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Variations in killer-cell immunoglobulin-like receptor and human leukocyte antigen genes and immunity to malaria

Cellular & Molecular Immunology 2020年第8期17卷 799-806页

作者： Stephen Tukwasibwe Annettee Nakimuli James Traherne Olympe Chazara Jyothi Jayaraman John Trowsdale Ashley Moffett Prasanna Jagannathan Philip JRosenthal Stephen Cose francesco colucci Makerere University KampalaUganda University of Cambridge CambridgeUK University of Cambridge Centre for Trophoblast Research CambridgeUK School of Medicine Stanford UniversityStanfordCAUSA University of California San FranciscoCAUSA MRC/UVRI and LSHTM Uganda Research Unit KampalaUganda Department of Obstetrics&Gynaecology National Institute for Health Research Cambridge Biomedical Research CentreUniversity of CambridgeCambridgeCB20SWUK

Malaria is one of the deadliest infectious diseases in the world. Immune responses to Plasmodium falciparum malaria vary among individuals and between populations. Human genetic variation in immune system genes is likely to play a role in this heterogeneity. Natural killer (NK) cells produce inflammatory cytokines in response to malaria infection, kill intraerythrocytic Plasmodium falciparum parasites by cytolysis, and participate in the initiation and development of adaptive immune responses to plasmodial infection. These functions are modulated by interactions between killer-cell immunoglobulin-like receptors (KIRs) and human leukocyte antigens (HLAs). Therefore, variations in KIR and HLA genes can have a direct impact on NK cell functions. Understanding the role of KIRs and HLAs in immunity to malaria can help to better characterize antimalarial immune responses. In this review, we summarize the different KIRs and HLAs associated with immunity to malaria thus far.

关键词： Genetic variation Human Leukocyte Antigen Innate immunity Killer-cell immunoglobulin-like receptor Malaria Natural killer cells

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Biology and pathology of the uterine micro environ merit and its natural killer cells

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Cellular & Molecular Immunology 2021年第9期18卷 2101-2113页

作者： Fuyan Wang Anita Ellen Qualls Laia Marques-Fernandez francesco colucci Department of Obstetrics&Gynaecology University of CambridgeNational Institute for Health Research Cambridge Biomedical Research CentreCambridge CB20SWUK Department of Biochemistry and Molecular Biology and Zhejiang Key Laboratory of PathophysiologySchool of MedicineNingbo UniversityNingbo 315211China Centre for Trophoblast Research University of CambridgeCambridge CB23EGUK

Tissues are the new frontier of discoveries in immunology.Cells of the immune system are an integral part of tissue physiology and immunity.Determining how immune cells inhabit,housekeep,and defend gut,lung,brain,liver,uterus,and other organs helps revealing the intimate details of tissue physiology and may offer new therapeutic targets to treat pathologies.The uterine microenvironment modulates the development and function of innate lymphoid cells[ILC,largely represented by natural killer(NK)cells],macrophages,T cells,and dendritic cells.These immune cells,in turn,contribute to tissue homeostasis.Regulated by ovarian hormones,the human uterine mucosa(endometrium)undergoes ~400 monthly cycles of breakdown and regeneration from menarche to menopause,with its fibroblasts,glands,blood vessels,and immune cells remodeling the tissue into the transient decidua.Even more transformative changes occur upon blastocyst implantation.Before the placenta is formed,the endometrial glands feed the embryo by histiotrophic nutrition while the uterine spiral arteries are stripped of their endothelial layer and smooth muscle actin.This arterial remodeling is carried out by invading fetal trophoblast and maternal immune cells,chiefly uterine NK(uNK)cells,which also assist fetal growth.The tran sformed arteries no Ion ger resp ond to mater nal stimuli and meet the increasi ng dema nds of the growing fetus.This review focuses on how the everchanging uterine microenvironment affects uNK cells and how uNK cells regulate homeostasis of the decidua,placenta development,and fetal growth.Determining these pathways will help understand the causes of major pregnancy complications.

关键词： Natural killer cells Uterine microenvironment Pregnancy Decidua uNK

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胸苷酸合成酶和拓扑异构酶-1及Ki-67对伊立替康联合5-氟脲嘧啶治疗晚期大肠癌的预测价值

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中华肿瘤杂志 2005年第5期27卷 312-315页

作者：徐建明朱步东 Mangia Anita Simone Gianni Montemurro Severino Giuliani francesco Maiello Evaristo colucci Giuseppe Paradiso Angelo 军事医学科学院附属医院肿瘤中心北京大学临床肿瘤学院内科 70126 Bari Via Amendola 209National Cancer InstituteItaly

目的探讨胸苷酸合成酶(TS)、拓扑异构酶1(Topo1)和肿瘤增殖指标Ki67对伊立替康(CPT11)联合5氟脲嘧啶(5Fu)治疗晚期大肠癌患者的临床疗效和预后的预测价值。方法采用免疫组化方法检测了CPT11+5Fu一线治疗78例大肠癌患者的TS、Topo1和Ki6... 详细信息

目的探讨胸苷酸合成酶(TS)、拓扑异构酶1(Topo1)和肿瘤增殖指标Ki67对伊立替康(CPT11)联合5氟脲嘧啶(5Fu)治疗晚期大肠癌患者的临床疗效和预后的预测价值。方法采用免疫组化方法检测了CPT11+5Fu一线治疗78例大肠癌患者的TS、Topo1和Ki67的表达,并与化疗疗效和患者的临床预后进行了分析。结果各检测指标的表达水平与临床疗效之间无关,但是临床预后不同。其中,TS低表达患者表现明显长的肿瘤进展时间(TTP,P<0.05)和存活期(OS,P<0.05);Ki67低表达也预示长的OS(P<0.05)。与单个指标相比较,两个指标的联合也不能预测临床疗效,但是对预后的判断作用明显提高。TS低表达、Ki67低表达以及TS和Ki67均低表达患者的中位TTP分别为9,8和17个月(P=0.02);TS低表达、Topo1低表达以及TS和Topo1均低表达患者的中位TTP分别为9,9和13个月(P=0.03);而Topo1低表达、Ki67低表达、Ki67和Topo1均低表达患者的中位TTP分别为8,9和11个月(P=0.05)。其中任何两个指标均低表达肿瘤的TTP和OS均明显长于高表达者(P<0.05)。结论TS、Topo1和Ki67不能预测大肠癌患者CPT11+5Fu的疗效,但对其临床预后有一定的预测作用。其中任何两个指标的联合,比单一指标对患者预后的预测价值明显提高。

关键词：胸苷酸合成酶拓扑异构酶-l Ki-67 伊立替康 5-氟脲嘧啶结肠肿瘤直肠肿瘤

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