR and numerical modelling to assess tailings pond slope deformation affected by reservoir water
Slope stability in tailings ponds is crucial for both environmental safety and operational efficiency, as instability can lead to significant hazards. This study introduces a novel integrated approach combining SBAS-InSAR and fluid–structure interaction numerical modeling to enhance the monitoring and stability analysis of tailing pond slopes. A fluid–structure interaction model is presented, incorporating the effects of pore pressure generated by reservoir water level on slope stability, thereby improving the accuracy of internal stress and deformation analysis. Sentinel-1 SAR data were used to monitor surface displacements over a 2-year period (2021–2023), while a three-dimensional numerical model was employed to simulate the mechanical behavior of the tailings dam, considering different material properties and reservoir water level conditions. The results reveal notable spatial patterns of slope deformation, with the presence of reservoir water level and stratigraphic boundaries leading to significant changes in stress and displacement profiles. Comparison between the InSAR results and numerical simulations shows a high level of agreement, with error and statistical analyses, respectively, validating the robustness of the integrated approach. This study provides a comprehensive multi-source method for tailing pond slope monitoring, offering a more accurate and reliable technique for predicting slope instability and improving risk assessment.
Journal Article
Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases
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.
Journal Article
Multiple Functions of B Cells in the Pathogenesis of Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by excessive autoantibody production and multi-organ involvement. Although the etiology of SLE still remains unclear, recent studies have characterized several pathogenic B cell subsets and regulatory B cell subsets involved in the pathogenesis of SLE. Among pathogenic B cell subsets, age-associated B cells (ABCs) are a newly identified subset of autoreactive B cells with T-bet-dependent transcriptional programs and unique functional features in SLE. Accumulation of T-bet+ CD11c+ ABCs has been observed in SLE patients and lupus mouse models. In addition, innate-like B cells with the autoreactive B cell receptor (BCR) expression and long-lived plasma cells with persistent autoantibody production contribute to the development of SLE. Moreover, several regulatory B cell subsets with immune suppressive functions have been identified, while the impaired inhibitory effects of regulatory B cells have been indicated in SLE. Thus, further elucidation on the functional features of B cell subsets will provide new insights in understanding lupus pathogenesis and lead to novel therapeutic interventions in the treatment of SLE.
Journal Article
Designing new low alloyed Mg—RE alloys with high strength and ductility via high-speed extrusion
Two new low-alloyed Mg—2RE—0.8Mn—0.6Ca—0.5Zn (wt%, RE = Sm or Y) alloys are developed, which can be produced on an industrial scale via relatively high-speed extrusion. These two alloys are not only comparable to commercial AZ31 alloy in extrudability, but also have superior mechanical properties, especially in terms of yield strength (YS). The excellent extrudability is related to less coarse second-phase particles and high initial melting point of the two as-cast alloys. The high strength—ductility mainly comes from the formation of fine grains, nano-spaced submicron/nano precipitates, and weak texture. Moreover, it is worth noting that the YS of the two alloys can maintain above 160 MPa at elevated temperature of 250°C, significantly higher than that of AZ31 alloy (YS: 45 MPa). The Zn/Ca solute segregation at grain boundaries, the improved heat resistance of matrix due to addition of RE, and the high melting points of strengthening particles (Mn, MgZn
2
, and Mg—Zn—RE/Mg—Zn—RE—Ca) are mainly responsible for the excellent high-temperature strength.
Journal Article
Epigenetic regulation of B cells and its role in autoimmune pathogenesis
B cells play a pivotal role in the pathogenesis of autoimmune diseases. Although previous studies have shown many genetic polymorphisms associated with B-cell activation in patients with various autoimmune disorders, progress in epigenetic research has revealed new mechanisms leading to B-cell hyperactivation. Epigenetic mechanisms, including those involving histone modifications, DNA methylation, and noncoding RNAs, regulate B-cell responses, and their dysregulation can contribute to the pathogenesis of autoimmune diseases. Patients with autoimmune diseases show epigenetic alterations that lead to the initiation and perpetuation of autoimmune inflammation. Moreover, many clinical and animal model studies have shown the promising potential of epigenetic therapies for patients. In this review, we present an up-to-date overview of epigenetic mechanisms with a focus on their roles in regulating functional B-cell subsets. Furthermore, we discuss epigenetic dysregulation in B cells and highlight its contribution to the development of autoimmune diseases. Based on clinical and preclinical evidence, we discuss novel epigenetic biomarkers and therapies for patients with autoimmune disorders.
Journal Article
Roles of IL-25 in Type 2 Inflammation and Autoimmune Pathogenesis
Interleukin-17E (IL-25) is a member of the IL-17 cytokine family that includes IL-17A to IL-17F. IL-17 family cytokines play a key role in host defense responses and inflammatory diseases. Compared with other IL-17 cytokine family members, IL-25 has relatively low sequence similarity to IL-17A and exhibits a distinct function from other IL-17 cytokines. IL-25 binds to its receptor composed of IL-17 receptor A (IL-17RA) and IL-17 receptor B (IL-17RB) for signal transduction. IL-25 has been implicated as a type 2 cytokine and can induce the production of IL-4, IL-5 and IL-13, which in turn inhibits the differentiation of T helper (Th) 17. In addition to its anti-inflammatory properties, IL-25 also exhibits a pro-inflammatory effect in the pathogenesis of Th17-dominated diseases. Here, we review recent advances in the roles of IL-25 in the pathogenesis of inflammation and autoimmune diseases.
Journal Article
The Multiple Roles of B Cells in the Pathogenesis of Sjögren’s Syndrome
Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disease characterized by lymphocytic infiltration and tissue destruction of exocrine glands such as salivary glands. Although the formation of ectopic lymphoid tissue in exocrine glands and overproduction of autoantibodies by autoreactive B cells highlight the critical involvement of B cells in disease development, the precise roles of various B cell subsets in pSS pathogenesis remain partially understood. Current studies have identified several novel B cell subsets with multiple functions in pSS, among which autoreactive age-associated B cells, and plasma cells with augmented autoantibody production contribute to the disease progression. In addition, tissue-resident Fc Receptor-Like 4 (FcRL4) + B cell subset with enhanced pro-inflammatory cytokine production serves as a key driver in pSS patients with mucosa-associated lymphoid tissue (MALT)-lymphomas. Recently, regulatory B (Breg) cells with impaired immunosuppressive functions are found negatively correlated with T follicular helper (Tfh) cells in pSS patients. Further studies have revealed a pivotal role of Breg cells in constraining Tfh response in autoimmune pathogenesis. This review provides an overview of recent advances in the identification of pathogenic B cell subsets and Breg cells, as well as new development of B-cell targeted therapies in pSS patients.
Journal Article
Inflammasome and Its Therapeutic Targeting in Rheumatoid Arthritis
Inflammasome is a cytoplasmic multiprotein complex that facilitates the clearance of exogenous microorganisms or the recognition of endogenous danger signals, which is critically involved in innate inflammatory response. Excessive or abnormal activation of inflammasomes has been shown to contribute to the development of various diseases including autoimmune diseases, neurodegenerative changes, and cancers. Rheumatoid arthritis (RA) is a chronic and complex autoimmune disease, in which inflammasome activation plays a pivotal role in immune dysregulation and joint inflammation. This review summarizes recent findings on inflammasome activation and its effector mechanisms in the pathogenesis of RA and potential development of therapeutic targeting of inflammasome for the immunotherapy of RA.
Journal Article