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LILRB4, an immune checkpoint on myeloid cells

Blood Science 2022年第2期4卷 49-56页

作者： Ting Yang Yixin Qian Xiaoting Liang Jianbo Wu Ming Zou Mi Deng Peking University International Cancer Institute Health Science CenterPeking UniversityBeijingChina Peking University Cancer Hospital and Institute Peking UniversityBeijingChina

Leukocyte immunoglobulin-like receptor B4(LILRB4)is an inhibitory receptor in the LILR family mainly expressed on normal and malignant human cells of myeloid *** binding to ligands,LILRB4 is activated and subsequently recruits adaptors to cytoplasmic immunoreceptor tyrosine inhibitory motifs to initiate different signaling cascades,thus playing an important role in physiological and pathological conditions,including autoimmune diseases,microbial infections,and *** normal myeloid cells,LILRB4 regulates intrinsic cell activation and *** disease-associated or malignant myeloid cells,LILRB4 is significantly correlated with disease severity or patient survival and suppresses T cells,thereby participating in the pathogenesis of various *** summary,LILRB4 functions as an immune checkpoint on myeloid cells and may be a promising therapeutic target for various human immune diseases,especially for cancer immunotherapy.

关键词： autoimmune disease Cancer Immune checkpoint Immunotherapy Inhibitory receptor LILR LILRB4,MDSC Myeloid cell TAM

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The Immune Potential and Immunopathology of Cytokineproducing B Cell Subsets

The Immune Potential and Immunopathology of Cytokineproducin...

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第十届全国免疫学学术大会

作者： Yan Bao Xuetao Cao Center for Tranlational Medicine Changzheng Hospital The Second Military Medical University National Key Laboratory of Medical Immunology & Institute of Immunology The Second Military Medical University

B lymphocytes are generally recognized for their potential to mediate humoral immunity by producing different antibody isotypes and being involved in opsonization and complement fixation. Nevertheless, the non-classical, antibodyindependent immune potential of B cell subsets has attracted much attention especially in the past decade. These B cells can release a broad variety of cytokines(such as IL-2, IL-4, IL-6, IL-10, IL-17, IFN-α, IFN-γ, TNF-α, TGF-β, LT), and can be classified into distinct subsets depending on the particular cytokine profile, thus emerging the concept of cytokineproducing B cell subsets. Although there is still controversy surrounding the key cell surface markers, intracellular factors and cellular origins of cytokine-producing B cell subsets, accumulating evidence indicates that these B cells are endowed with great potential to regulate both innate and adaptive arms of immune system though releasing cytokines. On the one hand, they promote immune responses through mounting Th1/Th2/Th17 and neutrophil response, inducing DC maturation and formation of lymphoid structures, increasing NK cell and macrophage activation, enhancing development of themselves and sustaining antibody production. On the other hand, they can negatively regulate immune responses by suppressing Th cell responses, inhibiting Tr1 cells and Foxp3 Tregs differentiation, impairing APC function and proinflammatory cytokine release by monocytes, and inducing CD8 T cell anergy and CD4 T cell apoptosis. Therefore, cytokine-producing B cell subsets have multifunctional functions in health and diseases, playing pathologic as well as protective roles in autoimmunity, infection, allergy, and even malignancy. In this review, we revisit the history of discovering cytokine-producing B cells, describe the identification of cytokine-producing B cell subsets, introduce the origins of cytokine-producing B cell subsets as well as molecular and cellular mechanisms for their differentiation, and

关键词： Cytokine-producing B cells Immune regulation autoimmune disease Infection Cancer

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Advances in the research of anticardiolipin antibodies

Advances in the research of anticardiolipin antibodies

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第十三届全国免疫学学术大会

作者： Jiexin Zhang Shichang Zhang Department of Laboratory Medicine Jiangsu Province Hospital

Anticardiolipin antibody(ACA) is a kind of autoantibody, one of antiphospholipidantibodies(APL).The phospholipids with negative charge on platelets and endothelial cell membranes are used as target *** is common in systemic lupus erythematosus and other autoimmune diseases, and is closely associated with thrombosis, thrombocytopenia and spontaneous *** 1983, Harris et *** a method for the determination of ACA, the research on the antibody has gained worldwide attention and developed rapidly.

