cytokine

摘要： Glaucoma is a multifactorial disease and occurs in many different species.In humans,glaucoma is accounted one of the leading causes for blindness worldwide.Due to glaucoma's complexity,it is still unclear what pathomechanisms may be involved in its development in humans as well as in other species,such as canines.Diagnosis of glaucoma can be delayed because patients often do not notice a visual field loss until approximately30%of retinal ganglion cells(RGCs)are lost(Kerrigan-Baumrind et al.,2000).Although the exact undergoing pathomechanisms of glaucoma disease are not fully understood yet,an increased intraocular pressure(IOP)is related to RGCdeath and is considered the main risk factor.

摘要： Interleukin-27 is a pleiotropic cytokine that is involved in tissue responses to infection,cell stress,neuronal disease,and tumors.Recent studies in various tissues indicate that interleukin-27 has complex activating and inhibitory properties in innate and acquired immunity.The availability of recombinant interleukin-27 protein and mice with genetic deletions of interleukin-27,its receptors and signaling mediators have helped define the role of interleukin-27 in neurodegenerative diseases.Interleukin-27 has been well-characterized as an important regulator of T cell activation and differentiation that enhances or suppresses T cell responses in autoimmune conditions in the central nervous system.Evidence is also accumulating that interleukin-27 has neuroprotective activities in the retina and brain.Interleukin-27 is secreted from and binds to infiltrating microglia,macrophage,astrocytes,and even neurons and it promotes neuronal survival by regulating pro-and anti-inflammatory cytokines,neuroinflammatory pathways,oxidative stress,apoptosis,autophagy,and epigenetic modifications.However,interleukin-27 can have the opposite effect and induce inflammation and cell death in certain situations.In this review,we describe the current understanding of regulatory activities of interleukin-27 on cell survival and inflammation and discuss its mechanisms of action in the brain,spinal cord,and retina.We also review evidence for and against the therapeutic potential of interleukin-27 for dampening harmful neuroinflammatory responses in central nervous system diseases.

摘要： The original study by Alessio et al reported that skinny people (SP) serum canpromote the formation of brown adipocytes, but not the differentiation of whiteadipocytes. This finding may explain why SP do not often become obese, despiteconsuming more calories than the body needs. More importantly, theydemonstrated that circulating factors in SP serum can promote the expression ofUCP-1 protein, thereby reducing fat accumulation. In this study, only male serumsamples were evaluated to avoid the interference of sex hormones in experiments,but adult males also synthesize estrogen, which is produced by the cells of thetestes. At the same time, adult females secrete androgens, and females synthesizeandrogens that are mainly produced by the adrenal cortex. We believe that theapproach of excluding sex hormone interference by sex selection alone may beflawed, so we comment on the article and debate the statistical analysis of thearticle.

摘要： BACKGROUND Chronic hepatitis C virus(HCV)infection induces profound alterations in the cytokine and chemokine signatures in peripheral blood.Clearance of HCV by antivirals results in host immune modification,which may interfere with immune-mediated cancer surveillance.Identifying HCV patients who remain at risk of hepatocellular carcinoma(HCC)following HCV eradication remains an unmet need.We hypothesized that antiviral therapy-induced immune reconstruction may be relevant to HCC development.AIM To investigate the impact of differential dynamics of cytokine expression on the development of HCC following successful antiviral therapy.METHODS One hundred treatment-naïve HCV patients with advanced fibrosis(F3/4)treated with direct-acting antivirals(DAAs)or peginterferon/ribavirin who achieved sustained virologic response[SVR,defined as undetectable HCV RNA throughout 12 wk(SVR12)for the DAA group or 24 wk(SVR24)for the interferon group after completion of antiviral therapy]were enrolled since 2003.The primary endpoint was the development of new-onset HCC.Standard HCC surveillance(abdominal ultrasound andα-fetoprotein)was performed every six months during the followup.Overall,64 serum cytokines were detected by the multiplex immunoassay at baseline and 24 wk after end-of-treatment.RESULTS HCC developed in 12 of the 97 patients over 459 person-years after HCV eradication.In univariate analysis,the Fibrosis-4 index(FIB-4),hemoglobin A1c(HbA1c),the dynamics of tumor necrosis factor-α(TNF-α),and TNF-like weak inducer of apoptosis(TWEAK)after antiviral therapy were significant HCC predictors.The multivariate Cox regression model showed thatΔTNF-α(≤-5.7 pg/mL)was the most important risk factor for HCC(HR=11.54,95%CI:2.27-58.72,P=0.003 in overall cases;HR=9.98,95%CI:1.88-52.87,P=0.007 in the interferon group).An HCC predictive model comprising FIB-4,HbA1c,ΔTNF-α,andΔTWEAK had excellent performance,with 3-,5-,10-,and 13-year areas under the curve of 0.882,0.864,0.903,and 1.000,respectively.The 5-year accumulative risks of HCC were 0%,16.9%,and 40.0%in the low-,intermediate-,and high-risk groups,respectively.CONCLUSION Downregulation of serum TNF-αsignificantly increases the risk of HCC after HCV eradication.A predictive model consisting of cytokine kinetics could ameliorate personalized HCC surveillance strategies for post-SVR HCV patients.

