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Liver immunology and its role in inflammation and homeostasis

Cellular & Molecular Immunology 2016年第3期13卷 267-276页

作者： Mark W Robinson Cathal Harmon Cliona O'Farrelly School of Biochemistry and Immunology Trinity Biomedical Sciences Institute Trinity College Dublin Dublin D2 Ireland School of Medicine TrinityBiomedical Sciences Institute Trinity College Dublin Dublin D2 Ireland

The human liver is usually perceived as a non-immunological organ engaged primarily in metabolic, nutrient storage and detoxification activities. However, we now know that the healthy liver is also a site of complex immunological activity mediated by a diverse immune cell repertoire as well as non-hematopoietic cell populations. In the nondiseased liver, metabolic and tissue remodeling functions require elements of inflammation. This inflammation, in combination with regular exposure to dietary and microbial products, creates the potential for excessive immune activation. In this complex microenvironment, the hepatic immune system tolerates harmless molecules while at the same time remaining alert to possible infectious agents, malignant cells or tissue damage. Upon appropriate immune activation to challenge by pathogens or tissue damage, mechanisms to resolve inflammation are essential to maintain liver homeostasis. Failure to clear ＇dangerous＇ stimuli or regulate appropriately activated immune mechanisms leads to pathological inflammation and disrupted tissue homeostasis characterized by the progressive development of fibrosis, cirrhosis and eventual liver failure. Hepatic inflammatory mechanisms therefore have a spectrum of roles in the healthy adult liver; they are essential to maintain tissue and organ homeostasis and, when dysregulated, are key drivers of the liver pathology associated with chronic infection, autoimmunity and malignancy. In this review, we explore the changing perception of inflammation and inflammatory mediators in normal liver homeostasis and propose targeting of liver-specific immune regulation pathways as a therapeutic approach to treat liver disease.

关键词： homeostasis immunology inflammation liver tolerance

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Chemokines in homeostasis and diseases

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Cellular & Molecular Immunology 2018年第4期15卷 324-334页

作者： Keqiang Chen Zhiyao Bao Peng Tang Wanghua Gong Teizo Yoshimura Ji Ming Wang Cancer and Inflammation Program Center for Cancer ResearchNational Cancer Institute at FrederickFrederickMD 21702USA Department of Pulmonary&Critical Care Medicine Ruijin HospitalShanghai Jiaotong University School of MedicineShanghai 200025P.R.China Department of Breast Surgery Southwest HospitalThird Military Medical UniversityChongqing 400038China Basic Research Program Leidos Biomedical ResearchInc.FrederickMD 21702USA Department of Pathology and Experimental Medicine Graduate School of MedicineDentistry and Pharmaceutical SciencesOkayama UniversityOkayama 700-8558Japan

For the past twenty years,chemokines have emerged as a family of critical mediators of cell migration during immune surveillance,development,inflammation and cancer progression.Chemokines bind to seven transmembrane G protein-coupled receptors(GPCRs)that are expressed by a wide variety of cell types and cause conformational changes in trimeric G proteins that trigger the intracellular signaling pathways necessary for cell movement and activation.Although chemokines have evolved to benefit the host,inappropriate regulation or utilization of these small proteins may contribute to or even cause diseases.Therefore,understanding the role of chemokines and their GPCRs in the complex physiological and diseased microenvironment is important for the identification of novel therapeutic targets.This review introduces the functional array and signals of multiple chemokine GPCRs in guiding leukocyte trafficking as well as their roles in homeostasis,inflammation,immune responses and cancer.

