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dc.contributor.authorMuriuki, Beatrice M.
dc.contributor.authorForconi, Catherine S
dc.contributor.authorOluoch, Peter O.
dc.contributor.authorBailey, Jeffrey A.
dc.contributor.authorGhansah, Anita
dc.contributor.authorMoormann, Ann M.
dc.contributor.authorOng'echa, John M.
dc.date2022-08-11T08:10:00.000
dc.date.accessioned2022-08-23T16:51:58Z
dc.date.available2022-08-23T16:51:58Z
dc.date.issued2021-05-31
dc.date.submitted2021-10-04
dc.identifier.citation<p>Muriuki BM, Forconi CS, Oluoch PO, Bailey JA, Ghansah A, Moormann AM, Ong'echa JM. Association of killer cell immunoglobulin-like receptors with endemic Burkitt lymphoma in Kenyan children. Sci Rep. 2021 May 31;11(1):11343. doi: 10.1038/s41598-021-90596-7. PMID: 34059753; PMCID: PMC8166913. <a href="https://doi.org/10.1038/s41598-021-90596-7">Link to article on publisher's site</a></p>
dc.identifier.issn2045-2322 (Linking)
dc.identifier.doi10.1038/s41598-021-90596-7
dc.identifier.pmid34059753
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41960
dc.description.abstractEndemic Burkitt lymphoma (eBL) is an aggressive pediatric B cell lymphoma, common in Equatorial Africa. Co-infections with Epstein-Barr virus (EBV) and Plasmodium falciparum, coupled with c-myc translocation are involved in eBL etiology. Infection-induced immune evasion mechanisms to avoid T cell cytotoxicity may increase the role of Natural killer (NK) cells in anti-tumor immunosurveillance. Killer immunoglobulin-like receptor (KIR) genes on NK cells exhibit genotypic and allelic variations and are associated with susceptibility to diseases and malignancies. However, their role in eBL pathogenesis remains undefined. This retrospective study genotyped sixteen KIR genes and compared their frequencies in eBL patients (n = 104) and healthy geographically-matched children (n = 104) using sequence-specific primers polymerase chain reaction (SSP-PCR) technique. The relationship between KIR polymorphisms with EBV loads and eBL pathogenesis was investigated. Possession of > /= 4 activating KIRs predisposed individuals to eBL (OR = 3.340; 95% CI 1.530-7.825; p = 0.004). High EBV levels were observed in Bx haplogroup (p = 0.016) and AB genotypes (p = 0.042) relative to AA haplogroup and AA genotype respectively, in eBL patients but not in healthy controls. Our results suggest that KIR-mediated NK cell stimulation could mute EBV control, contributing to eBL pathogenesis.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=34059753&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectCancer
dc.subjectImmunology
dc.subjectMolecular biology
dc.subjectHemic and Lymphatic Diseases
dc.subjectImmune System Diseases
dc.subjectImmunology of Infectious Disease
dc.subjectImmunopathology
dc.subjectInternational Public Health
dc.subjectNeoplasms
dc.subjectPediatrics
dc.subjectVirus Diseases
dc.titleAssociation of killer cell immunoglobulin-like receptors with endemic Burkitt lymphoma in Kenyan children
dc.typeJournal Article
dc.source.journaltitleScientific reports
dc.source.volume11
dc.source.issue1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5797&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/4764
dc.identifier.contextkey25262259
refterms.dateFOA2022-08-23T16:51:58Z
html.description.abstract<p>Endemic Burkitt lymphoma (eBL) is an aggressive pediatric B cell lymphoma, common in Equatorial Africa. Co-infections with Epstein-Barr virus (EBV) and Plasmodium falciparum, coupled with c-myc translocation are involved in eBL etiology. Infection-induced immune evasion mechanisms to avoid T cell cytotoxicity may increase the role of Natural killer (NK) cells in anti-tumor immunosurveillance. Killer immunoglobulin-like receptor (KIR) genes on NK cells exhibit genotypic and allelic variations and are associated with susceptibility to diseases and malignancies. However, their role in eBL pathogenesis remains undefined. This retrospective study genotyped sixteen KIR genes and compared their frequencies in eBL patients (n = 104) and healthy geographically-matched children (n = 104) using sequence-specific primers polymerase chain reaction (SSP-PCR) technique. The relationship between KIR polymorphisms with EBV loads and eBL pathogenesis was investigated. Possession of > /= 4 activating KIRs predisposed individuals to eBL (OR = 3.340; 95% CI 1.530-7.825; p = 0.004). High EBV levels were observed in Bx haplogroup (p = 0.016) and AB genotypes (p = 0.042) relative to AA haplogroup and AA genotype respectively, in eBL patients but not in healthy controls. Our results suggest that KIR-mediated NK cell stimulation could mute EBV control, contributing to eBL pathogenesis.</p>
dc.identifier.submissionpathoapubs/4764
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.contributor.departmentDivision of Infectious Diseases and Immunology, Department of Medicine
dc.source.pages11343


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Copyright © The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
Except where otherwise noted, this item's license is described as Copyright © The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.