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CD300a inhibits CD16-mediated NK cell effector functions in HIV-1-infected patients

作     者:Joana Vitallé Iñigo Terrén Ane Orrantia Raquel Pérez-Garay Francesc Vidal JoséA.Iribarren Carmen Rodríguez Ana M.López Lirola Enrique Bernal Olatz Zenarruzabeitia Francisco Borrego 

作者机构:Immunopathology GroupBiocruces Bizkaia Health Research InstituteBarakaldoSpain Hospital Universitari de Tarragona Joan XXIIIIISPVUniversitat Rovira i VirgiliTarragonaSpain Servicio de Enfermedades InfecciosasHospital Universitario DonostiaInstituto de Investigación Sanitaria BiodonostiaDonostia-San SebastiánSpain Centro Sanitario SandovalHospital Clínico San CarlosInstituto de Investigación Sanitaria San CarlosMadridSpain Hospital Universitario de CanariasSanta Cruz de TenerifeSpain Department of Clinical MedicineUniversidad de Murcia and Hospital General Universitario Reina SofíaMurciaSpain IkerbasqueBasque Foundation for ScienceBilbaoSpain 

出 版 物:《Cellular & Molecular Immunology》 (中国免疫学杂志(英文版))

年 卷 期:2019年第16卷第12期

页      面:940-942页

核心收录:

学科分类:0710[理学-生物学] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100401[医学-流行病与卫生统计学] 10[医学] 

基  金:supported by grants to F.B.from Instituto de Salud CarlosⅢ(ISCⅢ)-Subdirección de Evaluación y Fondo Europeo de Desarrollo Regional(FEDER)(Grant PI13/00889) Marie-Curie Actions,Career Integration Grant,European Commission(Grant CIG 631674) .J.V.and I.T.are recipients of a predoctoral contract funded by the Department of Education,Basque Government(PRE_2018_2_0211 and PRE_2018_1_0032) I.T.is the recipient of a fellowship from the Jesús de Gangoiti Barrera Foundation(FJGB17/003) funded by ISCIII-Contratos Sara Borrell(CD17/0128) supported by ISCIII,Spanish Health Ministry(Grant no.RD06/0006/0035,RD12/0017/0037,and RD16/0025/0019) funded by the ISCIII through the RIS(RIS C03/173,RD12/0017/0018,and RD16/0002/0006) the Plan Nacional R+D+I and cofinanced by ISCIII-Subdirección General de Evaluación y FEDER 

主  题:CD16 CD30 ADCC 

摘      要:Natural killer(NK)cell-mediated antibody-dependent cellular cytotoxicity(ADCC)through CD16 plays a critical role in antihuman immunodeficiency virus(HIV)responses.1–3 CD300a is a surface receptor highly expressed on NK cells that has the capacity to inhibit NK cell-mediated cytotoxicity in healthy donors.4 The CD300a molecule has been related to several viral infections and is able to diminish the NK cell killing of pseudorabies-infected cells through interactions with its ligands phosphatidylserine and phosphatidylethanolamine.5 In addition,CD300a expression on B and CD4+T lymphocytes is altered during HIV-1 infection,and combined antiretroviral therapy(cART)does not restore nonpathological expression levels.5,6 However,the expression and function of CD300a on NK cells during HIV-1 infection is still *** have determined the surface expression of CD300a on different NK cell subsets and the capacity of this receptor to inhibit CD16-induced NK cell effector functions in healthy and HIV-1 infected individuals.

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