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You had me at PELO:a"Ribosome Rescuer"induces NLR inflammasome assembly

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Cellular & Molecular immunology 2024年第1期21卷 1-2页

作者： Zoie Magri Alexander Poltorak Graduate Program in Immunology Tufts Graduate School of Biomedical Sciences136 Harrison AvenueBostonMA02111USA Department of immunology Tufts University School of MedicineBostonMA02111USA

Pyroptosis,an inflammatory form of programmed cell death,eliminates a niche where pathogens replicate,providing overall benefits to a host.When left uncontrolled,pyroptosis can lead to severe pathology.Overactive pyroptotic activation has been implicated in neuroinflammation,cardiovascular disease,acute respiratory distress syndrome(ARDS),and many other diseases[1,2,3].Because of its multiple and permanent consequences,pyroptosis is a highly regulated signaling pathway.Major regulators of pyroptosis are NLR inflammasomes,which are activated by various“danger”signals such as ATP.

关键词： inflam NLR distress

Two distinct subpopulations of marginal zone B cells exhibit differential antibody-producing capacities and radioresistance

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Cellular & Molecular immunology 2024年第4期21卷 393-408页

作者： Sujin Lee Yeunjung Ko Hyun Woo Lee Won Joon Oh Hun Gi Hong Dinuka Ariyaratne Se Jin Im Tae Jin Kim Department of immunology Graduate School of Basic Medical ScienceSungkyunkwan University School of MedicineSuwon16419Republic of Korea Department of immunology and Molecular Medicine Faculty of Medical SciencesUniversity of Sri JayewardenepuraNugegodaSri Lanka Present address:immunology and Microbiology Graduate program Baylor College of MedicineHoustonTX77030USA

Marginal zone(MZ)B cells,which are splenic innate-like B cells that rapidly secrete antibodies(Abs)against blood-borne pathogens,are composed of heterogeneous subpopulations.Here,we showed that MZ B cells can be divided into two distinct subpopulations according to their CD80 expression levels.CD80^(high)MZ B cells exhibited greater Ab-producing,proliferative,and IL-10-secreting capacities than did CD80^(low)MZ B cells.Notably,CD80^(high)MZ B cells survived 2-Gy whole-body irradiation,whereas CD80^(low)MZ B cells were depleted by irradiation and then repleted with one month after irradiation.Depletion of CD80^(low)MZ B cells led to accelerated development of type II collagen(CII)-induced arthritis upon immunization with bovine CII.CD80^(high)MZ B cells exhibited higher expression of genes involved in proliferation,plasma cell differentiation,and the antioxidant response.CD80^(high)MZ B cells expressed more autoreactive B cell receptors(BCRs)that recognized double-stranded DNA or CII,expressed more immunoglobulin heavy chain sequences with shorter complementarity-determining region 3 sequences,and included more clonotypes with no N-nucleotides or with B-1a BCR sequences than CD80^(low)MZ B cells.Adoptive transfer experiments showed that CD21^(+)CD23^(+)transitional 2 MZ precursors preferentially generated CD80^(low)MZ B cells and that a proportion of CD80^(low)MZ B cells were converted into CD80^(high)MZ B cells;in contrast,CD80^(high)MZ B cells stably remained CD80^(high)MZ B cells.In summary,MZ B cells can be divided into two subpopulations according to their CD80 expression levels,Ab-producing capacity,radioresistance,and autoreactivity,and these findings may suggest a hierarchical composition of MZ B cells with differential stability and BCR specificity.

