Fathman C G, Goronzy J, Weyand C
Ann N Y Acad Sci. 1986;475:24-31. doi: 10.1111/j.1749-6632.1986.tb20853.x.
In speculating about mechanisms that might give rise to T-cell epitopes appearing within different HLA-DR frameworks, we return to the hypothesis expressed above that suggests that gene-conversion-like events might be involved in shuffling the hypervariable segments of HLA-D region exons into alternative HLA-D region frameworks where they will still be recognized by the T cell (but not typed by conventional serology or mixed lymphocyte typing) as the "disease associated" HLA product. This might well explain the lack of stringent association between rheumatoid arthritis and HLA-DR4. It is possible, through the use of such alloreactive T-cell clones, that we might eventually define subgroups based upon presumed genetic susceptibility markers, which might allow therapeutic or prognostic assignment of patients with seropositive rheumatoid arthritis.
在推测可能导致T细胞表位出现在不同HLA - DR框架内的机制时,我们回到上述假说,该假说认为类似基因转换的事件可能参与将HLA - D区外显子的高变段改组到其他HLA - D区框架中,在那里它们仍会被T细胞识别(但不能通过传统血清学或混合淋巴细胞分型鉴定)为“疾病相关”的HLA产物。这很可能解释了类风湿性关节炎与HLA - DR4之间缺乏严格关联的原因。通过使用此类同种异体反应性T细胞克隆,我们最终有可能基于假定的遗传易感性标志物定义亚组,这可能有助于对血清阳性类风湿性关节炎患者进行治疗或预后评估。