Changes in macrophage infiltration and podocyte injury in lupus nephritis patients with repeated renal biopsy: Report of three cases

BACKGROUND In this study,we retrospectively analysed macrophage infiltration and podocyte injury in three patients with diffuse proliferative lupus nephritis(LN)who un-derwent repeated renal biopsy.CASE SUMMARY Clinical data of three diffuse proliferative LN patients with different pathological characteristics(case 1 was LN IV-G(A),case 2 was LN IV-G(A)+V,and case 3 was LN IV-G(A)+thrombotic microangiopathy)were reviewed.All patients underwent repeated renal biopsies 6 mo later,and renal biopsy specimens were studied.Macrophage infiltration was assessed by CD68 expression detected by immunohistochemical staining,and an immunofluorescence assay was used to detect podocin expression to assess podocyte damage.After treatment,Case 1 changed to LN III-(A),Case 2 remained as type V LN lesions,and Case 3,which changed to LN IV-S(A),had the worst prognosis.We observed reduced macro-phage infiltration after therapy.However,two of the patients with active lesions after treatment still showed macrophage infiltration in the renal interstitium.Before treatment,the three patients showed discontinuous expression of podocin.Notably,the integrity of podocin was restored after treatment in Case 1.CONCLUSION It may be possible to reverse podocyte damage and decrease the infiltrating ma-crophages in LN patients through effective treatment.

Effect of UBR5 on the tumor microenvironment and its related mechanisms in cancer

Objective UBR5,recently identified as a potential target for cancer therapeutics,is overexpressed in multiple malignant tumors.In addition,it is closely associated with the growth,prognosis,metastasis,and treatment response of multiple types of cancer.Although emerging evidence supports the relationship between UBR5 and cancer,there are limited cancer analyses available.Methods In this study,online databases(TIMER2,GEPIA2,UALCAN,c-BioPortal,STRING)were employed to comprehensively explore expression levels and prognostic values of the UBR5 gene in cancer,using bioinformatic methods.Results We found that various characteristics of the UBR5 gene such as gene expression,survival value,genetic mutation,protein phosphorylation,immune infiltration,and pathway activities in the normal tissue were remarkably different from those in the primary tumor.Furthermore,“protein processing in spliceosome”and“ubiquitin mediated proteolysis”have provided evidence for their potential involvement in the development of cancer.Conclusion Our findings may provide insights for the selection of novel immunotherapeutic targets and prognostic biomarkers for cancer.

Exploring the regulatory mechanism of tRNA-derived fragments 36 in acute pancreatitis based on small RNA sequencing and experiments

BACKGROUND Acute pancreatitis(AP)is a disease featuring acute inflammation of the pancreas and histological destruction of acinar cells.Approximately 20%of AP patients progress to moderately severe or severe pancreatitis,with a case fatality rate of up to 30%.However,a single indicator that can serve as the gold standard for prognostic prediction has not been discovered.Therefore,gaining deeper insights into the underlying mechanism of AP progression and the evolution of the disease and exploring effective biomarkers are important for early diagnosis,progression evaluation,and precise treatment of AP.AIM To determine the regulatory mechanisms of tRNA-derived fragments(tRFs)in AP based on small RNA sequencing and experiments.METHODS Small RNA sequencing and functional enrichment analyses were performed to identify key tRFs and the potential mechanisms in AP.Reverse transcription quantitative polymerase chain reaction(RT-qPCR)was conducted to determine tRF expression.AP cell and mouse models were created to investigate the role of tRF36 in AP progression.Lipase,amylase,and cytokine levels were assayed to examine AP progression.Ferritin expression,reactive oxygen species,malondialdehyde,and ferric ion levels were assayed to evaluate cellular ferroptosis.RNA pull down assays and methylated RNA immunoprecipitation were performed to explore the molecular mechanisms.RESULTS RT-qPCR results showed that tRF36 was significantly upregulated in the serum of AP patients,compared to healthy controls.Functional enrichment analysis indicated that target genes of tRF36 were involved in ferroptosisrelated pathways,including the Hippo signaling pathway and ion transport.Moreover,the occurrence of pancreatic cell ferroptosis was detected in AP cells and mouse models.The results of interference experiments and AP cell models suggested that tRF-36 could promote AP progression through the regulation of ferroptosis.Furthermore,ferroptosis gene microarray,database prediction,and immunoprecipitation suggested that tRF-36 accelerated the progression of AP by recruiting insulin-like growth factor 2 mRNA binding protein 3(IGF2BP3)to the p53 mRNA m6A modification site by binding to IGF2BP3,which enhanced p53 mRNA stability and promoted the ferroptosis of pancreatic follicle cells.CONCLUSION In conclusion,regulation of nuclear pre-mRNA domain-containing protein 1B promoted AP development by regulating the ferroptosis of pancreatic cells,thereby acting as a prospective therapeutic target for AP.In addition,this study provided a basis for understanding the regulatory mechanisms of tRFs in AP.

