Genetic susceptibility to childhood common acute lymphoblastic leukaemia is associated with polymorphic peptide-binding pocket profiles in HLA-DPB1*0201.
Genetic susceptibility to childhood common acute lymphoblastic leukaemia is associated with polymorphic peptide-binding pocket profiles in HLA-DPB1*0201.
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对儿童常见急性淋巴细胞白血病的遗传易感性与 HLA-DPB1*0201 中的多态性肽结合袋谱相关。
DOI:
10.1093/hmg/11.14.1585
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发表时间:
2002
影响因子:
3.5
通讯作者:
U. Investigators
中科院分区:
文献类型:
--
作者:
G. M. Taylor;S. Dearden;P. Ravetto;M. Ayres;P. Watson;A. Hussain;M. Greaves;F. Alexander;O. Eden;U. Investigators
In a previous study, we obtained preliminary evidence in a small series of patients (n = 63) suggesting that susceptibility to childhood common acute lymphoblastic leukaemia (c-ALL) was associated with an allele at the HLA-DPB1 locus, DPB1*0201. We have now tested this hypothesis by comparing the frequency of children with leukaemia (n = 982) who typed for specific DPB1 alleles and two groups of non-leukaemic children, one consisting of children with solid tumours, excluding lymphomas (n = 409), the other consisting of normal infants (n = 864). We found that significantly more children with c-ALL and T-ALL, but not pro-B ALL or acute non-ALL typed for DPB1*0201 as compared with children with solid tumours [odds ratio (OR), 95% confidence interval (CI) for c-ALL: 1.76, 1.20-2.56; T-ALL: 1.93, 1.01-3.80] and normal infants (OR, 95% CI for c-ALL: 1.83, 1.34-2.48; T-ALL: 2.00, 1.10-3.82). In childhood c-ALL, significantly more children than those with solid tumours or normal infants typed for DPB1 alleles coding specific polymorphic amino acids lining the antigen-binding site of the DPbeta1*0201 allotypic protein, suggesting that susceptibility to childhood c-ALL may be influenced by DPbeta ABS amino acid polymorphisms shared by DPbeta1*0201 and other DPbeta1 allotypes. These results point to a mechanism of c-ALL susceptibility that involves the presentation of specific antigenic peptides, possibly derived from infectious agents, by DPbeta1*0201-related allotypic proteins, leading to the activation of helper T cells mediating proliferative stress on preleukaemic cells.
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影响因子:
11.4
作者:
Buckley,JD;Buckley,CM;Ruccione,K;Sather,HN;Waskerwitz,MJ;Woods,WG;Robison,LL
通讯作者:
Robison,LL
DOI:
10.1093/jnci/92.14.1151
发表时间:
2000-07-19
期刊:
JOURNAL OF THE NATIONAL CANCER INSTITUTE
影响因子:
--
作者:
Wacholder, S;Rothman, N;Caporaso, N
通讯作者:
Caporaso, N
DOI:
--
发表时间:
1997
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Chicz,RM;Graziano,DF;Trucco,M;Strominger,JL;Gorga,JC
通讯作者:
Gorga,JC
DOI:
10.1016/s1201-9712(98)90116-3
发表时间:
1998
期刊:
International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases
影响因子:
--
作者:
Hayney,MS;Poland,GA;Jacobson,RM;Rabe,D;Schaid,DJ;Jacobsen,SJ;Lipsky,JJ
通讯作者:
Lipsky,JJ
影响因子:
4.4
作者:
A. Begovich;G. McClure;V. Suraj;R. Helmuth;N. Fildes;T. Bugawan;H. Erlich;W. Klitz
通讯作者:
A. Begovich;G. McClure;V. Suraj;R. Helmuth;N. Fildes;T. Bugawan;H. Erlich;W. Klitz