关键词： chemokines chemotaxis diseases GPCRs homeostasis inflammatory cells

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GOLM1 restricts colitis and colon tumorigenesis by ensuring Notch signaling equilibrium in intestinal homeostasis

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Signal Transduction and Targeted Therapy 2021年第5期6卷 1511-1525页

作者： Yang Pu Ya Song Mengdi Zhang Caifeng Long Jie Li Yanan Wang Yinzhe Xu Fei Pan Na Zhao Xinyu Zhang Yanan Xu Jianxin Cui Hongying Wang Yan Li Yong Zhao Di Jin Hongbing Zhang State Key Laboratory of Medical Molecular Biology Department of PhysiologyInstitute of Basic Medical Sciences and School of Basic MedicinePeking Union Medical College and Chinese Academy of Medical SciencesBeijingChina lnstitute of Cancer Stem Cell Dalian Medical UniversityDalianLiaoningChina Chinese PLA General Hospital BeijingChina State Key Laboratory of Biomembrane and Membrane Biotechnology Institute of ZoologyChinese Academy of SciencesBeijingChina State Key Laboratory of Molecular Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijingChina Department of Anatomy and Physiology College of Basic Medical SciencesShanghai Jiao Tong UniversityShanghaiChina

Intestinal epithelium serves as the first barrier against the infections and injuries that mediate colonic inflammation.Colorectal cancer is often accompanied with chronic inflammation.Differed from its well-known oncogenic role in many malignancies,we present here that Golgi membrane protein 1(G0LM1,also referred to as GP73)suppresses colorectal tumorigenesis via maintenance of intestinal epithelial barrier.G0LM1 deficiency in mice conferred susceptibility to mucosal inflammation and colitis-induced epithelial damage,which consequently promoted colon cancer.Mechanistically,depletion of G0LM1 in intestinal epithelial cells(lECs)led to aberrant Notch activation that interfered with IEC differentiation,maturation,and lineage commitment in mice.Pharmacological inhibition of Notch pathway alleviated epithelial lesions and restrained pro-tumorigenic inflammation in G0LM1-deficient mice.Therefore,G0LM1 maintains IEC homeostasis and protects against colitis and colon tumorigenesis by modulating the equilibrium of Notch signaling pathway.

关键词： colon homeostasis Notch

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Altered surfactant protein A gene expression and protein homeostasis in rats with emphysematous changes

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Chinese Medical Journal 2008年第13期121卷 1177-1182页

作者： HU Qiong-jie XIONG Sheng-dao ZHANG Hui-lan SHI Xue-mei XU Yong-jian ZHANG Zhen-xiang ZHEN Guo-hua ZHAO Jian-ping Department of Respiratory Medicine Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China

Background The decrease of surfactant protein （SP） secreted by the alveolar type Ⅱ cell is one of the important causes of limiting air of pulmonary emphysema. However, the SP-A gene and protein changes in this disease are rarely studied. This study was undertaken to investigate alterations in SP-A gene activity and protein, and to explore their roles in the pathogenesis of emphysematous changes. Methods Twenty Wistar rats were divided randomly into a normal control group （n=10） and a cigarette smoking （CS）＋ lipopolysaccharide （LPS） group （n=10）. Ultra-structural changes were observed under an electron microscope. The number of cells positive for SP-A was measured by immunohistochemistry. The mRNA expression and protein level of SP-A in the lung tissues were determined by quantitative polymerase chain reaction （qPCR） and Western blot separately. The protein level of SP-A in lavage fluid was determined by Western blot. Results The number of cells positive for SP-A of the CS＋LPS group （0.35±0.03） was lower than that of the blank control group （0.72±0.06, P 〈0.05）. The level of SP-A in the lung tissues of rats in the CS＋LPS group （0.2765±0.0890） was lower than that in the blank control group （0.6875±0.1578, P 〈0.05）. The level of SP-A in the lavage fluid of rats in the CS＋LPS group （0.8567±0.1458） was lower than that in the blank control group （1.3541±0.2475, P 〈0.05）. The lung tissues of rats in the CS＋LPS group showed an approximate increase （0.4-fold） in SP-A mRNA levels relative to β-actin mRNA （P 〈0.05）. Conclusions The changes of SP-A may be related to emphysematous changes in the lung. And cigarette smoke and LPS alter lung SP-A gene activity and protein homeostasis.

