Objective To review the osteoimmunomodulatory effects and related mechanisms of inorganic biomaterials in the process of bone repair. Methods A wide range of relevant domestic and foreign literature was reviewed, the characteristics of various inorganic biomaterials in the process of bone repair were summarized, and the osteoimmunomodulatory mechanism in the process of bone repair was discussed. Results Immune cells play a very important role in the dynamic balance of bone tissue. Inorganic biomaterials can directly regulate the immune cells in the body by changing their surface roughness, surface wettability, and other physical and chemical properties, constructing a suitable immune microenvironment, and then realizing dynamic regulation of bone repair. Conclusion Inorganic biomaterials are a class of biomaterials that are widely used in bone repair. Fully understanding the role of inorganic biomaterials in immunomodulation during bone repair will help to design novel bone immunomodulatory scaffolds for bone repair.
Using the techniques of monoclonal antibody and radioactive isotope,we found that the total glueosides of paeony (TGP) could almost regain peripheral blood T cell subsets increased or decreased ,supressed cellular immune function and disordered humor immune function of the patients with endogenous uveitis(ElJ) to normal level ,but could not regain those evidently of the patients in control group. The result suggested that TGP might possess double immunomodulatory effect on the patients with EU. （Chin J Ocul Fundus Dis,1994,10:146-148）
ObjectiveTo investigate the pan-cancer expression profile, prognostic value, co-expression networks, immune regulatory roles of BRF1, and its biological functions and molecular mechanisms in esophageal squamous cell carcinoma (ESCC). MethodsIntegrated analysis of TCGA pan-cancer datasets was performed to evaluate BRF1 expression differences between tumor/normal tissues, survival correlations, co-expressed gene-enriched pathways, and immune features (immune checkpoints, cytokines, immune cell infiltration). GEO datasets were used to validate BRF1 expression in ESCC. BRF1 was knocked down using siRNA in ESCC cells, with MTT and Transwell assays assessing proliferation/migration, and Western blot analyzing proliferation- (PCNA) and migration-related proteins (Vimentin, MMP, E-Cadherin). TCGA data were analyzed to explore BRF1-ferroptosis correlations. ResultsBRF1 was significantly upregulated in over 20 cancer types. High BRF1 expression predicted poor prognosis in adrenocortical carcinoma (ACC) and prostate adenocarcinoma (PRAD). BRF1 positively regulated T cell-mediated cell death pathways in ESCA and circadian rhythm pathways in PAAD. BRF1 exhibited cancer-type-specific correlations with immune checkpoints, cytokine networks, and immune cell infiltration. In vitro, BRF1 knockdown suppressed ESCC proliferation (PCNA downregulation) and migration (Vimentin/MMP downregulation, E-Cadherin upregulation). BRF1 expression positively correlated with ferroptosis antagonists (GPX4, HSPA5, SLC7A11). ConclusionBRF1 demonstrates complex pan-cancer expression and functional heterogeneity, modulating tumor progression and immune infiltration. BRF1 promotes ESCC proliferation and migration, potentially via ferroptosis resistance regulation, highlighting its potential as a therapeutic target in ESCC.
Age-related macular degeneration (AMD) is an age-related degenerative disease with complex pathogenesis, whose initial lesion is accompanied with immune inflammatory response. Amyloid beta (Aβ), a small-molecule protein generated by the hydrolysis of amyloid precursor protein, as the main component, is involved in the formation of drusen, which serves as the early characteristic of AMD. In the local inflammatory response of AMD, Aβ is an important pathological deposit, promoting the proliferation and differentiation of macrophages as well as changing their morphology to accelerate the progression of AMD. In addition, Aβ can also regulate immune molecules and the complement system by activating inflammatory pathways, thus mediating chronic retinal inflammation and promoting the course of AMD. However, since AMD is not caused by inflammation alone, only the immunosuppression may not be effective in inhibiting the course of AMD, and thus the future development is to rebalance the disordered immune system in AMD patients eyes.
Objective To summarize research progress of the mechanism of natural killer cells (NK cells) acted in regulating the T cell immunity in chronic infectious disease. Method Literatures about recent studies concerning how NK cells act as a regulator for T cells in chronic infectious disease were reviewed according to the results obtained from PubMed, Embase, CNKI, CBM, and Wanfang databases. Results NK cells that acted as regulators of T cell immunity could affect T cell immune responses through influencing antigen presentation, secreting cytokine, and presenting lytic activities, thus playing an important role in the immunological therapy of chronic infectious diseases. Conclusion NK cells are critical for T cell immune regulation, which could provide noval strategies for immunological therapy of chronic infectious disease, transplantation-related immune rejection, and autoimmune disease.
