期刊论文详细信息
Developmental Biology
Cellular Immune Response to Parasite Infection in the Drosophila Lymph Gland Is Developmentally Regulated
Richard Paul Sorrentino1  Shubha Govind1  Yves Carton1 
[1] Department of Biology, City College of New York and Graduate School and University Center of the City University of New York, 138th Street and Convent Avenue, New York, New York, 10031
关键词: cellular immune competence;    steroid hormone;    signal transduction;    parasites;    Drosophila;   
DOI  :  10.1006/dbio.2001.0542
学科分类:生物科学(综合)
来源: Academic Press
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【 摘 要 】

Themechanismsbywhichanorganismbecomesimmunecompetentduringitsdevelopmentarelargelyunknown.Wheninfectedbyeggsofparasiticwasps,Drosophilalarvaemountacomplexcellularimmunereactioninwhichspecializedhostbloodcells,lamellocytesandcrystalcells,areactivatedandrecruitedtobuildacapsulearoundtheparasiteeggtoblockitsdevelopment.Here,wereportthatparasitizationbythewaspLeptopilinaboulardileadstoadramaticincreaseinthenumberofbothlamellocytesandcrystalcellsintheDrosophilalarvallymphgland.Furthermore,alimitedburstofmitosisfollowsshortlyafterinfection,suggestingthatbothcelldivisionanddifferentiationoflymphglandhemocytesarerequiredforencapsulation.Thesechanges,observedinthelymphglandsofthird-instar,butneverofsecond-instarhosts,arealmostalwaysaccompaniedbydispersaloftheanteriorlobesthemselves.Toconfirmalinkbetweenhostdevelopmentandimmunecompetence,weinfectedmutanthostsinwhichdevelopmentisblockedduringlarvalorlatelarvalstages.Wefoundthat,ingeneticbackgroundswhereecdysonelevelsarelow(ecdysoneless)orecdysonesignalingisblocked(nonpupariatingalleleofthetranscriptionfactorbroad),theencapsulationresponseisseverelycompromised.Inthethird-instarecdysonelesshosts,postinfectionmitoticamplificationinthelymphglandsisabsentandthereisareductionincrystalcellmaturationandpostinfectioncirculatinglamellocyteconcentration.Theseresultssuggestthatanecdysone-activatedpathwaypotentiatesprecursorsofeffectorcelltypestorespondtoparasitizationbyproliferationanddifferentiation.Weproposethat,byaffectingaspecificpoolofhematopoieticprecursors,thispathwaythusconfersimmunecapacitytothird-instarlarvae.

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