关键词： emphysema alveolar type Ⅱ cells surfactant protein A gene homeostasis

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A novel CCCH-type zinc finger protein SAW1 activates OsGA20ox3 to regulate gibberellin homeostasis and anther development in rice

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Journal of Integrative Plant Biology 2020年第10期62卷 1594-1606页

作者： Bin Wang Ruiqiu Fang Faming Chen Jingluan Han Yao-Guang Liu Letian Chen Qinlong Zhu State Key Laboratory for Conservation and Utilization of Subtropical Agro-Bioresources South China Agricultural UniversityGuangzhou 510642China Guangdong Laboratory for Lingnan Modern Agriculture Guangzhou 510642China Guangdong Provincial Key Laboratory of Protein Function and Regulation in Agricultural Organisms South China Agricultural UniversityGuangzhou 510642China College of Life Sciences South China Agricultural UniversityGuangzhou 510642China Dongyang Institute of Maize Research Zhejiang Academy of Agricultural SciencesDongyang 322100China

Male sterility is a prerequisite for hybrid seed production.The phytohormone gibberellin(GA)is in-volved in regulating male reproductive development,but the mechanism underlying GA homeostasis in anther development remains less understood.Here,we report the isolation and characterization of a new positive regulator of GA homeostasis,swollen anther wall 1(SAW1),for anther development in rice(Oryza sativa L.).Rice plants carrying the recessive mutant allele saw1 produces abnormal anthers with swollen anther wall and aborted pollen.Clustered regularly interspaced short palindromic repeats(CRISPR)/CRIPSR-associated protein 9-mediated knockout of SAW1 in rice generated similar male sterile plants.SAW1 encodes a novel nucleus-localizing CCCH-tandem zinc finger protein,and this protein could directly bind to the promoter region of the GA synthesis gene OsGA20ox3 to induce its anther-specific expression.In the saw1 anther,the significantly decreased OsGA20ox3 expression resulted in lower bio-active GA content,which in turn caused the lower expression of the GA-inducible anther-regulator gene OsGAMYB.Thus,our results disclose the mechanism of the SAW1-GA20ox3-GAMYB pathway in controlling rice anther development,and provide a new target gene for the rapid generation of male sterile lines by genome editing for hybrid breeding.

关键词： sterile homeostasis anther

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Regulation of Virus Replication and T Cell homeostasis by N^6-Methyladenosine

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Virologica Sinica 2019年第1期34卷 22-29页

作者： Jing Yang Hong Wang Wenyan Zhang Institute of Virology and AIDS Research The First Hospital of Jilin University

RNA modifications are abundant in eukaryotes, bacteria, and archaea. N^6-methyladenosine(m^6A), a type of RNA modification mainly found in messenger RNA(mRNA), has significant effects on the metabolism and function of m RNAs. This modification is governed by three types of proteins, namely methyltransferases as ‘‘writers' ', demethylases as ‘‘erasers' ',and specific m^6A-binding proteins(YTHDF1-3) as ‘‘readers' '. Further, it is important for the regulation of cell fate and has a critical function in many biological processes including virus replication, stem cell differentiation, and cancer development, and exerts its effect by controlling gene expression. Herein, we summarize recent advances in research on m^6A in virus replication and T cell regulation, which is a rapidly emerging field that will facilitate the development of antiviral therapies and the study of innate immunity.

关键词： RNA modification N^6-methyladenosine (m^6A) Virus replication T cell homeostasis

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Oryza sativa FER-LIKE FE DEFICIENCY-INDUCED TRANSCRIPTION FACTOR(OsFIT/OsbHLH156)interacts with OsIRO2 to regulate iron homeostasis

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Journal of Integrative Plant Biology 2020年第5期62卷 668-689页

作者： Gang Liang Huimin Zhang Yang Li Mengna Pu Yujie Yang Chenyang Li Chengkai Lu Peng Xu Diqiu Yu CAS Key Laboratory of Tropical Plant Resources and Sustainable Use Xishuangbanna Tropical Botanical GardenThe Innovative Academy of Seed DesignChinese Academy of SciencesKunming 650223China Center of Economic Botany Core Botanical GardensChinese Academy of SciencesMenglunMengla 666303China University of Chinese Academy of Sciences Beijing 100049China State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan Yunnan UniversityKunming 650091China