Correlation between Combined Urinary Metal Exposure and Grip Strength under Three Statistical Models:A Cross-sectional Study in Rural Guangxi

Objective This study aimed to investigate the potential relationship between urinary metals copper(Cu),arsenic(As),strontium(Sr),barium(Ba),iron(Fe),lead(Pb)and manganese(Mn)and grip strength.Methods We used linear regression models,quantile g-computation and Bayesian kernel machine regression(BKMR)to assess the relationship between metals and grip strength.Results In the multimetal linear regression,Cu(β=−2.119),As(β=−1.318),Sr(β=−2.480),Ba(β=0.781),Fe(β=1.130)and Mn(β=−0.404)were significantly correlated with grip strength(P<0.05).The results of the quantile g-computation showed that the risk of occurrence of grip strength reduction was−1.007(95%confidence interval:−1.362,−0.652;P<0.001)when each quartile of the mixture of the seven metals was increased.Bayesian kernel function regression model analysis showed that mixtures of the seven metals had a negative overall effect on grip strength,with Cu,As and Sr being negatively associated with grip strength levels.In the total population,potential interactions were observed between As and Mn and between Cu and Mn(P_(interactions) of 0.003 and 0.018,respectively).Conclusion In summary,this study suggests that combined exposure to metal mixtures is negatively associated with grip strength.Cu,Sr and As were negatively correlated with grip strength levels,and there were potential interactions between As and Mn and between Cu and Mn.

Clinical observation of Shengxuebao Mixture in treating anemia after concurrent chemoradiotherapy for cervical cancer

Objective:To investigate the efficacy of the Shengxuebao Mixture in treating anemia after concurrent chemoradiotherapy for cervical cancer.Methods:The patients who met the criteria were randomly divided into the study group(n=30)and the control group(n=30).The study group was treated with Shengxuebao Mixture(15 ml once,three times a day)for 30 days,and the control group was treated with ferrous succinate tablets(0.1 g,twice a day),folic acid tablets(5 mg,three times a day),and vitamin B12 tablets(25μg,once a day)for 30 days.Observed the hemoglobin level,erythropoietin level,TCM syndrome score,karnofsky performance status score before and after treatment in the two groups,compared the relevant data and clinical efficacy between the two groups and observed the adverse drug reactions at the same time.Results:The age,pathological type,stage,baseline hemoglobin level,erythropoietin level,TCM syndrome score,and karnofsky performance status score were comparable between the two groups(P>0.05).The hemoglobin level of the two groups after treatment was higher than before treatment(P<0.05).After treatment,the hemoglobin level in the study group was significantly higher than that in the control group(P<0.05),and the number of effective cases in the study group was more than that in the control group,and the effective rate in the study group was higher than that in the control group(P<0.05).The erythropoietin level of the two groups after treatment was lower than before treatment(P<0.05).After treatment,the erythropoietin level in the study group was significantly lower than that in the control group(P<0.05).The TCM syndrome score of the study group decreased significantly after treatment(P<0.05),but there was no significant change in the control group(P>0.05).After treatment,the TCM syndrome score of the study group was significantly lower than that of the control group(P<0.05),and the number of effective cases in the study group was more than that in the control group,and the effective rate in the study group was higher than that in the control group(P<0.05).There was no significant change in the karnofsky performance status score of the study group after treatment(P>0.05),but the karnofsky performance status score of the control group decreased significantly(P<0.05).After treatment,the karnofsky performance status score of the study group was higher than that of the control group(P<0.05),and the number of effective cases in the study group was more than that of the control group,and the effective rate was higher than that of the control group(P<0.05).And there were no obvious adverse reactions in this study.Conclusion:To some extent,this study showed that the Shengxuebao Mixture has a definite effect in treating anemia after concurrent chemoradiotherapy for cervical cancer,can promote the use of erythropoietin,improve TCM syndromes and stabilize the quality of life of patients.

