ArticleThe Journal of infectious diseases2011
Genetic and functional evidence implicating DLL1 as the gene that influences susceptibility to visceral leishmaniasis at chromosome 6q27.
Article in The Journal of infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Human genetics of leishmania infections.Human genetics · 2020Review
- Notch signalling in T cell homeostasis and differentiation.Open biology · 2019Review
- CD45RO+ T Cells and T Cell Activation in the Long-Lasting Immunity afterThe American journal of tropical medicine and hygiene · 2018Article
- A Mother's Gift: Congenital Transmission of Trypanosoma and Leishmania Species.PLoS pathogens · 2016Review
- A Novel Molecular Test to Diagnose Canine Visceral Leishmaniasis at the Point of Care.The American journal of tropical medicine and hygiene · 2015Article
- Common variants in the HLA-DRB1-HLA-DQA1 HLA class II region are associated with susceptibility to visceral leishmaniasis.Nature genetics · 2013Article
- Mapping the genes for susceptibility and response to Leishmania tropica in mouse.PLoS neglected tropical diseases · 2013Article
- Genetic and functional evaluation of the role of DLL1 in susceptibility to visceral leishmaniasis in India.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2012Article
- Redundant Notch1 and Notch2 signaling is necessary for IFNγ secretion by T helper 1 cells during infection with Leishmania major.PLoS pathogens · 2012Article
- Vaccine Development Against Leishmania donovani.Frontiers in immunology · 2012Article
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Authors and funding
18 authors at 9 institutions in 5 countries.
Funding
Abstract
backgroundVisceral leishmaniasis (VL) is caused by Leishmania donovani and Leishmania infantum chagasi. Genome-wide linkage studies from Sudan and Brazil identified a putative susceptibility locus on chromosome 6q27.
methodsTwenty-two single-nucleotide polymorphisms (SNPs) at genes PHF10, C6orf70, DLL1, FAM120B, PSMB1, and TBP were genotyped in 193 VL cases from 85 Sudanese families, and 8 SNPs at genes PHF10, C6orf70, DLL1, PSMB1, and TBP were genotyped in 194 VL cases from 80 Brazilian families. Family-based association, haplotype, and linkage disequilibrium analyses were performed. Multispecies comparative sequence analysis was used to identify conserved noncoding sequences carrying putative regulatory elements. Quantitative reverse-transcription polymerase chain reaction measured expression of candidate genes in splenic aspirates from Indian patients with VL compared with that in the control spleen sample.
resultsPositive associations were observed at PHF10, C6orf70, DLL1, PSMB1, and TBP in Sudan, but only at DLL1 in Brazil (combined P = 3 × 10(-4) at DLL1 across Sudan and Brazil). No functional coding region variants were observed in resequencing of 22 Sudanese VL cases. DLL1 expression was significantly (P = 2 × 10(-7)) reduced (mean fold change, 3.5 [SEM, 0.7]) in splenic aspirates from patients with VL, whereas other 6q27 genes showed higher levels (1.27 × 10(-6) < P < .01) than did the control spleen sample. A cluster of conserved noncoding sequences with putative regulatory variants was identified in the distal promoter of DLL1.
conclusionsDLL1, which encodes Delta-like 1, the ligand for Notch3, is strongly implicated as the chromosome 6q27 VL susceptibility gene.
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