关键词： Marginal Zone B Cell CD80 Autoreactivity Radioresistance

Physiology of gangliosides and the role of antiganglioside antibodies in human diseases

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Cellular & Molecular immunology 2020年第4期17卷 313-322页

作者： Gianni Cutillo Anna-Helena Saariaho Seppo Meri Translational immunology Research program and the Department of Bacteriology and immunology University of HelsinkiHelsinkiFinland Humanitas University MilanRozzanoItaly Helsinki University Hospital Laboratory(HUSLAB) HelsinkiFinland

Gangliosides are structurally and functionally polymorphic sialic acid containing glycosphingolipids that are widely distributed in the human body.They play important roles in protecting us against immune attacks,yet they can become targets for autoimmunity and act as receptors for microbes,like the influenza viruses,and toxins,such as the cholera toxin.The expression patterns of gangliosides vary in different tissues,during different life periods,as well as in different animals.Antibodies against gangliosides(AGA)can target immune attack e.g.,against neuronal cells and neutralize their complement inhibitory activity.AGAs are important especially in acquired demyelinating immune-mediated neuropathies,like Guillain–Barrésyndrome(GBS)and its variant,the Miller–Fisher syndrome(MFS).They can emerge in response to different microbial agents and immunological insults.Thereby,they can be involved in a variety of diseases.In addition,antibodies against GM3 were found in the sera of patients vaccinated with Pandemrix®,who developed secondary narcolepsy,strongly supporting the autoimmune etiology of the disease.

关键词： ganglioside Guillain-Barre syndrome complement narcolepsy sialic acid

Serotonin suppresses lung ILC2 activation and proliferation

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Cellular & Molecular immunology 2023年第5期20卷 546-547页

作者： Xiao-Hong Sun Oklahoma Medical Research Foundation Program in Arthritis and Clinical ImmunologyOklahoma CityOKUSA

In recent issue, Wang et al. [1] reported the suppressive effects of serotonin (5-hydroxytryptamine, 5-HT) on the activation and proliferation of group 2 innate lymphoid cells (ILC2s) in the lungs. ILC2s belong to a family of newly appreciated immune cells with a broad impact on a variety of immunological functions [2]. In particular, ILC2 activation has been implicated in the pathophysiology of asthma [3]. Although serotonin is known to play important roles in diverse physiological functions in the body [4], the effects of serotonin on innate lymphoid cells are less understood. The findings described here could potentially establish a new therapeutic avenue for respiratory disorders.

关键词： al. activation finding

Glucocorticosteroid therapy in inflammatory bowel diseases: From clinical practice to molecular biology

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World Journal of Gastroenterology 2017年第36期23卷 6628-6638页

作者： Karen Dubois-Camacho Payton A Ottum Daniel Franco-Munoz Marjorie De la Fuente Alejandro Torres-Riquelme David Díaz-Jiménez Mauricio Olivares-Morales Gonzalo Astudillo Rodrigo Quera Marcela A Hermoso Innate Immunity Laboratory Immunology ProgramInstitute of Biomedical SciencesFaculty of MedicineUniversidad de Chile Neuroimmunology Laboratory Immunology ProgramInstitute of Biomedical SciencesFaculty of MedicineUniversidad de Chile Division of Research Clínica Las Condes Gastroenterology Department Inflammatory Bowel Disease ProgramClínica Las Condes

Inflammatory bowel diseases(IBDs),such as ulcerative colitis and Crohn's disease,are chronic pathologies associated with a deregulated immune response in the intestinal mucosa,and they are triggered by environmental factors in genetically susceptible individuals.Exogenous glucocorticoids(GCs)are widely used as anti-inflammatory therapy in IBDs.In the past,patients with moderate or severe states of inflammation received GCs as a first line therapy with an important effectiveness in terms of reduction of the disease activity and the induction of remission.However,this treatment often results in detrimental side effects.This downside drove the development of second generation GCs and more precise(non-systemic)drugdelivery methods.Recent clinical trials show that most of these new treatments have similar effectiveness to first generation GCs with fewer adverse effects.The remaining challenge in successful treatment of IBDs concerns the refractoriness and dependency that some patients encounter during GCs treatment.A deeper understanding of the molecular mechanisms underlying GC response is key to personalizing drug choice for IBDs patients to optimize their response to treatment.In this review,we examine the clinical characteristics of treatment with GCs,followed by an in depth analysis of the proposed molecular mechanisms involved in its resistance and dependence associated with IBDs.This thorough analysis of current clinical and biomedical literature may help guide physicians in determining a course of treatment for IBDs patients and identifies important areas needing further study.