Highlights on FOXO3 and tumor-associated dendritic ：ells in prostate cancer

Cancer immunotherapy sometimes fails to provoke effective immune responsesbecause of immunosuppressive mechanisms present in the tumor-bearing host. Dendritic cells （DCs） are the most potent antigenpresenting cells. After internalizing tumorassociated antigens （TAAs） at the tumor site,

A novel in vitro prognostic model of bladder cancer based on urine-derived living tumor cells

Bladder cancer(BLCA)remains a difficult malignancy to manage because of its high recurrence,intense follow-up,and invasive diagnostic and treatment techniques.Immune checkpoint inhibitors(ICIs)have forged a new direction for the treatment of BLCA,but it is currently challenging to predict whether an individual patient will be sensitive to ICIs.We collected 43 urine/tumor samples from BLCA patients for primary bladder cancer cells(BCCs)culturing using our previously reported BCC culture platform.We used flow cytometry(FCM)to measure the expression levels of Programmed Death-Ligand 1(PD-L1)on BCCs before and after interferon-gamma(IFN-γ)treatment and found that PD-L1 expression and the sensitivities to IFN-γvaried among patients.RNA-sequencing,western blotting,and programmed death-1(PD-1)binding assays confirmed that the BCC FCM-based PD-L1 detection platform(BC-PD-L1)was reliable and was not hindered by the glycosylation of PD-L1.In the subsequent retrospective study,we found that IFN-γ-stimulated PD-L1(sPD-L1)expression on BCCs detected by BC-PD-L1 could predict the prognosis of BLCA patients.Importantly,the prognostic value was similar or even better in urine-derived BC-PD-L1(UBC-PD-L1).Transcriptome analysis showed that BCCs with high sPD-L1 tended to enrich genes associated with the collagen-containing extracellular matrix,cell–cell adhesion,and positive regulation of the immune system.In addition,the UBC-PD-L1 also exhibited predictive value for ICI response in BLCA patients.In conclusion,as a novel personalized urine-detection method,UBC-PD-L1 may provide a rapid,accurate,and non-invasive tool for monitoring tumor progression,predicting therapeutic responses,and helping improve BLCA clinical treatment in future.

Spontaneous NETosis and type I IFN signaling activation in resting neutrophils of chronic granulomatous disease patients with CYBB mutations

Mutations in CYBB,encoding gp91^(phox)subunit of NADPH oxidase in phagocytes,impair the respiratory burst of neutrophils and result in X-linked chronic granulomatous disease(CGD).While inflammatory response and NETosis are important modalities employed by neutrophils for pathogen clearance,variants in these cell functions in CGD neutrophils(CGD-PMN)could possibly explain the insufficient defense and accumulation of phagocytes in the sites of infection.

Self-anti-angiogenesis nanoparticles enhance anti-metastatic-tumor efficacy of chemotherapeutics

Beyond traditional endothelium-dependent vessel(EDV),vascular mimicry(VM)is another critical tumor angiogenesis that further forms in many malignant metastatic tumors.However,the existing anti-angiogenesis combined chemotherapeutics strategies are only efficient for the treatment of EDV-based subcutaneous tumors,but remain a great challenge for the treatment of in situ malignant metastatic tumor associated with EDV and VM.Here,we demonstrate a self-assembled nanoparticle(VE-DDP-Pro)featuring self-anti-EDV and-VM capacity enables to significantly enhance the treatment efficacy of cisplatin(DDP)against the growth and metastasis of ovarian cancer.The VE-DDP-Pro is constructed by patching DDP loaded cRGD-folate-heparin nanoparticles(VE)onto the surface of protamine(Pro)nanoparticle.We demonstrated the self-anti-angiogenesis capacity of VE-DDP-Pro was attributed to VE,which could significantly inhibit the formation of EDV and VM by regulating signaling pathway of MMP-2/VEGF,AKT/mTOR/MMP-2/Laminin and AKT/mTOR/EMT,facilitating chemotherapeutics to effectively suppress the development and metastasis of ovarian cancer.Thus,combing with the chemotherapeutics effectiveness of DDP,the VE-DDP-Pro can significantly enhance treatment efficacy and prolong median survival of mice with metastatic ovarian cancer.We believe our self-assembled nanoparticles integrating the anti-EDV and anti-VM capacity provide a new preclinical sight to enhance the efficacy of chemotherapeutics for the treatment malignant metastasis tumor.

Correction:Characteristic and fate determination of adipose precursors during adipose tissue remodeling

Correction:Cell Regen 12,13(2023).https://doi.org/10.1186/s13619-023-00157-8.Following publication of the original article(Ye et al.2023),the authors reported that the“Competing inter-ests”section needed to be updated.The original version was:The authors declare no competing interests.