Iron(Fe)is indispensable for the growth and development of plants.It is well known that FER-LIKE FE DEFICIENCY-INDUCED TRANSCRIPTION FACTOR(FIT)is a key regulator of Fe uptake in Arabidopsis.Here,we identify the Oryza sativa FIT(also known as Osb HLH156)as the interacting partner of IRON-RELATED BHLH TRANSCRIPTION FACTOR 2(OsIRO2)that is critical for regulating Fe uptake.The OsIRO2 protein is localized in the cytoplasm and nucleus,but OsFIT facilitates the accumulation of OsIRO2 in the nucleus.Loss-of-function mutations of OsFIT result in decreased Fe accumulation,severe Fe-deficiency symptoms,and disrupted expression of Feuptake genes.In contrast,OsFIT overexpression promotes Fe accumulation and the expression of Fe-uptake genes.Genetic analyses indicate that OsFIT and OsIRO2 function in the same genetic node.Further analyses suggest that OsFIT and OsIRO2 form a functional transcription activation complex to initiate the expression of Fe-uptake genes.Our findings provide a mechanism understanding of how rice maintains Fe homeostasis.

关键词： homeostasis maintain finding

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Epo/EpoR signaling in osteoprogenitor cells is essential for bone homeostasis and Epo-induced bone loss

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Bone Research 2021年第4期9卷 549-556页

作者： Martina Rauner Marta Murray Sylvia Thiele Deepika Watts Drorit Neumann Yankel Gabet Lorenz C.Hofbauer Ben Wielockx Department of Medicine III&Center for Healthy Aging Technische Universitat DresdenDresdenGermany lnstitute for Clinical Chemistry and Laboratory Medicine Technische Universitat DresdenDresdenGermany Department of Cell and Developmental Biology Sackler Faculty of MedicineTel Aviv UniversityTel AvivIsrael Department of Anatomy&Anthropology Sackler Faculty of MedicineTel Aviv UniversityTel AvivIsrael

High erythropoietin(Epo)levels are detrimental to bone health in adult organisms.Adult mice receiving high doses of Epo lose bone mass due to suppressed bone formation and increased bone resorption.In humans,high serum Epo levels are linked to fractures in elderly men.Our earlier studies indicated that Epo modulates osteoblast activity;however,direct evidence that Epo acts via its receptor(EpoR)on osteoblasts in vivo is still missing.Here,we created mice lacking EpoR in osteoprogenitor cells to specifically address this gap.Deletion of EpoR in osteoprogenitors(EpoR:Osx-cre,cKO)starting at 5 weeks of age did not alter red blood cell parameters but increased vertebral bone volume by 25%in 12-week-old female mice.This was associated with low bone turnover.Histological(osteoblast number,bone formation rate)and serum(P1NP,osteocalcin)bone formation parameters were all reduced,as were the number of osteoclasts and TRAP serum level.Differentiation of osteoblast precursors isolated from cKO versus control mice resulted in lower expression of osteoblast marker genes including Runx2,Alp,and Col1a1 on day 21,whereas the mineralization capacity was similar.Moreover,the RANKL70PG ratio,which determines the osteoclast-supporting potential of osteoblasts,was substantially decreased by 50%.Similarly,coculturing cKO osteoblasts with control or cKO osteoclast precursors produced significantly fewer osteoclasts than coculture with control osteoblasts.Finally,exposing female mice to Epo pumps(10 U-d_1)for 4 weeks resulted in trabecular bone loss(-25%)and increased osteoclast numbers(1.7-fold)in control mice only,not in cKO mice.Our data show that EpoR in osteoprogenitors is essential in regulating osteoblast function and osteoblast-mediated osteoclastogenesis via the RANKI70PG axis.Thus,osteogenic Epo/EpoR signaling controls bone mass maintenance and contributes to Epo-induced bone loss.