摘要： During this COVID-19 pandemic’s,scientists and researchers are developing vaccines and with help of country's health ministry and WHO.They try to reach out vaccination throughout the country but this process should take some time.Therefore,until vaccination can done we have to protect our immune system.In the year,2021 people may also get an infection of the third wave of COVID,which is a chance to arrive.Therefore,protecting our immunity and decreasing the severity of infection is the priority for that developing a new approach is necessary.Therefore,probiotics(Lactobacillus plantarum&Bifidobacterium breve)are good option for the person having post Covid Symptoms without side effects.Those probiotics can help people for developing immunity against COVID-19 infection.Those probiotics dosages are useful to patient because these probiotics are easily available,easy to administrate and it is useful in severe condition as well as in mild condition.

摘要： Crohn’s disease(CD)is driven by the loss of tolerance to intestinal microbiota and excessive production of pro-inflammatory cytokines.These pro-inflammatory cytokines are produced by macrophages and dendritic cells(DCs)upon sensing the intestinal microbiota by the pattern recognition receptors(PRRs).Impaired activation of PRR-mediated signaling pathways is associated with chronic gastrointestinal inflammation,as shown by the fact that loss-of-function mutations in the nucleotide-binding oligomerization domain 2 gene increase the risk of CD development.Autophagy is an intracellular degradation process,during which cytoplasmic nutrients and intracellular pathogens are digested.Given that impaired reaction to intestinal microbiota alters signaling pathways mediated by PRRs,it is likely that dysfunction of the autophagic machinery is involved in the development of CD.Indeed,the loss-of-function mutation T300A in the autophagy related 16 like 1(ATG16L1)protein,a critical regulator of autophagy,increases susceptibility to CD.Recent studies have provided evidence that ATG16L1 is involved not only in autophagy,but also in PRR-mediated signaling pathways.ATG16L1 negatively regulates pro-inflammatory cytokine responses of macrophages and DCs after these cells sense the intestinal microbiota by PRRs.Here,we discuss the molecular mechanisms underlying the development of CD in the T300A ATG16L1 mutation by focusing on PRR-mediated signaling pathways.

摘要： Tumor necrosis factors(TNFs)are a group of cytokines that play critical roles in regulating a diverse range of physiological processes in vertebrates.TNFs function by activating a large number of structurally related receptors,leading to TNF mediated biological processes which are evolutionarily conserved.Fish have a much diversified TNF family,partly due to the whole genome duplication events which have occurred in this lineage,providing an excellent model to investigate the neo-and subfunctionalised properties of TNF superfamily.Fish possess most of the TNFs and receptors found in mammals and also some homologues exclusively present in fish.It seems that TNFSF4(OX40),TNFSF7(CD27)and TNFSF8(CD30)and their cognate receptors are absent in teleosts.It has been shown that fish viruses are able to produce TNFR homologues to establish infection by manipulating the host immune system.Understanding the roles of TNFSFs in fish immune defence and the pathogenesis of fish diseases will provide insights into the functions of TNFSFs from an evolutionary perspective and better strategies for improving fish health and welfare in aquaculture.This review summarises recent advances in the study of fish TNF biology and focuses on the molecular properties and immunological functions of the TNF and TNFR superfamily.

摘要： The coronavirus disease 2019(COVID-19)caused by severe acute respiratory disease respiratory syndrome coronavirus-2 has significantly impacted the health care systems globally.Liver transplantation(LT)has faced an unequivocal challenge during this unprecedented time.This targeted review aims to cover most of the clinical issues,challenges and concerns about LT during the COVID-19 pandemic and discuss the most updated literature on this rapidly emerging subject.

摘要： Solitary organ autoimmune disorders,formerly known as autoimmune pancreatitis(AIP),autoimmune sialadenitis,and autoimmune sclerosing cholangitis,are now considered organ-specific manifestations of systemic immunoglobulin G4-related disease(IgG4-RD).AIP and IgG4-RD are characterized by elevated serum concentration of IgG4 antibody(Ab),accumulation of IgG4-expressing plasmacytes in the affected organs,and involvement of multiple organs.It is well established that enhanced IgG4 Ab responses are a hallmark of AIP and IgG4-RD for diagnosis and monitoring disease activity.However,a significant fraction of patients with AIP and IgG4-RD who develop chronic fibroinflammatory responses have normal serum concentrations of this IgG subtype.In addition,disease flare-up is sometimes seen even in the presence of normalized serum concentrations of IgG4 Ab after successful induction of remission by prednisolone.Therefore,it is necessary to identify new biomarkers based on the understanding of the pathophysiology of AIP and IgG4-RD.Recently,we found that activation of plasmacytoid dendritic cells producing both interferon-α(IFN-α)and interleukin-33(IL-33)mediate murine AIP and human IgG4-RD.More importantly,we provided evidence that serum concentrations of IFN-αand IL-33 could be useful biomarkers for the diagnosis and monitoring of AIP and IgG4-RD activity after induction of remission in these autoimmune disorders.In this Frontier article,we have summarized and discussed biomarkers of AIP and IgG4-RD,including Igs,autoAbs,and cytokines to provide useful information not only for clinicians but also for researchers.

摘要： Hematopoietic stem cell transplantation(HSCT)is widely performed as a treatment for malignant blood disorders,such as leukemia.To achieve good clinical outcomes in HSCT,it is necessary to minimize the unfavorable effects of acute graft-vs-host disease(GVHD)and induce the more tolerable,chronic form of the disease.For better management of GVHD,sensitive and specific biomarkers that predict the severity and prognosis of the disease have been intensively investigated using proteomics,transcriptomics,genomics,cytomics,and tandem mass spectrometry methods.Here,I will briefly review the current understanding of GVHD biomarkers and future prospects.