Vitamin C exerts anti-cadmium induced fracture functions/targets:bioinformatic and biostructural findings

Background:Epidemiological data indicate an association between cadmium exposure and risk of bone fracture;however,clinical treatment of cadmium-induced fracture is limited.Although vitamin C(VC)reportedly reduces cadmium-induced fracture,its pharmacological mechanism remains unexplored.Methods:Thus,we used a network pharmacology approach and molecular docking analysis to identify core targets,functional processes,and biological pathways involved in the anti-fracture action of VC.Results:Bioinformatics identified 17 intersection targets of VC and cadmium-induced fracture,Nine core targets were characterized,including tumor protein p53,epidermal growth factor receptor,proto-oncogene c,mitogen-activated protein kinase-1(MAPK1),MAPK3,signal transducer and activator of transcription-3,MAPK14,prostaglandin-endoperoxide synthase 2,and estrogen receptor alpha.Interestingly,findings of molecular docking analysis indicated that VC exerted effective binding capacity in cadmium-induced fracture.Furthermore,biological processes,cell components,molecular functions,and pharmacological pathways involved in the action of VC against cadmium-induced fracture were identified and visualized.Conclusions:Based on these findings,we conclude that VC exhibits its anti-cadmium-induced fracture effects by promoting osteoblastic regeneration and proliferation,and inhibiting inflammatory stress.The core targets may serve as biomarkers for diagnosing cadmium-induced fractures.

Progress research on non-drug therapy in cancer-related fatigue

Cancer-related fatigue is the most prevalent and persistently symptom in cancer survivors than any other symptom,which is caused by both the disease and its treatment.Patients with cancer show a severe symptom of fatigue,which cannot be relieved by general rest or sleep.Cancer-related fatigue negatively impacts a patient's physical and emotional function,social ability and even patients’prognosis.At present,the mechanism of cancer-related fatigue remain unclear despite much research,and a variety of mechanisms may contribute to its occurrence and development,including inflammatory reaction,metabolism dysregulation,immune activation,hormonal changes,central nervous system dysfunction,etc.Now a broad variety of drugs and non-drugs interventions are used against cancer-related fatigue.The intervention of conventional western medicine mainly contains hematopoietic stimulants,hormones,mental stimulants,and antidepressants,but their widely clinical application is limited by their effectiveness and possible side effects to a certain degree.There are also many forms of non-drug interventions for managing cancer-related fatigue,such as exercise intervention,psychological intervention,sleep intervention,nutrition intervention,bright white light therapy,etc.The aim of this review is to provide recommendations of non-drug interventions for patients with CRF during and after cancer treatment,in order to provide an evidence-based guideline for clinicians.

Characteristic and fate determination of adipose precursors during adipose tissue remodeling

Adipose tissues are essential for actively regulating systemic energy balance,glucose homeostasis,immune responses,reproduction,and longevity.Adipocytes maintain dynamic metabolic needs and possess heterogeneity in energy storage and supply.Overexpansion of adipose tissue,especially the visceral type,is a high risk for diabetes and other metabolic diseases.Changes in adipocytes,hypertrophy or hyperplasia,contribute to the remodeling of obese adipose tissues,accompanied by abundant immune cell accumulation,decreased angiogenesis,and aberrant extracellular matrix deposition.The process and mechanism of adipogenesis are well known,however,adipose precursors and their fate decision are only being defined with recent information available to decipher how adipose tissues generate,maintain,and remodel.Here,we discuss the key findings that identify adipose precursors phenotypically,with special emphasis on the intrinsic and extrinsic signals in instructing and regulating the fate of adipose precursors under pathophysiological conditions.We hope that the information in this review lead to novel therapeutic strategies to combat obesity and related metabolic diseases.