关键词： progenitor homeostasis doses

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Mechanical force-driven TNFαendocytosis governs stem cell homeostasis

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Bone Research 2021年第1期9卷 37-49页

作者： Wenjing Yu Chider Chen Xiaoxing Kou Bingdong Sui Tingting Yu Dawei Liu Runci Wang Jun Wang Songtao Shi Department of Anatomy and Cell Biology School of Dental MedicineUniversity of PennsylvaniaPhiladelphiaPA 19104USA State Key Laboratory of Oral Diseases National Clinical Research Center for Oral DiseasesWest China Hospital of StomatologySichuan UniversityChengdu 610041 SichuanChina South China Center of Craniofacial Stem Cell Research Guanghua School and Hospital of StomatologySun Yat-sen UniversityGuangzhou 510055 GuangdongChina Research and Development Center for Tissue Engineering School of StomatologyFourth Military Medical UniversityXi’an 710032 ShaanxiChina Department of Orthodontics Peking University School and Hospital of Stomatology100081 BeijingChina

Mesenchymal stem cells(MSCs)closely interact with the immune system,and they are known to secrete inflammatory cytokines in response to stress stimuli.The biological function of MSC-derived inflammatory cytokines remains elusive.Here,we reveal that even under physiological conditions,MSCs produce and release a low level of tumor necrosis factor alpha(TNFα),which is unexpectedly required for preserving the self-renewal and differentiation of MSCs via autocrine/paracrine signaling.Furthermore,TNFαcritically maintains MSC function in vivo during bone homeostasis.Mechanistically,we unexpectedly discovered that physiological levels of TNFαsafeguard MSC homeostasis in a receptor-independent manner through mechanical force-driven endocytosis and that endocytosed TNFαbinds to mammalian target of rapamycin(mTOR)complex 2 and restricts mTOR signaling.Importantly,inhibition of mTOR signaling by rapamycin serves as an effective osteoanabolic therapeutic strategy to protect against TNFαdeficiency and mechanical unloading.Collectively,these findings unravel the physiological framework of the dynamic TNFαshuttlebased mTOR equilibrium that governs MSC and bone homeostasis.

关键词： homeostasis maintain endocytosis

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A double-edged sword of immuno-microenvironment in cardiac homeostasis and injury repair

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Signal Transduction and Targeted Therapy 2021年第3期6卷 779-794页

作者： Kang Sun Yi-yuan Li Jin Jin MOE Laboratory of Biosystem homeostasis and Protection and Life Sciences InstituteZhejiang UniversityHangzhou 310058China Key Laboratory for Developmental Genes and Human Disease Ministry of EducationInstitute of Life SciencesJiangsu Province High-Tech Key Laboratory for Bio-Medical ResearchSoutheast UniversityNanjing 210096China Sir Run Run Shaw Hospital College of Medicine Zhejiang UniversityHangzhou 310016China

The response of immune cells in cardiac injury is divided into three continuous phases:inflammation,proliferation and maturation.The kinetics of the inflammatory and proliferation phases directly influence the tissue repair.In cardiac homeostasis,cardiac tissue resident macrophages(cTMs)phagocytose bacteria and apoptotic cells.Meanwhile,NK cells prevent the maturation and transport of inflammatory cells.After cardiac injury,cTMs phagocytose the dead cardiomyocytes(CMs),regulate the proliferation and angiogenesis of cardiac progenitor cells.NK cells prevent the cardiac fibrosis,and promote vascularization and angiogenesis.Type 1 macrophages trigger the cardioprotective responses and promote tissue fibrosis in the early stage.Reversely,type 2 macrophages promote cardiac remodeling and angiogenesis in the late stage.Circulating macrophages and neutrophils firstly lead to chronic inflammation by secreting proinflammatory cytokines,and then release anti-inflammatory cytokines and growth factors,which regulate cardiac remodeling.In this process,dendritic cells(DCs)mediate the regulation of monocyte and macrophage recruitment.Recruited eosinophils and Mast cells(MCs)release some mediators which contribute to coronary vasoconstriction,leukocyte recruitment,formation of new blood vessels,scar formation.In adaptive immunity,effector T cells,especially Th17 cells,lead to the pathogenesis of cardiac fibrosis,including the distal fibrosis and scar formation.CMs protectors,Treg cells,inhibit reduce the inflammatory response,then directly trigger the regeneration of local progenitor cell via IL-10.B cells reduce myocardial injury by preserving cardiac function during the resolution of inflammation.

关键词： cardiac homeostasis inflammation

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