关键词： anticardiolipin antibody autoantibody autoimmune disease

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Programmed cell death 5(PDCD5) negatively regulates autoimmunity

Programmed cell death 5(PDCD5) negatively regulates autoimmu...

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第十届全国免疫学学术大会

作者： Ge Li Juan Xiao Yingyu Chen Department of Immunology Peking University School of Basic Medical Sciences Peking University Center for Human Disease Genomics Medical College Hubei University of Arts and Science

Purpose:This study aims to investigate the roles of PDCD5 in autoimmune disease and to probe into its molecular mechanism of ***:We constructed some autoimmune disease models such as autoimmune encephalomyelitis(EAE),collageninduced arthritis(CIA)and DSS-induced ulcerative colitis(UC)to detect whether increased PDCD5 protein could relieve autoimmune *** these models,PDCD5 transgenic mice were used,or rh PDCD5 were injected to mice or rats.

关键词： PDCD5 autoimmune disease Regulatory T cell FOXP3

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IFN-γ-STAT1-iNOS Induces Myeloid Progenitors to Acquire Immunosuppressive Activity

IFN-γ-STAT1-iNOS Induces Myeloid Progenitors to Acquire Imm...

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第十二届全国免疫学学术大会

作者： Yang shuhan Li Liang Xie Yuqing Yao Yuan Gao Caiyue Liao Lianghuan Ma Hongdi Lian Zhexiong University of Science and Technology of China South China University of Technology Hefei National Laboratory for Physical Sciences at Microscale

autoimmune diseases often induce dysregulated hematopoiesis with altered number and function of hematopoietic stem and progenitor cells(HSPCs).However,there are limited studies on the direct regulation of HSPCs on T cells,which are often detrimental to *** we found that in a murine model of Concanavalin A induced autoimmune hepatitis,LSK(Lineage’Sca-1c-Kit)-like cells accumulated in liver,spleen and bone marrow,which were myeloid progenitors(Lineage"Sca-1c-Kit) that upregulated Sca-1 expression upon T cell derived IFN-γ ***,bone marrow LSK-like cells from mice induced by Con A to develop autoimmune hepatitis or alternatively myeloid progenitors from wild type mice possessed strong in vitro suppressive *** suppressive function depended on T cell derived IFN-γ in a paracrine fashion,which induced STAT1 phosphorylation,inducible Nitric Oxide Synthase expression and nitric oxide *** IFN-γ/IFN-γ receptor interaction,knockout of STAT1 or iNOS inhibition abrogated their suppressive *** addition,the suppressive function was independent of differentiation;mitomycin C treated myeloid progenitors maintained T cell suppressive ability in *** data demonstrate a mechanism of inflammation induced suppressive function of myeloid progenitors which may participate directly in suppressing T cell mediated immunopathology.

关键词： Immunosuppression autoimmune disease myeloid progenitors T cells Bone marrow IFN-γ STAT1 iNOS

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Structure and degradation of circular RNAs regulate PKR activation in innate immunity

Structure and degradation of circular RNAs regulate PKR acti...

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中国生物化学与分子生物学会2019年全国学术会议暨学会成立四十周年

作者： Chu-Xiao Liu Xiang Li Fang Nan Shan Jiang Xiang Gao Si-Kun Guo Wei Xue Yange Cui Kaige Dong Huihua Ding Bo Qu Zhaocai Zhou Nan Shen Li Yang Ling-Ling Chen State Key Laboratory of Molecular Biology Shanghai Key Laboratory of Molecular Andrology CAS Center for Excellence in Molecular Cell Science Shanghai Institute of Biochemistry and Cell Biology University of Chinese Academy of Sciences Chinese Academy of Sciences Key Laboratory of Computational Biology CAS-MPG Partner Institute for Computational Biology Shanghai Institute of Nutrition and Health Shanghai Institutes for Biological Sciences University of Chinese Academy of Sciences Chinese Academy of Sciences School of Life Science and Technology ShanghaiTech University Laboratory of Molecular Rheumatology Shanghai Institute of Nutrition and Health Shanghai Institutes for Biological Sciences University of Chinese Academy of Sciences Chinese Academy of Sciences Shanghai Institute of Rheumatology China-Australia Centre for Personalized Immunology Renji Hospital School of Medicine Shanghai Jiao Tong University Center for autoimmune Genomics and Etiology Cincinnati Children’s Hospital Medical Center Department of Pediatrics University of Cincinnati College of Medicine

