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dc.contributor.authorLu, M. F.zh_CN
dc.contributor.authorZhang, M.zh_CN
dc.contributor.authorTakashima, A.zh_CN
dc.contributor.authorWeiss, J.zh_CN
dc.contributor.authorApicella, M. A.zh_CN
dc.contributor.authorLi, X. H.zh_CN
dc.contributor.authorYuan, D.zh_CN
dc.contributor.authorMunford, R. S.zh_CN
dc.contributor.author袁东星zh_CN
dc.date.accessioned2013-12-12T02:08:43Z
dc.date.available2013-12-12T02:08:43Z
dc.date.issued2005zh_CN
dc.identifier.citationNature Immunology,6(10):989-994zh_CN
dc.identifier.issn1529-2908zh_CN
dc.identifier.otherISI:000232027200017zh_CN
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/60753
dc.description.abstractT cell - independent type 1 agonists such as Gram-negative bacterial lipopolysaccharides can stimulate B lymphocytes to proliferate and produce antibodies by signaling through Toll-like receptors. This phenomenon is well established in vitro, yet polyclonal B cell responses after bacterial infection in vivo are often weak and short-lived. We show here that B cell proliferation and polyclonal antibody production in response to Gram-negative bacterial infection are modulated by acyloxyacyl hydrolase, a host enzyme that deacylates bacterial lipopolysaccharides. Deacylation of lipopolysaccharide occurred over several days, allowing lipopolysaccharide to act as an innate immune stimulant yet limiting the eventual amount of B cell proliferation and polyclonal antibody production. Control of lipopolysaccharide activation by acyloxyacyl hydrolase indicates that mammals can regulate immune responses to bacterial infection by chemical modification of a Toll-like receptor agonist.zh_CN
dc.language.isoen_USzh_CN
dc.subjectPERITONEAL INFLAMMATORY EXUDATEzh_CN
dc.subjectACYLOXYACYL HYDROLASEzh_CN
dc.subjectNEISSERIAL PORINSzh_CN
dc.subjectIMMUNE-RESPONSESzh_CN
dc.subjectEXTRACELLULAR COMPONENTSzh_CN
dc.subjectPOLYCLONAL ACTIVATIONzh_CN
dc.subjectENDOTOXIN EXPOSUREzh_CN
dc.subjectC57BL/10SCCR MICEzh_CN
dc.subjectGENETIC-CONTROLzh_CN
dc.subjectIN-VIVOzh_CN
dc.titleLipopolysaccharide deacylation by an endogenous lipase controls innate antibody responses to Gram-negative bacteriazh_CN
dc.typeArticlezh_CN


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