Malignant and normal T cells show random use of T-cell receptor alpha chain variable regions in patients with cutaneous T-cell lymphoma.

Malignant and normal T cells show random use of T-cell receptor alpha chain variable regions in patients with cutaneous T-cell lymphoma.
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皮肤 T 细胞淋巴瘤患者的恶性和正常 T 细胞显示 T 细胞受体 α 链可变区的随机使用。

DOI:
10.1111/1523-1747.ep12312571
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发表时间:
1995
期刊:
The Journal of investigative dermatology
影响因子:
--
通讯作者:
Tigelaar,R
Tigelaar,R
中科院分区:
--
文献类型:
--
作者:
Longley,J;Tyrrell,L;Lu,SZ;Farrell,J;Ding,TG;Yan,S;Sallee,D;Heald,P;Berger,C;Tigelaar,R

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皮肤T细胞淋巴瘤(CTCL)是成熟T淋巴细胞的恶性肿瘤,其中大多数表达α/β型T细胞受体(TCR)。 CTCL 的病因尚不清楚,但已提出假设超抗原或致白血病病毒对 TCR 进行慢性刺激。这两种机制都可能对恶性细胞使用的 TCR 可变 (V) 区类型产生偏差。为了确定 TCR α 在 CTCL 中的使用是否受到限制,我们使用逆转录和聚合酶链反应来确定从 CTCL 白血病患者外周血中纯化的恶性细胞对 Vα 和 Vβ 的使用。链 V 区片段的使用完全是随机的;从 6 名患者中每人分离出的恶性淋巴细胞使用了不同的 Vα 区域。正如之前报道的,13 链 V 区的使用也没有发现偏差。除了每位患者的恶性细胞中生产性(框内)TCR V 区 mgNA 外,我们还在 6 名患者中的 2 人中检测到这些细胞中的非生产性(框外)13 链转录物,并在 6 名患者中的 5 人中检测到非生产性 α 链转录物。这些患者的残余正常外周血淋巴细胞显示出随机、多克隆或寡克隆的 V 区使用模式。我们的结论是,CTCL 中 V 区的使用不存在偏差,因此超抗原或病毒与 TCR V 区之间的相互作用不太可能在 CTCL 的发病机制中发挥作用。
Cutaneous T-cell lymphoma (CTCL) is a malignancy of mature T lymphocytes, most of which express α/β type T-cell receptors (TCRs). The cause of CTCL is unknown, but hypotheses postulating chronic stimulation of TCRs by superantigen or by a leukemogenic virus have been proposed. Either mechanism might produce bias in the TCR variable (V) region types used by the malignant cells. To determine if TCR α use is restricted in CTCL, we used reverse transcription and the polymerase chain reaction to determine Vα and Vβ usage by malignant cells purified from the peripheral blood of leukemic patients with CTCL. Usage of a chain V region segments appeared totally random; malignant lymphocytes isolated from each of six patients used different Vα regions. As has been previously reported, no bias was found in 13 chain V region usage either. In addition to productive (in frame) TCR V region mgNAs in malignant cells from each patient, we detected non-productive (out of frame) 13 chain transcripts in these cells in two of six patients, and non-productive α chain transcripts in five of six. Residual normal peripheral blood lymphocytes from these patients showed a random, polyclonal or oligoclonal pattern of V region usage. We conclude that there is no bias in V region usage in CTCL, making it unlikely that interactions between superantigen or virus and the TCR V regions play a role in the pathogenesis of CTCL.