Occurrence of autoantibodies in chronic graft vs. host disease after allogeneic stem cell transplantation.
Occurrence of autoantibodies in chronic graft vs. host disease after allogeneic stem cell transplantation.
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同种异体干细胞移植后慢性移植物抗宿主病中自身抗体的出现。
DOI：
10.1111/j.1365-2257.2005.00699.x
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
M. Ganzckowski
中科院分区：
文献类型：
--
作者：
A. Wechalekar;T. Cranfield;D. Sinclair;M. Ganzckowski
慢性移植物抗宿主病（GVHD）仍然是同种异体干细胞移植（SCT）后发病和死亡的主要原因。慢性 GVHD (cGVHD) 与新发自身免疫性疾病有许多相似之处。虽然这些疾病中自身抗体的存在和关联已得到充分报道，但 SCT 后其作用和临床应用仍然是一个较少研究的领域。我们报告 SCT 受者体内存在自身抗体，并且可能与 cGVHD 存在相关。在例行随访期间，对 13 名 SCT 受者的外周血样本进行了以下检测：类风湿因子 (RF)、抗核抗体 (ANA)、双链 DNA (dsDNA)、抗线粒体抗体、抗平滑肌抗体 (Anti Sm)、抗肌内膜抗体、抗网织蛋白抗体、抗甲状腺过氧化物酶抗体和可提取核抗原筛查。 13 名患者中有 6 名 (46%) 具有一种或多种自身抗体。所有有抗体的患者都患有cGVHD，而没有cGVHD的患者没有任何自身抗体（P = 0.025）。三名 (23%) 患者仅具有一种自身抗体，其中三名 (23%) 患者具有超过一种自身抗体。 3 名患者 (23.3%) 呈 ANA 阳性，4 名患者 (30.7%) 呈双链 DNA，1 名患者 (7.6%) 呈 RF 阳性，2 名患者 (15.3%) 呈抗 Sm 肌肉阳性。在本研究中，自身抗体主要在存在 cGVHD 的患者中检测到。它们似乎在未操作的移植物中更常见，因此在 T 细胞耗尽的同种异体移植物患者中较少。在 13 名患者中，只有两名患者的抗体滴度与皮肤症状的发作之间似乎存在关联。总之，本系列文章提出了有关 SCT 后自身抗体的存在和作用及其与 cGVHD 的关联的有趣问题。
Chronic graft vs. host disease (GVHD) remains a major cause of morbidity and mortality after allogeneic stem cell transplantation (SCT). Chronic GVHD (cGVHD) has many similarities to de novo autoimmune disorders. While the presence and association of autoantibodies is well reported in these disorders, their role and clinical use remains a less studied area after SCT. We report the presence of autoantibodies in SCT recipients and a possible association with presence of cGVHD. During routine follow-up visits peripheral blood samples were tested for: rheumatoid factor (RF), antinuclear antibody (ANA), double stranded DNA (dsDNA), antimitochondrial antibody, antismooth muscle antibody (Anti Sm), antiendomysial, antireticulin antibodies, antithyroid peroxidase antibodies and an extractable nuclear antigen screen, in 13 SCT recipients. Six of 13 (46%) patients had one or more autoantibodies. All the patients with antibodies had cGVHD where as none of the patients without cGVHD had any autoantibodies (P = 0.025). Three (23%) patients had only one autoantibody and three (23%) of them had more than one autoantibody. ANA was positive in three (23.3%) patients, double stranded DNA in four (30.7%) patients, RF in one (7.6%) and Anti Sm muscle in two (15.3%) patients. In the present study, autoantibodies were detected predominantly in patients with presence of cGVHD. They also appeared to be more frequent in an unmanipulated graft and so less in patients with a T-cell depleted allograft. In two of 13 patients only there appeared to be an association between the antibody titre and flare up in skin symptoms. In conclusion, this small series raises interesting questions about the presence and role of autoantibodies after SCT and their association with cGVHD.