Serum level of soluble interleukin-2 receptor correlates with CD25 expression in patients with T lymphoblastic lymphoma.
Serum level of soluble interleukin-2 receptor correlates with CD25 expression in patients with T lymphoblastic lymphoma.
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T 淋巴细胞淋巴瘤患者中可溶性白细胞介素 2 受体的血清水平与 CD25 表达相关。
DOI：
10.1136/jclinpath-2015-202934
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Yoshino T.
中科院分区：
文献类型：
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作者：
Toji T;Takata K;Sato Y;Miyata-Takata T;Hayashi E;Habara T;Maeda Y;Tanimoto M;Yoshino T.
急性淋巴母细胞白血病/淋巴瘤（ALL/LBL）是一种侵袭性形式的非霍奇金淋巴瘤（NHL），分别影响B细胞或T细胞。血清可溶性白细胞介素-2受体（sIL-2 R）水平反映了侵袭性NHL的免疫活性和肿瘤体积;然而，在LBL中sIL-2 R的释放尚未得到广泛研究。此外，sIL-2 R释放与IL-2 R α亚基（CD 25）表达水平之间的关系尚不清楚。本文检测了23例T淋巴母细胞性淋巴瘤（T-LBL）患者血清sIL-2 R水平，并与20例T急性淋巴细胞白血病（T-ALL）、40例弥漫性大B细胞淋巴瘤（DLBCL）和40例外周T细胞淋巴瘤（PTCL）进行了比较。T-LBL患者血清sIL-2 R水平明显低于T-ALL、DLBCL和PTCL患者（P<0.001）。免疫组化结果显示，T-LBL患者CD 25表达与血清sIL-2 R水平相关（p=0.0069），而DLBCL（p=0.348）和PTCL（p=0.266）患者血清sIL-2 R水平与CD 25表达无相关性。此外，双重免疫组织化学分析显示，CD 25阳性细胞也被发现是Foxp 3阳性非肿瘤性T细胞。总之，T-LBL中的CD 25阳性非肿瘤性T细胞被认为是sIL-2 R的主要来源，与其他侵袭性和高度侵袭性淋巴瘤相比，存在的细胞数量少导致释放到血清中的sIL-2 R水平较低。
Acute lymphoblastic leukaemia/lymphoma (ALL/LBL) is an aggressive form of non-Hodgkin's lymphoma (NHL) affecting B-cells or T-cells, respectively. The serum level of soluble interleukin-2 receptor (sIL-2R) is known to reflect the immune activity and tumour volume in aggressive NHL; however, the release of sIL-2R in LBL has not been extensively studied. Further, the relationship between sIL-2R release and the expression level of IL-2R α subunit (CD25) remains unknown. In the present study, we examined the serum level of sIL-2R in 23 patients with T lymphoblactic lymphoma (T-LBL) and compared these with the levels in 20 patient with T acute lymphoblastic leukaemia (T-ALL), 40 patients with diffuse large B-cell lymphoma (DLBCL) and 40 patients with peripheral T-cell lymphoma (PTCL), not otherwise specified. The release of sIL-2R into the serum in patients with T-LBL was significantly lower than that for T-ALL, DLBCL and PTCL (p<0.001). Immunohistochemistry revealed that CD25 expression was correlated with the serum level of sIL-2R in T-LBL (p=0.0069), whereas no correlation was found to exist between serum sIL-2R levels and CD25 expression in patients with DLBCL (p=0.348) and PTCL (p=0.266). Furthermore, double immunohistochemical analysis revealed that CD25-positive cells were also found to be Foxp3-positive non-neoplastic T-cells. In conclusion, CD25-positive non-neoplastic T-cells in T-LBL are presumed to be the primary source of sIL-2R, and the low number of cells present results in a lower level of sIL-2R released into the serum compared with the other aggressive and highly aggressive lymphomas.