Autoimmune markers in lymphoid malignancies
Autoimmune markers in lymphoid malignancies
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DOI：
10.1111/j.1365-3083.2008.02095.x
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发表时间：
2008-05-01
影响因子：
3.7
通讯作者：
Svensson, P.
中科院分区：
文献类型：
--
作者：
Sjoberg, K.;Roth, E. B.;Svensson, P.
幽门螺杆菌 (hp) 感染、干燥综合征或乳糜泻等慢性免疫刺激可能引发非霍奇金淋巴瘤 (NHL)。也有相反的情况（自身免疫的出现）的报道。本研究的目的是描述淋巴恶性肿瘤患者中这些免疫标记物的模式。采用 ELISA 分析 96 名 NHL 患者（中位年龄 72，范围 38-88，F/M 41/55）的血清，以确定抗豚鼠 (gp) 和人重组 (hr) 转谷氨酰胺酶 2 型 (Tg2)、hr 因子 XIII 亚基 a*（Tg 家族的一部分）、可提取核抗原 (ENA) 和 hp 的抗体频率。由于 HP 抗体在较年轻的年龄组中下降，因此使用了由 768 人组成的性别和年龄匹配的对照组。使用商业试剂盒对转谷氨酰胺酶抗体的对照人群由 59 名献血者（中位年龄 42 岁，范围 19-65）组成。 Gp-Tg2-IgG 阳性率为 72%，hr-Tg2-IgG 阳性率为 15%（两者均为 5% 阳性对照；分别为 P < 0.001 和 ns）。对于 IgA，3% 具有 gp-Tg2 和 4% hr-Tg2（对照中 5%：两者均为 ns）。 22% 的人呈抗 FXIII-IgA 阳性（对照组为 5%；P = 0.03）。 24% 的人呈非特异性抗 ENA-IgG 阳性 (P < 0.001)，而只有 2% 的人具有特异性 ENA 自身抗体。此外，36% 的人抗 hp-IgG 呈阳性，而对照组的 54% 呈阳性（P < 0.001）。非特异性自身抗体的频率增加。特定自身抗体 (hr-Tg2-IgA) 没有发现差异。相比之下，抗 HP 阳性的人数少于预期。与自身免疫性疾病相似，免疫反应缺陷可能导致淋巴恶性肿瘤的发病机制。
Chronic immune stimulation such as Helicobacter pylori (hp) infection, Sjogren's syndrome or coeliac disease may initiate non-Hodgkin lymphoma (NHL). The opposite (appearance of autoimmunity) has also been reported. The aim of this study was to describe the pattern of these immune markers in patients with lymphoid malignancies. Sera from 96 patients with NHL (median age 72, range 38-88, F/M 41/55) were analysed with ELISA to determine the frequency of antibodies against guinea pig (gp) and human recombinant (hr) transglutaminase type 2 (Tg2), and hr factor XIII subunit a* (part of the Tg-family), extractable nuclear antigen (ENA), and hp. As hp antibodies decrease in younger age cohorts a sex- and age-matched control group of 768 persons was used. The control population for transglutaminase antibodies consisted of 59 blood donors, (median 42 years, range 19-65) was analysed with a commercial kit. Gp-Tg2-IgG positivity was documented in 72% and hr-Tg2-IgG positivity in 15% (5% positive controls for both; P < 0.001 and ns, respectively). For IgA 3% had gp-Tg2 and 4% hr-Tg2 (5% in controls: ns for both). Anti-FXIII-IgA positivity was found in 22% (5% in controls; P = 0.03). Unspecific anti-ENA-IgG positivity was found in 24% (P < 0.001), while only 2% had specific ENA autoantibodies. Moreover, 36% were positive for anti-hp-IgG, while controls were positive in 54% (P < 0.001). The frequency of unspecific autoantibodies was increased. No differences could be noted in specific autoantibodies (hr-Tg2-IgA). In contrast, fewer than expected were anti-hp-positive. A defective immune response, similar to that in autoimmune diseases, could contribute to the pathogenesis of lymphoid malignancies.