关键词： Inflammatory bowel diseases Ulcerative colitis Crohn's disease Glucocorticoid dependence Glucocorticoid resistance

Chimera RNA interference knockdown of γ-synuclein in human cortical astrocytes results in mitotic catastrophe

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Neural Regeneration Research 2020年第10期15卷 1894-1902页

作者： Timmy Le Cynthia L.Winham Fotis Andromidas Adam C.Silver Evan R.Jellison Aime A.Levesque Andrew O.Koob Graduate program in Neuroscience Biology DepartmentUniversity of HartfordWest HartfordCTUSA Department of immunology UCONN Health CenterFarmingtonCTUSA

Elevated levels of γ-synuclein(γ-syn)expression have been noted in the progression of glioblastomas,and also in the cerebrospinal fluid of patients diagnosed with neurodegenerative diseases.γ-Syn can be either internalized from the extracellular milieu or expressed endogenously by human cortical astrocytes.Internalizedγ-syn results in increased cellular proliferation,brain derived neurotrophic factor release and astroprotection.However,the function of endogenousγ-syn in primary astrocytes,and the relationship to these two opposing disease states are unknown.γ-Syn is expressed by astrocytes in the human cortex,and to gain a better understanding of the role of endogenous γ-syn,primary human cortical astrocytes were treated with chimera RNA interference(RNAi)targeting γ-syn after release from cell synchronization.Quantitative polymerase chain reaction analysis demonstrated an increase in endogenousγ-syn expression 48 hours after release from cell synchronization,while RNAi reduced γ-syn expression to control levels.Immunocytochemistry of Ki67 and 5-bromodeoxyuridine showed chimera RNAi γ-syn knockdown reduced cellular proliferation at 24 and 48 hours after release from cell synchronization.To further investigate the consequence of γ-syn knockdown on the astrocytic cell cycle,phosphorylated histone H3 pSer10(pHH3)and phosphorylated cyclin dependent kinase-2 pTyr15(pCDK2)levels were observed via western blot analysis.The results revealed an elevated expression of pHH3,but not pCDK2,indicating γ-syn knockdown leads to disruption of the cell cycle and chromosomal compaction after 48 hours.Subsequently,flow cytometry with propidium iodide determined that increases in apoptosis coincided with γ-syn knockdown.Therefore,γ-syn exerts its effect to allow normal astrocytic progression through the cell cycle,as evidenced by decreased proliferation marker expression,increased pHH3,and mitotic catastrophe after knockdown.In this study,we demonstrated that the knockdown of γ-syn within primary human cortical astrocytes using chime

关键词： apoptosis astrocyte cell cycle glioblastomas phospho-histone H3 proliferation synuclein

Dissecting the multifactorial nature of demyelinating disease

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Neural Regeneration Research 2018年第4期13卷 628-632页

作者： Karolina Kucharova William B.Stallcup Sanford Burnham Prebys Medical Discovery Institute Cancer Center Tumor Microenvironment and Cancer Immunology ProgramLa Jolla CA USA

Chondroitin sulfate proteoglycan-4(CSPG4) is a surface component of two key cell types(oligodendrocyte progenitor cells(OPCs) and myeloid cells) present in lysolecithin-induced lesions in mouse spinal cord.Two types of CSPG4 manipulations have been used to study the roles of these cells in myelin damage and repair:(1) OPC and myeloid-specific ablation of CSPG4,and(2) transplantation of enhanced green fluorescent protein(EGFP)-labeled progenitors to distinguish between bone marrow-derived macrophages and resident microglia.Ablation of CSPG4 in OPCs does not affect myelin damage,but decreases myelin repair,due to reduced proliferation of CSPG4-null OPCs that diminishes generation of mature oligodendrocytes for remyelination.Ablation of CSPG4 in myeloid cells greatly decreases recruitment of macrophages to spinal cord lesions,resulting in smaller initial lesions,but also in significantly diminished myelin repair.In the absence of macrophage recruitment,OPC proliferation is greatly impaired,again leading to decreased generation of myelinating oligodendrocytes.Macrophages may promote OPC proliferation via phagocytosis of myelin debris and/or secretion of factors that stimulate OPC mitosis.Microglia are not able to substitute for macrophages in promoting OPC proliferation.An additional feature of lesions in myeloid-specific CSPG4 null mice is the persistence of poorly-differentiated platelet-derived growth factor receptor α(PDGFRα) + macrophages that may prolong damage.

