Increased severity of acute graft versus host disease as a result of differential expression following a homozygous gene deletion. (22nd June 2012)
- Record Type:
- Journal Article
- Title:
- Increased severity of acute graft versus host disease as a result of differential expression following a homozygous gene deletion. (22nd June 2012)
- Main Title:
- Increased severity of acute graft versus host disease as a result of differential expression following a homozygous gene deletion
- Authors:
- Jervis, S.
Collins, P.
Tate, D.
Foster, L.
Bowman, V.
Adhern, C.
Bloor, A.
Yin, J.
Wynn, R.
Poulton, K. - Abstract:
- <abstract abstract-type="main" id="iji1138-abs-0001"> <title>Summary</title> <p>Acute graft versus host disease (aGvHD) is a major cause of early morbidity post‐haematopoietic stem cell transplantation with minor histocompatibility antigens being a contributing factor. One mHA encoded by the UDP glycosyltransferase 2 family polypeptide B17 (UGT2B17) gene has been shown to be immunogenic because of differential expression in the donor and recipient. We investigated the effects of a homozygous gene deletion of UGT2B17 on the severity of acute aGvHD post‐HSCT in HLA‐matched related donors. 115 donor and recipient HLA and UGT2B17 genotypes were determined using PCR‐SSO and PCR‐SSP, respectively. aGvHD grading was determined using routine criteria and dichotomized into either nonclinically significant (0–I) or clinically significant (II–IV). For all analyses, <italic>P</italic>‐values of ≤ 0.05 were considered significant. The frequency of the gene deletion within the total cohort tested was 29.1%. A significant increase in aGvHD severity (grades II‐IV) was seen in UGT2B17 recipients expressing the protein when transplanted with a UGT2B17 disparate donor (<italic>P</italic> = 0.011). We observed a significant association between UGT2B17 expressing recipients and UGT2B17 deficient donors with the severity of aGvHD. This study provides additional evidence that genomic variations may predispose to more severe aGvHD, but are not a mechanism for GvHD.</p> </abstract>
- Is Part Of:
- International journal of immunogenetics. Volume 40:Number 2(2013:Apr.)
- Journal:
- International journal of immunogenetics
- Issue:
- Volume 40:Number 2(2013:Apr.)
- Issue Display:
- Volume 40, Issue 2 (2013)
- Year:
- 2013
- Volume:
- 40
- Issue:
- 2
- Issue Sort Value:
- 2013-0040-0002-0000
- Page Start:
- 116
- Page End:
- 119
- Publication Date:
- 2012-06-22
- Subjects:
- Immunogenetics -- Periodicals
571.9648 - Journal URLs:
- http://eu.wiley.com/WileyCDA/WileyTitle/productCd-IJI.html ↗
http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1744-313X ↗
http://www.blackwell-synergy.com/servlet/useragent?func=showIssues&code=eji ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/j.1744-313X.2012.01138.x ↗
- Languages:
- English
- ISSNs:
- 1744-3121
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4542.300300
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 4147.xml