CircRNAs produced from back-splicing of exons of pre-mRNAs are widely expressed, but current understanding of their functions is limited. These RNAs are stable in general and are thought to have unique structural conformations distinct from their linear RNA cognates. Here we uncover that endogenous circRNAs tend to form 16-26 bp imperfect RNA duplexes and act as inhibitors of double-stranded RNA(dsRNA)-activated protein kinase(PKR) related to innate immunity. Upon poly(I:C) stimulation or viral infection, circRNAs are globally degraded by RNase L, a process required for PKR activation in early cellular innate immune responses. Augmented PKR phosphorylation and circRNA reduction are found in peripheral blood mononuclear cells(PBMCs) derived from patients of autoimmune disease systemic lupus erythematosus(SLE). Importantly, over-expression of the dsRNA-containing circRNA in PBMCs or T cells derived from SLE can alleviate the aberrant PKR activation cascade, thus providing a connection between circRNAs and SLE.

关键词： Circular RNAs(circRNAs) circRNA structure circRNA degradation double-stranded RNAs(dsRNAs) RNase L PKR innate immune responses autoimmune disease SHAPE-MaP systemic lupus erythematosus(SLE)

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miR-99a regulates CD4+ T cell differentiation by m TOR mediated glycolysis suppression

miR-99a regulates CD4+ T cell differentiation by m TOR media...

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第三届免疫学博士生论坛

作者：钱柳 Hong Zhou Congfeng Xu Yanyun Zhang 上海交通大学医学院 Shanghai Institute of Immunology Institutes of Medical Sciences Shanghai Jiao Tong University School of Medicine (SJTUSM) and Key Laboratory of Stem Cell Biology Institute of Health Sciences Shanghai Institutes for Biological Sciences Chinese Academy of Sciences & SJTUSM

Metabolic demands are dramatically different in distinct activated status and subsets of CD4+ T cells, during which mammalian target of rapamycin(m TOR) is of indispensable importance as both a sensor of external environment and a regulator on multiple downstream signaling cascades. Elaborated regulation of m TOR is vital for appropriate T cell function, and micro RNAs(mi RNA) could have potential role on that process, however, there are only superficial touch in that perspective. In the present study, with the assistance of bioinformatics, we identified mi R-99 a as a powerful regulator of m TOR, and in turn modulating glycolysis of CD4+ T cells. Further exploration demonstrated that TGF-β upregulates mi R-99 a and reprograms cellular glycolysis, through meddling m TOR signaling, thus contributes to the inhibition of Th1 differentiation and in favor of Treg induction. Deregulation of glycolysis contributes to the pathogenesis of rheumatoid arthritis(RA), and our data did show that mi R-99 a was dramatically decreased in CD4+ T cells of RA patients, potentially leading to higher glycolysis. In conclusion, we identified mi R-99 a, a novel regulator of m TOR function, which essentially regulates T cell biology through glycolysis manipulation, providing a potential therapeutic approach on autoimmune diseases.

关键词： m TOR mi R-99a glycolysis T cell differentiation TGF-β autoimmune disease

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Association of Rare and Common Variants with Juvenile Idiopathic Arthritis

Association of Rare and Common Variants with Juvenile Idiopa...

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第十四届全国免疫学学术大会

作者： Jin Li Xinyi Meng Jie Yang Tianjin Medical University

Juvenile idiopathic arthritis(JIA) is the most common pediatric rheumatic disease and is one of the most common chronic autoimmune diseases among *** remains to be understood about JIA etiology and the number of JIA genetic loci that have been reported is very limited compared to that of rheumatoid arthritis,the adult counterpart of JIA,though genetics makes large contributions to the development of JIA based on heritability *** aimed to identify rare coding variants and common single nucleotide polymorphism(SNPs) associated with JIA at the genome-wide *** rare variant study,we established a rare variant calling and filtering pipeline based on RNA-seq *** performed rare coding variant and gene-based association analyses on three RNA-seq datasets composed of 228 JIA patients in the Gene Expression Omnibus against different sets of *** identified 66 recurrent rare coding variants only present in JIA patients but not *** these variants three were reported in literature as JIA causal variants and 10 were replicated in our replication study using whole-exome sequencing data of JIA *** the common variant study,we attempted to tackle unknown molecular mechanisms of JIA underlying its heterogeneous clinical phenotypes by systematically identifying genetic signatures of each JIA subtypes with a heterogeneity sensitive *** identified 11 novel genome-wide significant loci from previously published GWAS *** annotation and pathway analysis suggest that candidate genes at these loci are highly expressed in immune cell types and function in Th17 cell *** on the association between these loci and each JIA subtype,the 7 JIA subtypes could be classified into two groups,reflecting their autoimmune vs autoinflammatory nature *** of the candidate genes in these JIA loci are targets of drugs used in clinic,with known medications used for other inflammation *** ident

