Gelmez Metin Y, Teker Aysegul B A, Aday Aynur D, Yavuz Akif S, Soysal Teoman, Deniz Gunnur, Aktan Melih
Department of Immunology, Institute of Experimental Medicine (DETAE), Istanbul University , Istanbul , Turkey.
Leuk Lymphoma. 2014 Feb;55(2):326-30. doi: 10.3109/10428194.2013.803225. Epub 2013 Jul 15.
Activation induced cytidine deaminase (AID) enzyme, which converts cytosine into uracil and is expressed only by activated B lymphocytes, plays a role in B cells in both the mechanisms of somatic hypermutation (SHM) and class switch recombination (CSR). There are studies showing that AID can cause numerous translocations in different lymphoproliferative diseases. Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of monoclonal B cells in bone marrow and peripheral blood. The predictability and clinical status of B-CLL are difficult to determine. About 30-50% of patients have chromosomal abnormalities. AID, which is thought to create fraction segments for translocations, might also cause deletions in DNA regions of 17p13, 11q22.3, 13q14 and 13q34 that are associated with prognostic implications in patients with CLL. In this study, the AID gene expression in patients with CLL with and without deletions was investigated. When compared to healthy subjects and patients without deletions, increased levels of AID expression in patients with deletions of 17p13, 11q22.3 or 13q14 were found, but not for the 13q34 region. Our results show that AID expression may be associated with deletions in patients with CLL.
激活诱导胞苷脱氨酶（AID）可将胞嘧啶转化为尿嘧啶，且仅由活化的B淋巴细胞表达，它在B细胞的体细胞高频突变（SHM）和类别转换重组（CSR）机制中均发挥作用。有研究表明，AID可在不同的淋巴增殖性疾病中引发大量易位。慢性淋巴细胞白血病（CLL）的特征是骨髓和外周血中出现单克隆B细胞积聚。B-CLL的可预测性和临床状况难以确定。约30%-50%的患者存在染色体异常。AID被认为会产生易位的片段，它也可能导致17p13、11q22.3、13q14和13q34等DNA区域的缺失，这些区域与CLL患者的预后相关。在本研究中，对有或无缺失的CLL患者的AID基因表达进行了研究。与健康受试者和无缺失的患者相比，发现17p13、11q22.3或13q14缺失的患者中AID表达水平升高，但13q34区域未出现这种情况。我们的结果表明，AID表达可能与CLL患者的缺失有关。