关键词：疾病性质 EGFP 巨噬细胞 OPC 房间硫酸盐蛋白质

RBP-J is required for M2 macrophage polarization in response to chitin and mediates expression of a subset of M2 genes

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Protein & Cell 2016年第3期7卷 201-209页

作者： Julia Foldi Yingli Shang Baohong Zhao Lionel B. Ivashkiv Xiaoyu Hu Graduate Program in Immunology and Microbial Pathogenesis Weill Cornell Graduate School of Medical Sciences New York NY 10021 USA School of Medicine and Institute for immunology Tsinghua University Beijing 100084 China Arthritis and Tissue Degeneration program Hospital for Special Surgery New York NY 10021 USA

开发或者激活(M2 ) 巨噬细胞显型是被小径和因素的过多并列地调整的一个复杂过程。这里，我们报导那 RBP-J，集成的 DNA 有约束力的蛋白质包括槽口小径从多重小径发信号，极其涉及 M2 巨噬细胞的极化。在在 myeloid 分隔空间的 RBP-J ... 详细信息

开发或者激活(M2 ) 巨噬细胞显型是被小径和因素的过多并列地调整的一个复杂过程。这里，我们报导那 RBP-J，集成的 DNA 有约束力的蛋白质包括槽口小径从多重小径发信号，极其涉及 M2 巨噬细胞的极化。在在 myeloid 分隔空间的 RBP-J 缺乏的老鼠在 M2 极化的一个导致几丁质的模型在 vivo 展出了损害 M2 显型。与一致在里面 vivo 调查结果， M2 极化部分在包括 arginase 由 M2 受动器分子的一个子集的减少的表示示威了的 Rbpj 缺乏的巨噬细胞在 vitro 被损害 1。机能上地， myeloid Rbpj 缺乏包括嗜曙红血球的招募和 T 房间增长的抑制损害了 M2 受动器功能。一起，我们作为区别的一个必要管理者和或者激活的巨噬细胞的功能识别了 RBP-J。

关键词：巨噬细胞极化响应甲壳素 DNA结合蛋白子集基因介导嗜酸性粒细胞

Immune regulation in the tumor microenvironment and its relevance in cancer therapy

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Cellular & Molecular immunology 2022年第1期19卷 1-2页

作者： Weiping Zou Department of Surgery Center of Excellence for Cancer Immunology and ImmunotherapyUniversity of Michigan Rogel Cancer CenterAnn ArborMIUSA Department of Pathology Graduate Program in Immunology and Graduate Program in Cancer BiologyUniversity of Michigan School of MedicineAnn ArborMIUSA

Cancer immunotherapy,including immune checkpoint blockade and CAR-T cell therapy,has introduced revolutionary approaches to treating patients with cancer.The success and hope of cancer immunotherapy have continuously stimulated high interest in dissecting immunotherapy resistance mechanisms,researching previously unknown therapeutic targets,and informing novel clinical trials in cancer therapy.The notion that the tumor microenvironment holds the key to understanding tumor immunity and developing novel immunotherapy has been well established in the field of tumor immunology and medical oncology[1].This special issue of Cellular&Molecular immunology(CMI)compiles a series of review articles,presenting state-ofthe-art literature and concepts focused on several important aspects concerning the most recent advancement in immune sensitive and resistant mechanisms in the tumor microenvironment,and their relevance in cancer therapy.

关键词： cancer immunity Immune