首页> 外文OA文献 >Soluble Interleukin-2 Receptors Inhibit Interleukin 2-Dependent Proliferation and Cytotoxicity: Explanation for Diminished Natural Killer Cell Activity in Cutaneous T-Cell Lymphomas In Vivo?
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Soluble Interleukin-2 Receptors Inhibit Interleukin 2-Dependent Proliferation and Cytotoxicity: Explanation for Diminished Natural Killer Cell Activity in Cutaneous T-Cell Lymphomas In Vivo?

机译:可溶性白细胞介素2受体抑制白细胞介素2依赖性增殖和细胞毒性:体内皮肤T细胞淋巴瘤中自然杀伤细胞活性降低的解释?

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摘要

In patients with cutaneous T-cell lymphomas (CTCL), soluble interleukin-2 receptor serum levels (sIL-2R) were determined by ELISA technique, and natural killer cell (NK) activity, by a 4-h chromium-51 release assay. Decrease of NK activity correlated with the augmentation of serum sIL-2R. After a 4-d stimulation with interleukin 2 CTCL patients' peripheral mononuclear cells (PMC) showed an increase of cytotoxic activity similar to that in healthy donors' PMC. Normal donors' PMC demonstrated a diminished IL-2-induced cytotoxic activity in 25% CTCL serum (sIL-2R of 3000, 7330, and 10700 U/mI, respectively) compared to control serum (sIL-2R of 400, 340, and 420 U/ml, respectively). IL-2-dependent proliferation of 2-d phytohemagglutinin (PHA) blasts was lower in CTCL serum than in control serum. sIL-2R was enriched from one CTCL patient's serum by IL-2 affinity chromatography. Transfection of the Tac gene into NIH/3T3 fibroblasts resulted in the production of a recombinant sIL-2R. The presence Of enriched native or recombinant slL-2R inhibited interleukin-2-dependent generation of cytotoxic activity and PHA blast proliferation. We suggest that elevated sIL- 2R levels account for diminished NK activity by neutralizing iriterleukin 2 in CTCL patients.
机译:在皮肤T细胞淋巴瘤(CTCL)患者中,通过ELISA技术测定可溶性白介素2受体血清水平(sIL-2R),并通过4-h铬51释放测定法测定自然杀伤细胞(NK)活性。 NK活性的降低与血清sIL-2R的增加有关。白介素2 CTCL刺激4天后,患者外周血单个核细胞(PMC)的细胞毒性活性增加,类似于健康捐献者的PMC。正常捐献者的PMC与25%CTCL血清(sIL-2R分别为3000、7330和10700 U / mI)相比,IL-2诱导的细胞毒性活性降低,而对照血清(sIL-2R分别为400、340和109)分别为420 U / ml)。 CTCL血清中2-d植物血凝素(PHA)母细胞的IL-2依赖性增殖低于对照血清。通过IL-2亲和层析从一名CTCL患者的血清中富集了sIL-2R。 Tac基因转染到NIH / 3T3成纤维细胞中导致了重组sIL-2R的产生。丰富的天然或重组slL-2R的存在抑制了IL-2依赖的细胞毒活性和PHA blast增殖的产生。我们建议升高的sIL-2R水平可通过中和CTCL患者的iriterleukin 2来降低NK活性。

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