Anti-hepatic carcinoma mechanisms of calycosin through targeting ferroptosis

Background Ferroptosis,a pathologic state induced by lipid-driven oxidative stress,is associated with the development of human cancers.Calycosin,a natural compound with antioxidant and anti-inflammatory activities,has promising antitumor effects.However,the ferroptosis-related mechanism of calycosin in the treatment of hepatic carcinoma has not been reported.Methods This study applied network pharmacology and bioinformatic approaches(including Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis)to investigate the pharmacologic targets and mechanism of action of calycosin in the treatment of hepatic carcinoma through targeting ferroptosis.By searching online databases including The Cancer Genome Atlas,FerrDb,GeneCards,SwissTargetPrediction,SuperPred,BindingDB,TargetNet,BATMAN-TCM,and Drugbank,we identified 13 ferroptosis-related putative target genes of calycosin against hepatic carcinoma including IL-6,PTGS2,SRC,HRAS,NQO1,NOX4,PGK1,G6PD,GPI,MIF,NOS2,ALDOA,and SQSTM1.Results Molecular docking analysis revealed that calycosin potentially binded directly with the target proteins IL-6,PTGS2,and SRC.Functional enrichment analysis of these proteins indicated that they were involved in gluconeogenesis and apoptosis through regulation of ERK1,ERK2,and MAPK activities(P<0.05).Conclusion Calycosin exerts antitumor effects in hepatic carcinoma by targeting ferroptosis through regulation of IL-6,PTGS2,and SRC.

Tumor microenvironments self-activated nanoscale metal-organic frameworks for ferroptosis based cancer chemodynamic/photothermal/chemo therapy

Ferroptosis,as a newly discovered cell death form,has become an attractive target for precision cancer therapy.Several ferroptosis therapy strategies based on nanotechnology have been reported by either increasing intracellular iron levels or by inhibition of glutathione(GSH)-dependent lipid hydroperoxidase glutathione peroxidase 4(GPX4).However,the strategy by simultaneous iron delivery and GPX4 inhibition has rarely been reported.Herein,novel tumor microenvironments(TME)-activated metal-organic frameworks involving Fe&Cu ions bridged by disulfide bonds with PEGylation(FCSP MOFs)were developed,which would be degraded specifically under the redox TME,simultaneously achieving GSH-depletion induced GPX4 inactivation and releasing Fe ions to produce ROS via Fenton reaction,therefore causing ferroptosis.More ROS could be generated by the acceleration of Fenton reaction due to the released Cu ions and the intrinsic photothermal capability of FCSP MOFs.The overexpressed GSH and H2O2 in TME could ensure the specific TME self-activated therapy.Better tumor therapeutic efficiency could be achieved by doxorubicin(DOX)loading since it can not only cause apoptosis,but also indirectly produce H2O2 to amplify Fenton reaction.Remarkable anti-tumor effect of obtained FCSP@DOX MOFs was verified via both in vitro and in vivo assays.

A review of the risk factors associated with juvenile-onset recurrent respiratory papillomatosis:genetic,immune and clinical aspects

Background Juvenile-onset recurrent respiratory papillomatosis(JoRRP)is one of the most common benign lesions of hyperplastic respiratory epithelial tissue in children and is predominantly caused by human papillomaviruses(HPVs)6 and 11.The clinical course of the disease is variable,and some patients even develop a malignancy.The purpose of this review was to summarize the related factors affecting the disease course in patients with JoRRP.Data sources We used databases,including PubMed and Google Scholar,to search for publications on factors associated with the genetic,immune,and clinical aspects of JoRRP.The most relevant articles to the scope of this review were chosen for analysis.Results Mother-to-child transmission is the most important mode of disease transmission;other factors,such as immune condition or genetic susceptibility,may be important determinants of JoRRP occurrence.Genetically,the presence of DRBI*0301 and HFV 6/11 E6/E7 is associated with a more severe disease.Immunewise,patients have an enhanced T helper 2-like response.In addition,regulatory T cells are enriched in tumors and may become one of the effective prognostic indicators.For clinical characteristics,patients infected with HPV-11 have more aggressive disease.However,compared with HPV type,age at first onset is a more important factor related to the aggressiveness of JoRRP.Furthermore,socioeconomic status may also affect the course.Conclusions Genetic,immune,and some clinical factors have been noted to play an important role in the course of JoRRP.Exploring definite influencing factors will be an important direction of research in the future.

In-silico analysis reveals the core targets and mechanisms of CA028,a new derivative of calycosin,in the treatment of colorectal cancer

