Silman A J, Hay E M, Worthington J, Thomson W, Pepper L, Davidson J, Dyer P A, Ollier W E
ARC Epidemiology Research Unit, University of Manchester, United Kingdom.
Ann Rheum Dis. 1995 Apr;54(4):311-3. doi: 10.1136/ard.54.4.311.
To reproduce findings from previous reports that non-inherited maternal HLA class II antigens might contribute to rheumatoid arthritis (RA) susceptibility in the offspring.
Families were recruited from the Arthritis and Rheumatism Council's National Repository of RA families and HLA-DRB1 alleles were examined in these individuals and their first degree relatives using DNA typing methods.
There was no evidence of an increase in either non-inherited maternal HLA-DR4 or the HLA-DRB1 shared epitope as a whole compared with the frequency expected using the non-inherited paternal antigens as controls.
The numbers of probands who were shared epitope negative were small, but we are unable to confirm in these families the findings that non-inherited maternal HLA contributes an additional susceptibility factor to rheumatoid arthritis.
重现先前报告中的研究结果,即非遗传性母体人类白细胞抗原(HLA)II类抗原可能会增加后代患类风湿性关节炎(RA)的易感性。
从关节炎与风湿病理事会的全国类风湿性关节炎家系库中招募家系,并使用DNA分型方法对这些个体及其一级亲属的HLA - DRB1等位基因进行检测。
与以非遗传性父系抗原作为对照所预期的频率相比,没有证据表明非遗传性母体HLA - DR4或整个HLA - DRB1共享表位增加。
共享表位阴性的先证者数量较少,但我们无法在这些家系中证实非遗传性母体HLA为类风湿性关节炎贡献额外易感性因素这一研究结果。