关键词： Juvenile idiopathic arthritis autoimmune disease rare variants common SNPs,genetic association

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MTOR signaling is essential for the development of thymic epithelial cells and the induction of central immune tolerance

MTOR signaling is essential for the development of thymic ep...

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第十二届全国免疫学学术大会

作者： Liang Zhanfeng Zhang Lianjun Su Huiting Luan Rong Zhao Yong Institute of Zoology Chinese Academy of Sciences

Thymic epithelial cells(TECs) are critical for the establishment and maintenance of appropriate microenvironment for the positive and negative selection of thymocytes and the induction of central immune ***,little about the molecular regulatory network on TEC development and function is ***,by using conditional knockout,flow cytometry,western blot,real-time PCR,immunofluorence et al,we want to demonstrate the role of MTOR(mechanistic target of rapamycin) signaling in the development of *** results showed that MTOR is essential for proper development and functional maturation of *** inhibition of MTOR activity by rapamycin(RPM) causes severe thymic atrophy and reduction of ***-specific deletion of Mtor causes the severe reduction of mTECs,the blockage of thymocyte differentiation and output,the reduced generation of thymic regulatory T(Treg) cells and the impaired expression of tissue-restricted antigens(TRAs) including Fabp2,Ins1,Tff3 and Chrnal ***,specific deletion of Mtor in TECs causes autoimmune diseases characterized by enhanced tissue immune cell infiltration and the presence of autoreactive ***,Mtor deletion causes overdegradation of Beta-Catenin due to excessive autophagy and the attenuation of WNT(wingless-type MMTV integration site family) signaling in *** inhibition of autophagy significantly rescued the poor mTEC development caused by Mtor ***,MTOR is essential for TEC development and maturation by regulating proliferation and WNT signaling activity through *** present study also implies that long-term usage of RPM might increase the risk of autoimmunity by impairing TEC maturation and function.

关键词： autoimmune disease immune tolerance Mtor T cells thymic epithelial cells

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Anti-serum with anti-autoantibody activity decreases autoantibody-positive B lymphocytes and type 1 diabetes of NOD mice

Anti-serum with anti-autoantibody activity decreases autoant...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者：陈思峰 Dan Meng Chao Lu Yanqiang Hou Rui Wang Alex F.Chen 复旦大学 Department of Physiology and Pathophysiology Fudan University Shanghai Medical College Department of Central Laboratory Songjiang Hospital Affiliated First People's HospitalShanghai Jiao Tong University

Poor blood and stem/progenitor cell supplies underlie wound healing impairment in diabetic *** pluripotent stem cells（i PSs）have great therapeutic potential;however,it is not clear whether i PSs can promote wound healing are *** application of i PSs on a body or wound surface has not yet been *** study aimed to demonstrate the effect and associated mechanisms of topically applied i PSs on wound healing in diabetic *** streptozocin-induced type 1 diabetic mice,we found that i PSs accelerated skin wound healing,and promoted re-epithelialization and angiogenesis,while increasing expression of proangiogenic factors and receptors in the diabetic *** applied cells survived in the lesion and many differentiated into vascular endothelial *** of heme oxygenase-1（HO-1）in i PSs blocked these beneficial effects and the differentiation of i *** mice did not develop teratoma after i PS treatment over a follow-up of 3 *** results show that i PSs accelerate diabetic wound healing through a proangiogenic effect in a HO-1–dependent *** delivery of i PSs may be a novel approach to achieve i PS therapy while circumventing the major shortcomings of existing i PS administration routes.

关键词： autoimmune disease type 1 diabetes autoantibody immune therapy

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