Evidence for Involvement of Th17 Type Responses in Post Kala Azar Dermal Leishmaniasis (PKDL) 英文参考文献.docVIP

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Evidence for Involvement of Th17 Type Responses in Post Kala Azar Dermal Leishmaniasis (PKDL) 英文参考文献.doc

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Evidence for Involvement of Th17 Type Responses in Post Kala Azar Dermal Leishmaniasis (PKDL) 英文参考文献

EvidenceforInvolvementofTh17TypeResponsesin PostKalaAzarDermalLeishmaniasis(PKDL) GajendraKumarKatara1,NasimAkhtarAnsari1¤,AvninderSingh1,V.Ramesh2,PoonamSalotra1* 1NationalInstituteofPathology(ICMR),SafdarjungHospitalCampus,NewDelhi,India,2DepartmentofDermatology,SafdarjungHospital,NewDelhi,India Abstract Background: Postkala-azar dermal leishmaniasis (PKDL), adermal sequelofvisceral leishmaniasis, causedby Leishmania donovani,constitutesanimportantreservoirfortheparasite.Parallelfunctioningofcounteractingimmuneresponses(Th1/ Th2) reflects a complex immunological scenario, suggesting the involvement of additional regulatory molecules in the diseasepathogenesis. Methodology/PrincipalFindings:Inthepresentstudy,humancytokine/chemokine/receptorspecificcDNAarraytechnique was employed to identify modulations in gene expression of host immuno-determinants during PKDL, followed by evaluation of Th17 type responses by analyzing mRNA andprotein expression of Th17 markers (IL-23, IL-17, RORct) and performing functional assays using Leishmania antigen (TSLA) or recombinant (rec)IL-17. Array analysis identified key immuno-regulatory molecules including cytokines (TNF-a, IFN-c, IL-10, IL-17), chemokines (MCP-1, MIP-1a), apoptotic molecules(FasL,TRAIL,IRF-1)andreceptors(CD40,Fas).UpregulationinlesionalexpressionofTh17markerswasobserved during PKDL compared to control (IL-17 and IL-23, P=0.0008; RORct, P=0.02). In follow-up samples, chemotherapy significantly down regulatedexpressionof allmarkers. In addition,lesional expression ofIL-17 wasconfirmed at protein levelbyImmuno-histochemistry. Further,systemicpresenceofTh17 responses(IL-17 andIL-23)wasobservedinplasma samples from PKDL patients. In functional assays, TSLA stimulated the secretion of IL-17 and IL-23 from PBMCs of PKDL patients,whilerecIL-17enhancedtheproductionofTNF-aaswellasnitricoxide(NO)inPKDLcomparedtocontrol(TNF-a, P=0.0002;NO,P=0.0013).Further,apositivecorrelationwasevidentbetweenlesionalmRNAexpressionofIL-