Please use this identifier to cite or link to this item: https://doi.org/10.1038/srep26210
DC FieldValue
dc.titleMice lacking Programmed cell death-1 show a role for CD8 + T cells in long-term immunity against blood-stage malaria
dc.contributor.authorHorne-Debets, J.M
dc.contributor.authorKarunarathne, D.S
dc.contributor.authorFaleiro, R.J
dc.contributor.authorPoh, C.M
dc.contributor.authorRenia, L
dc.contributor.authorWykes, M.N
dc.date.accessioned2020-09-09T01:33:41Z
dc.date.available2020-09-09T01:33:41Z
dc.date.issued2016
dc.identifier.citationHorne-Debets, J.M, Karunarathne, D.S, Faleiro, R.J, Poh, C.M, Renia, L, Wykes, M.N (2016). Mice lacking Programmed cell death-1 show a role for CD8 + T cells in long-term immunity against blood-stage malaria. Scientific Reports 6 : 26210. ScholarBank@NUS Repository. https://doi.org/10.1038/srep26210
dc.identifier.issn20452322
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/174961
dc.description.abstractEven after years of experiencing malaria, caused by infection with Plasmodium species, individuals still have incomplete immunity and develop low-density parasitemia on re-infection. Previous studies using the P. chabaudi (Pch) mouse model to understand the reason for chronic malaria, found that mice with a deletion of programmed cell death-1 (PD-1KO) generate sterile immunity unlike wild type (WT) mice. Here we investigated if the mechanism underlying this defect during acute immunity also impacts on long-term immunity. We infected WT and PD-1KO mice with Pch-malaria and measured protection as well as immune responses against re-infections, 15 or 20 weeks after the original infection had cleared. WT mice showed approximately 1% parasitemia compared to sterile immunity in PD-1KO mice on re-infection. An examination of the mechanisms of immunity behind this long-term protection in PD-1KO mice showed a key role for parasite-specific CD8 + T cells even when CD4 + T cells and B cells responded to re-infection. These studies indicate that long-term CD8 + T cell-meditated protection requires consideration for future malaria vaccine design, as part of a multi-cell type response.
dc.publisherNature Publishing Group
dc.sourceUnpaywall 20200831
dc.subjectPdcd1 protein, mouse
dc.subjectprogrammed death 1 receptor
dc.subjectanimal
dc.subjectC57BL mouse
dc.subjectCD8+ T lymphocyte
dc.subjectdeficiency
dc.subjectdisease model
dc.subjectimmunology
dc.subjectknockout mouse
dc.subjectmalaria
dc.subjectmetabolism
dc.subjectPlasmodium chabaudi
dc.subjectAnimals
dc.subjectCD8-Positive T-Lymphocytes
dc.subjectDisease Models, Animal
dc.subjectMalaria
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectPlasmodium chabaudi
dc.subjectProgrammed Cell Death 1 Receptor
dc.typeArticle
dc.contributor.departmentDEPT OF MICROBIOLOGY & IMMUNOLOGY
dc.description.doi10.1038/srep26210
dc.description.sourcetitleScientific Reports
dc.description.volume6
dc.description.page26210
Appears in Collections:Elements
Staff Publications

Show simple item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_1038_srep26210.pdf2.43 MBAdobe PDF

OPEN

NoneView/Download

SCOPUSTM   
Citations

16
checked on Apr 15, 2021

Page view(s)

52
checked on Apr 16, 2021

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.