Sepsis is a worldwide problem. Although there are many related researchs and animal experiments about sepsis, the mortality of sepsis is still high. In the early stage of sepsis, after the pathogenic bacteria invade the body, the immune response produced by the body promotes the synthesis and secretion of a series of cytokines. Among them, there are proinflammatory cytokines that promote inflammatory response and anti-inflammatory cytokines that inhibit inflammatory response. These cytokines interact with each other and maintain a dynamic balance in complex cell grid. This is to restore the steady state of the body after resisting and eliminating the invaders.Anti-inflammatory cytokines play an important role in it. They act on specific immune cells or immune regulatory receptors. Anti-inflammatory cytokines limit persistent or excessive inflammatory responses after killing invaders, and reduce or block pro-inflammatory cytokine activities. These anti-inflammatory cytokines also can heal body to restore the normal immune physiological level of the organism. This article will review the related research of anti-inflammatory cytokines in sepsis.
Objective To explore the role of high endothelial venule (HEV) in chronic obstructive pulmonary disease (COPD) at the single cell level. Methods A total of 219257 cells from the lung tissues of 18 COPD patients and 28 healthy controls in the GEO public database (GSE136831) were used to analyze the relationship between HEV with T lymphocytes, B lymphocytes, and dendritic cells. Results Endothelial cells were extracted using single cell analysis technique, and sorting out venous endothelium, CCL14, IGFBP7, POSTN were used as marker genes for HEV endothelial cells. The ratio of HEV endothelial cells was also identified as up-regulated expression in COPD. The function of the differential genes of HEV endothelial cells was analyzed, suggesting the presence of immune regulation. By trajectory analysis, it was suggested that the differential genes of HEV endothelial cells were enriched for extracellular matrix deposition in late development. Finally, by receptor-ligand pairing, it was suggested that HEV endothelial cells was recruited through a series of ligands with T lymphocytes, B lymphocytes, and dendritic cells. Conclusions HEV endothelial cells are elevated in COPD and have an immunomodulatory role by secreting a series of ligands after recruiting T lymphocytes, B lymphocytes as well as dendritic cells for immune action. HEV may be a potential target for the study of COPD therapy.
Objective To review the research progress in the construction strategy and application of bone/cartilage immunomodulating hydrogels. Methods The literature related to bone/cartilage immunomodulating hydrogels at home and abroad in recent years was reviewed and summarized from the immune response mechanism of different immune cells, the construction strategy of immunomodulating hydrogels, and their practical applications. Results According to the immune response mechanism of different immune cells, the biological materials with immunoregulatory effect is designed, which can regulate the immune response of the body and thus promote the regeneration of bone/cartilage tissue. Immunomodulating hydrogels have good biocompatibility, adjustability, and multifunctionality. By regulating the physical and chemical properties of hydrogel and loading factors or cells, the immune system of the body can be purposively regulated, thus forming an immune microenvironment conducive to osteochondral regeneration. ConclusionImmunomodulating hydrogels can promote osteochondral repair by affecting the immunomodulation process of host organs or cells. It has shown a wide application prospect in the repair of osteochondral defects. However, more data support from basic and clinical experiments is needed for this material to further advance its clinical translation process.
Since the emergence of novel coronavirus pneumonia in late 2019, it has quickly spread to many countries and regions around the world, causing a significant impact on human beings and society, posing a great threat to the global public health system. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was highly infectious, and some complications emerged rapidly in some patients, including acute respiratory distress syndrome, and multiple organ failure. The virus could trigger a series of immune responses, which might lead to excessive immune activation, thereby bringing about the immune system imbalance of the body. Up to now, there was no specific antiviral drug, and we conjectured that immunomodulatory therapy might play an essential part in the treatment of coronavirus disease 2019 (COVID-19) as adjuvant therapy. Therefore, we analyzed the possible mechanism of immune imbalance caused by the new coronavirus, and summarized the immunotherapeutic means of COVID-19 based on the mechanisms, to provide some reference for follow-up research and clinical prevention and treatment of COVID-19.