The impact of recipient cytokine genotype on acute rejection after renal transplantation.

被引:73
作者
Marshall, SE [1 ]
McLaren, AJ
Haldar, NA
Bunce, M
Morris, PJ
Welsh, KI
机构
[1] Churchill Hosp, Oxford Transplant Ctr, Oxford OX3 7LJ, England
[2] Oxford Radcliffe Hosp, Nuffield Dept Surg, Oxford, England
关键词
D O I
10.1097/00007890-200011270-00016
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background. Acute allograft rejection remains an important cause of morbidity after kidney transplantation, and has een shown to be a crucial determinant of long-term graft function. As cytokines are major regulators of the immune system, genetic variation in cytokine production or activity may influence susceptibility to acute rejection. This study sought to determine the impact of recipient cytokine and cytokine receptor polymorphism on acute rejection after renal transplantation. Methods. A total of 209 cadaveric renal transplant recipients were selected for analysis according to the presence or absence of graft rejection in the first 30 days after transplantation. DNA was genotyped for 22 polymorphisms in 11 cytokine receptor genes using the polymerase chain reaction with sequence specific primers. Results were stratified by incidence and severity of rejection, and by HLA-DR mismatching. Results. No association between any polymorphism and the incidence or severity of acute rejection was detected. In particular, no association was seen with tumor necrosis factor or interleukin-10 genotype, either alone or in combination. Conclusions. We have failed to demonstrate any association between recipient cytokine genotype and acute rejection after cadaveric renal transplantation. Although more extensive studies may disprove these findings, it would seem premature to use recipient cytokine genotyping to predict transplant outcome, or to guide immunosuppressive therapy after transplantation.
引用
收藏
页码:1485 / 1491
页数:7
相关论文
共 41 条
[11]   Polymerase chain reaction haplotyping using 3' mismatches in the forward and reverse primers: Application to the biallelic polymorphisms of tumor necrosis factor and lymphotoxin alpha [J].
Fanning, GC ;
Bunce, M ;
Black, CM ;
Welsh, KI .
TISSUE ANTIGENS, 1997, 50 (01) :23-31
[12]   The effect of novel polymorphisms in the interleukin-6 (IL-6) gene on IL-6 transcription and plasma IL-6 levels, and an association with systemic-onset juvenile chronic arthritis [J].
Fishman, D ;
Faulds, G ;
Jeffery, R ;
Mohamed-Ali, V ;
Yudkin, JS ;
Humphries, S ;
Woo, P .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 102 (07) :1369-1376
[13]   Independent regulation of cytokine genes in T cells - The paradox in the paradigm [J].
Fitzpatrick, DR ;
Kelso, A .
TRANSPLANTATION, 1998, 65 (01) :1-5
[14]   Tumor necrosis factor genetic polymorphsms correlate with infections after liver transplantation [J].
Freeman, RB ;
Tran, CL ;
Mattoli, J ;
Patel, K ;
Supran, S ;
Basile, FG ;
Krishnamurthy, S ;
Aihara, R .
TRANSPLANTATION, 1999, 67 (07) :1005-1010
[15]   Five novel intragenic dimorphisms in the human interleukin-1 genes combine to high informativity [J].
Guasch, JF ;
Bertina, RM ;
Reitsma, PH .
CYTOKINE, 1996, 8 (08) :598-602
[16]  
Hahn A. B., 1999, Human Immunology, V60, pS30
[17]   The association of atopy with a gain-of-function mutation in the alpha subunit of the interleukin-4 receptor [J].
Hershey, GKK ;
Friedrich, MF ;
Esswein, LA ;
Thomas, ML ;
Chatila, TA .
NEW ENGLAND JOURNAL OF MEDICINE, 1997, 337 (24) :1720-1725
[18]   The immunogenetics of human infectious diseases [J].
Hill, AVS .
ANNUAL REVIEW OF IMMUNOLOGY, 1998, 16 :593-617
[19]   Cytokine gene polymorphisms in autoimmune thyroid disease [J].
Hunt, PJ ;
Marshall, SE ;
Weetman, AP ;
Bell, JI ;
Wass, JAH ;
Welsh, KI .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2000, 85 (05) :1984-1988
[20]   Cytokine gene polymorphisms and relevance to forms of rejection [J].
Hutchinson, IV ;
Pravica, V ;
Perrey, C ;
Sinnott, P .
TRANSPLANTATION PROCEEDINGS, 1999, 31 (1-2) :734-736