Background Colorectal cancer(CRC)is a type of malignant gastroenteric tumors associated with a high mortal-ity rate worldwide.Calycosin,a natural phytoestrogen,possesses potent anti-cancer properties.We structurally modified calycosin to improve its physicochemical properties,and generated a novel small molecule termed CA028.Methods By using network pharmacology,followed by gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis and molecular docking,we aimed to predict and disclose the biological functions and mechanism of CA028 in the treatment of CRC through bioinformatic analyses.Results By searching the online Swiss Target Prediction and TargetNet databases,we identified 150 genes shared by CA028 and CRC.Using the Search Tool for the Retrieval of Interacting Genes(STRING)database and Cytoscape software,we identified 14 hub-functional genes,namely the FYN proto-oncogene,a Src family tyrosine kinase(F YN),mitogen-activated protein kinase 1(MAPK1),MAPK8,MAPK14,Rac family small GTPase 1(RAC1),epi-dermal growth factor receptor(EGFR),protein tyrosine kinase 2(PTK2),sphingosine-1-phosphate receptor 1(S1PR1),S1PR2,Janus kinase 1(JAK1),JAK2,the RELA proto-oncogene NF-𝜅B subunit(RELA),bradykinin re-ceptor B1(BDKRB1),and BDKRB2.Additionally,biological docking analysis using the Autodock Vina software revealed that FYN and MAPK1 were the main pharmacological proteins of CA028 against CRC.The gene ontol-ogy analysis using R-language packages further revealed the anti-CRC functions of CA028,including biological processes,cell components,and molecular pathways.Conclusion CA028 exhibits effective pharmacological activity against CRC by suppressing the proliferation of CRC cells and improving the tumor microenvironment.Importantly,certain predicted genes(e.g.,FYN and MAPK1)may be the pharmacological targets of CA028 in the treatment of CRC.

Immune microenvironment-reshaping Au@Bi_(2)Te_(3) nanoparticles for spectral computed tomography/photoacoustic imaging-guided synergetic photo/radio/immunotherapy

Radiotherapy(RT)mediated tumor immunogenicity offers an opportunity for simultaneous RT and immunotherapy via immunogenic cell death(ICD),which releases damaged-associated molecular patterns and generates“eat me”signals for the innate immune system to modulate the immunogenicity.However,tumor hypoxia significantly reduces the therapeutic efficacy of RT and hampers its mediation of ICD induction.Herein,Au@Bi_(2)Te_(3)-polyethylene glycol(PEG)was rationally constructed as theranostic nanozymes for mild photothermal therapy,tumor hypoxia modulation,and RT adjuvant cancer immunotherapy.The tumor-specific production of oxygen could not only augment the effects of RT by enhanced reactive oxygen species(ROS)generation,but also reduce hypoxia-related cytokines and downregulate programmed cell death-ligand 1(PD-L1)to unleash immune-enhancing T cells.Moreover,Au@Bi_(2)Te_(3)-PEG could act as an immune-blocking inhibitor by efficient ICD induction with the combination of mild-photothermal therapy+RT to inhibit the tumor immune escape and improve antitumor immune response.Increased amounts of CD^(4+) and CD^(8+) Tcells and elevated levels of cytokines could be observed that eventually led to effective post-medication inhibition of primary and abscopal tumors.Spectral computed tomography/photoacoustic imaging allowed noninvasive and real-time tracking of nanoparticle(NP)accumulation and oxygenation status at tumor sites.Collectively,Au@Bi_(2)Te_(3)-PEG NPs could serve as effective theranostic nanoregulators with remarkable synergistic mildphotothermal/RT/immunotherapy effects that helped reshape the immune microenvironment and had remarkable molecular imaging properties.

Circulating fibroblasts present neutrophil-like features in severe COVID-19 cases revealed by single-cell landscape analyses

Severe acute respiratory syndrome coronavirus-2(SARSCoV-2),which causes coronavirus disease 2019(COVID-19)and initially infects epithelial cells of the upper respiratory tract,has recently caused a global health emergency and is still a potential threat to humans.1 Multiple studies have suggested alterations in the immune system,including excessive neutrophil activation and lymphopenia,and excessive inflammatory responses as the key mechanisms for severesymptoms.2However,which cell types contribute to excessive inflammation remains to be explored.Further analysis of human blood immune cells provides insights into the coordinated response to SARSCoV-2 infections and is a significant task for restraining the virus and controlling disease progression.

MiRNAs and lncRNAs in NK cell biology and NK/T-cell lymphoma

The important role of lncRNAs and miRNAs in directing immune responses has become increasingly clear.Recent evidence conforms that miRNAs and lncRNAs are involved in NK cell biology and diseases through RNAeprotein,RNAeRNA,or RNAeDNA interactions.In this view,we summarize the contribution of miRNAs and lncRNAs to NK cell lineage devel-opment,activation and function,highlight the biological significance of functional miRNAs or lncRNAs in NKTL and discuss the potential of these miRNAs and lncRNAs as innovative bio-markers/targets for NKTL early diagnosis,target treatment and prognostic evaluations.