RGD Reference Report - Disruption of IL-21 signaling affects T cell-B cell interactions and abrogates protective humoral immunity to malaria. - Rat Genome Database

Send us a Message
Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   
Search RGD Grant Resources Citing RGD About Us Contact Us
Genes Variants Community Projects QTLs Strains Markers Genome Information Ontologies Cell Lines References Download Submit Data
OntoMate (Literature Search) JBrowse (Genome Browser) Synteny Browser (VCMap) Variant Visualizer Multi-Ontology Enrichment (MOET) Gene-Ortholog Location Finder (GOLF) InterViewer (Protein-Protein Interactions) PhenoMiner (Quatitative Phenotypes) Gene Annotator OLGA (Gene List Generator) AllianceMine GViewer (Genome Viewer)
Aging & Age-Related Disease Cancer & Neoplastic Disease Cardiovascular Disease Coronavirus Disease Developmental Disease Diabetes Hematologic Disease Immune & Inflammatory Disease Infectious Disease Liver Disease Neurological Disease Obesity & Metabolic Syndrome Renal Disease Respiratory Disease Sensory Organ Disease
Find Models   new Genetic Models Autism Models Rat PhenoMiner (Quantitative Phenotypes) Chinchilla PhenoMiner Expected Ranges (Quantitative Phenotype) PhenoMiner Term Comparison Hybrid Rat Diversity Panel Phenotypes Phenotypes in Other Animal Models Animal Husbandry Strain Medical Records Phylogenetics Strain Availability Calendar Rats 101 Submissions Photo Archive
Pathways
Rat Community Forum Directory of Rat Laboratories Video Tutorials News RGD Publications RGD Presentations Archive Nomenclature Guidelines Resource Links Laboratory Resources Employment Resources

Disruption of IL-21 signaling affects T cell-B cell interactions and abrogates protective humoral immunity to malaria.

Authors: Pérez-Mazliah, Damián  Ng, Dorothy Hui Lin  Freitas do Rosário, Ana Paula  McLaughlin, Sarah  Mastelic-Gavillet, Béatris  Sodenkamp, Jan  Kushinga, Garikai  Langhorne, Jean 
Citation: Pérez-Mazliah D, etal., PLoS Pathog. 2015 Mar 12;11(3):e1004715. doi: 10.1371/journal.ppat.1004715. eCollection 2015 Mar.
RGD ID: 127285358
Pubmed: PMID:25763578   (View Abstract at PubMed)
PMCID: PMC4370355   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.ppat.1004715   (Journal Full-text)

Interleukin-21 signaling is important for germinal center B-cell responses, isotype switching and generation of memory B cells. However, a role for IL-21 in antibody-mediated protection against pathogens has not been demonstrated. Here we show that IL-21 is produced by T follicular helper cells and co-expressed with IFN-γ during an erythrocytic-stage malaria infection of Plasmodium chabaudi in mice. Mice deficient either in IL-21 or the IL-21 receptor fail to resolve the chronic phase of P. chabaudi infection and P. yoelii infection resulting in sustained high parasitemias, and are not immune to re-infection. This is associated with abrogated P. chabaudi-specific IgG responses, including memory B cells. Mixed bone marrow chimeric mice, with T cells carrying a targeted disruption of the Il21 gene, or B cells with a targeted disruption of the Il21r gene, demonstrate that IL-21 from T cells signaling through the IL-21 receptor on B cells is necessary to control chronic P. chabaudi infection. Our data uncover a mechanism by which CD4+ T cells and B cells control parasitemia during chronic erythrocytic-stage malaria through a single gene, Il21, and demonstrate the importance of this cytokine in the control of pathogens by humoral immune responses. These data are highly pertinent for designing malaria vaccines requiring long-lasting protective B-cell responses.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
malaria exacerbatesISOIl21 (Mus musculus)127285358; 127285358 RGD 
malaria exacerbatesIMP 127285358 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Il21  (interleukin 21)

Genes (Mus musculus)
Il21  (interleukin 21)

Genes (Homo sapiens)
IL21  (interleukin 21)


Additional Information