FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2078421176> ?p ?o ?g. }

• W2078421176 endingPage "297" @default.
• W2078421176 startingPage "286" @default.
• W2078421176 abstract "ABSTRACT Unlike human malaria parasites that induce persistent infection, some rodent malaria parasites, like Plasmodium yoelii strain 17XNL (Py17XNL), induce a transient (self-curing) malaria infection. Cooperation between CD4 T cells and B cells to produce antibodies is thought to be critical for clearance of Py17XNL parasites from the blood, with major histocompatibility complex (MHC) class II molecules being required for activation of CD4 T cells. In order to better understand the correspondence between murine malaria models and human malaria, and in particular the role of MHC (HLA) class II molecules, we studied the ability of humanized mice expressing human HLA class II molecules to clear Py17XNL infection. We showed that humanized mice expressing HLA-DR4 (DR0401) molecules and lacking mouse MHC class II molecules (EA 0 ) have impaired production of specific antibodies to Py17XNL and cannot cure the infection. In contrast, mice expressing HLA-DR4 (DR0402), HLA-DQ6 (DQ0601), HLA-DQ8 (DQ0302), or HLA-DR3 (DR0301) molecules in an EA 0 background were able to elicit specific antibodies and self-cure the infection. In a series of experiments, we determined that the inability of humanized DR0401.EA 0 mice to elicit specific antibodies was due to expansion and activation of regulatory CD4 + Foxp3 + T cells (Tregs) that suppressed B cells to secrete antibodies through cell-cell interactions. Treg depletion allowed the DR0401.EA 0 mice to elicit specific antibodies and self-cure the infection. Our results demonstrated a differential role of MHC (HLA) class II molecules in supporting antibody responses to Py17XNL malaria and revealed a new mechanism by which malaria parasites stimulate B cell-suppressogenic Tregs that prevent clearance of infection." @default.
• W2078421176 created "2016-06-24" @default.
• W2078421176 creator A5028088897 @default.
• W2078421176 creator A5030177021 @default.
• W2078421176 creator A5038661648 @default.
• W2078421176 creator A5041731742 @default.
• W2078421176 creator A5048188374 @default.
• W2078421176 creator A5066842624 @default.
• W2078421176 creator A5069197438 @default.
• W2078421176 creator A5086141060 @default.
• W2078421176 creator A5087226925 @default.
• W2078421176 date "2014-01-01" @default.
• W2078421176 modified "2023-09-27" @default.
• W2078421176 title "HLA Class II (DR0401) Molecules Induce Foxp3⁺Regulatory T Cell Suppression of B Cells in Plasmodium yoelii Strain 17XNL Malaria" @default.
• W2078421176 cites W1499797787 @default.
• W2078421176 cites W151434624 @default.
• W2078421176 cites W1545456180 @default.
• W2078421176 cites W1552712171 @default.
• W2078421176 cites W1898099607 @default.
• W2078421176 cites W193852082 @default.
• W2078421176 cites W1966554631 @default.
• W2078421176 cites W1970520939 @default.
• W2078421176 cites W1981356490 @default.
• W2078421176 cites W1993276441 @default.
• W2078421176 cites W1996181732 @default.
• W2078421176 cites W1998858806 @default.
• W2078421176 cites W1999015837 @default.
• W2078421176 cites W2000587047 @default.
• W2078421176 cites W2002324166 @default.
• W2078421176 cites W2005817811 @default.
• W2078421176 cites W2006509079 @default.
• W2078421176 cites W2017861745 @default.
• W2078421176 cites W2018308106 @default.
• W2078421176 cites W2022554379 @default.
• W2078421176 cites W2026176809 @default.
• W2078421176 cites W2029148574 @default.
• W2078421176 cites W2035779622 @default.
• W2078421176 cites W2036014936 @default.
• W2078421176 cites W2040840100 @default.
• W2078421176 cites W2053365848 @default.
• W2078421176 cites W2058425124 @default.
• W2078421176 cites W2059193305 @default.
• W2078421176 cites W2066403587 @default.
• W2078421176 cites W2066499419 @default.
• W2078421176 cites W2075459855 @default.
• W2078421176 cites W2090041953 @default.
• W2078421176 cites W2095554063 @default.
• W2078421176 cites W2096354903 @default.
• W2078421176 cites W2096869658 @default.
• W2078421176 cites W2099387335 @default.
• W2078421176 cites W2107004072 @default.
• W2078421176 cites W2108011188 @default.
• W2078421176 cites W2109924214 @default.
• W2078421176 cites W2113929556 @default.
• W2078421176 cites W2117557757 @default.
• W2078421176 cites W2127132522 @default.
• W2078421176 cites W2130503023 @default.
• W2078421176 cites W2133945584 @default.
• W2078421176 cites W2137408395 @default.
• W2078421176 cites W2142578713 @default.
• W2078421176 cites W2142657250 @default.
• W2078421176 cites W2146943570 @default.
• W2078421176 cites W2149626878 @default.
• W2078421176 cites W2159346740 @default.
• W2078421176 cites W2159570476 @default.
• W2078421176 cites W2161951914 @default.
• W2078421176 cites W2164751322 @default.
• W2078421176 cites W2169908075 @default.
• W2078421176 cites W2170098434 @default.
• W2078421176 cites W4313307572 @default.
• W2078421176 doi "https://doi.org/10.1128/iai.00272-13" @default.
• W2078421176 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3911852" @default.
• W2078421176 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24166949" @default.
• W2078421176 hasPublicationYear "2014" @default.
• W2078421176 type Work @default.
• W2078421176 sameAs 2078421176 @default.
• W2078421176 citedByCount "13" @default.
• W2078421176 countsByYear W20784211762014 @default.
• W2078421176 countsByYear W20784211762015 @default.
• W2078421176 countsByYear W20784211762016 @default.
• W2078421176 countsByYear W20784211762017 @default.
• W2078421176 countsByYear W20784211762018 @default.
• W2078421176 countsByYear W20784211762019 @default.
• W2078421176 countsByYear W20784211762020 @default.
• W2078421176 countsByYear W20784211762021 @default.
• W2078421176 countsByYear W20784211762022 @default.
• W2078421176 crossrefType "journal-article" @default.
• W2078421176 hasAuthorship W2078421176A5028088897 @default.
• W2078421176 hasAuthorship W2078421176A5030177021 @default.
• W2078421176 hasAuthorship W2078421176A5038661648 @default.
• W2078421176 hasAuthorship W2078421176A5041731742 @default.
• W2078421176 hasAuthorship W2078421176A5048188374 @default.
• W2078421176 hasAuthorship W2078421176A5066842624 @default.
• W2078421176 hasAuthorship W2078421176A5069197438 @default.
• W2078421176 hasAuthorship W2078421176A5086141060 @default.
• W2078421176 hasAuthorship W2078421176A5087226925 @default.
• W2078421176 hasBestOaLocation W20784211761 @default.
• W2078421176 hasConcept C147483822 @default.

• next