Variable expression of CD3‐zeta and associated protein tyrosine kinases in lymphocytes from patients with myeloid malignancies
Variable expression of CD3‐zeta and associated protein tyrosine kinases in lymphocytes from patients with myeloid malignancies
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骨髓恶性肿瘤患者淋巴细胞中 CD3-zeta 和相关蛋白酪氨酸激酶的可变表达
作者：
Buggins;Hirst;Pagliuca;Mufti
在骨髓恶性肿瘤中，T细胞和NK功能已被证明会随着从白血病前期向晚期疾病的转变而恶化。实体瘤中的免疫功能障碍归因于异常信号转导，可能通过TCR/CD 3复合物（例如CD 3-κ B）、NK细胞上的受体及其相关蛋白酪氨酸激酶（PTK; p56 lck、p59 fyn和ZAP-70）的细胞内组分的表达改变。使用流式细胞术方法检测TCR/CD 3复合物的表面蛋白和细胞内组分的双重表达，我们研究了46例骨髓恶性肿瘤患者。64%的患者CD 3-β表达异常，在晚期疾病患者中更为突出。在治疗前和治疗后分析了3例CD 3-κ B降低的患者，CD 3-κ B表达的恢复与成功诱导缓解相关（PTK的表达是可变的，在所有疾病阶段均观察到水平降低）。这项研究的结果表明，信号蛋白的损失是不是直接接触的白血病细胞与淋巴细胞本身或白血病负担的程度的结果，但一些骨髓恶性肿瘤的特定属性，这是更频繁地获得更大的恶性转化。
In myeloid malignancies, T‐cell and NK function has been shown to deteriorate with transformation from pre‐leukaemia to advanced disease. Immune dysfunction in solid tumours has been attributed to abnormal signal transduction, possibly through altered expression of intracellular components of the TCR/CD3 complex (e.g. CD3‐ζ), receptors on NK cells and their associated protein tyrosine kinases (PTKs; p56lck, p59fyn and ZAP‐70). Using a flow cytometric method to detect dual‐expression of surface proteins and intracellular components of the TCR/CD3 complex, we have studied 46 patients with myeloid malignancies. CD3‐ζ expression was abnormal in 64% of patients, and was more prominent in those with advanced disease. Three patients with reduced CD3‐ζ were analysed both pre‐ and post‐treatment, and recovery of CD3‐ζ expression was associated with successful remission induction (expression of PTKs was variable and reduced levels were seen all disease stages). The results of this study suggest that loss of signalling proteins is not a result of direct contact of leukaemic cells with lymphocytes per se or the extent of the leukaemia burden, but to a specific property of some myeloid malignancies, which is more frequently acquired with greater malignant transformation.
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影响因子：
56.9
作者：
MIZOGUCHI, H;O'SHEA, JJ;OCHOA, AC
通讯作者：
OCHOA, AC
影响因子：
11.2
作者：
J. Finke;A. Zea;J. Stanley;D. Longo;H. Mizoguchi;R. Tubbs;R. Wiltrout;J. O’Shea;S. Kudoh
通讯作者：
J. Finke;A. Zea;J. Stanley;D. Longo;H. Mizoguchi;R. Tubbs;R. Wiltrout;J. O’Shea;S. Kudoh
尽管存在 T 细胞受体/CD3 相关激酶，但浸润非霍奇金 B 细胞淋巴瘤的 T 细胞显示出酪氨酸磷酸化模式的改变。
DOI：
--
发表时间：
1995
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Wang,Q;Stanley,J;Kudoh,S;Myles,J;Kolenko,V;Yi,T;Tubbs,R;Bukowski,R;Finke,J
通讯作者：
Finke,J
A-LAK 细胞毒性和增殖的减弱伴随着慢性粒细胞白血病的疾病进展。
影响因子：
20.3
作者：
Verfaillie,C;Kay,N;Miller,W;McGlave,P
通讯作者：
McGlave,P
通过逐渐生长的肿瘤来改变小鼠的宿主抗肿瘤防御机制。
影响因子：
11.2
作者：
Maccubbin,DL;Mace,KF;Ehrke,MJ;Mihich,E
通讯作者：
Mihich,E