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T淋巴细胞的去唾液酸化克服了商陆丝裂原诱导的T细胞活化对单核细胞的依赖性。

Desialylation of T lymphocytes overcomes the monocyte dependency of pokeweed mitogen-induced T-cell activation.

作者信息

Gallart T, Angel de la Fuente M, Josep Barceló J, Alberola-Ila J, Lozano F

机构信息

Serveì d'Immunologia, Hospital Clinic Universitari de Barcelona, Spain.

出版信息

Immunology. 1997 Jan;90(1):57-65. doi: 10.1046/j.1365-2567.1997.00129.x.

Abstract

Activation of T lymphocytes by pokeweed mitogen (PWM) is strictly monocyte (Mo)-dependent and results in T-cell mitogenesis and interleukin-2 (IL-2) secretion, coupled with an inability to utilize IL-2 due to an impaired expression of functional IL-2 receptor (IL-2R). Such IL-2R impairment could arise in PWM-activated T cells themselves or, alternatively, be the result of Mo-derived influences, as it is known that PWM binds Mo strongly and does not or poorly binds lymphocytes, and Mo becomes rapidly destroyed in PWM-stimulated cultures of blood mononuclear cells or T cells plus Mo. The present study investigated these possibilities. The results show for the first time that desialylation of T lymphocytes strongly increases their PWM-binding capacity and, in addition, overcomes the Mo requirement for PWM to induce T-cell mitogenesis and IL-2 secretion. Such secreted IL-2 levels were even higher that those found in cultures of Mo-dependent PWM-activated T lymphocytes but similarly to the latter, PWM-activated desialylated purified T lymphocytes exhibited negligible high-affinity IL-2 binding capacity and an inability to utilize the IL-2 they produced. These effects were not due to desialylation itself, as indicated by data obtained with peanut agglutinin, a lectin that becomes strongly reactive with desialylated T lymphocytes. The data clearly indicate the existence of PWM-related events capable of impairing the expression of functional IL-2R without affecting IL-2 secretion, and indicate that such events are due to mechanisms arising at the level of PWM-activated T cells themselves.

摘要

商陆丝裂原(PWM)激活T淋巴细胞严格依赖单核细胞(Mo),可导致T细胞有丝分裂和白细胞介素-2(IL-2)分泌,同时由于功能性IL-2受体(IL-2R)表达受损而无法利用IL-2。这种IL-2R损伤可能出现在PWM激活的T细胞自身,或者是Mo衍生影响的结果,因为已知PWM与Mo强烈结合,与淋巴细胞结合不强或结合不佳,并且在PWM刺激的血液单核细胞或T细胞加Mo的培养物中Mo会迅速被破坏。本研究调查了这些可能性。结果首次表明,T淋巴细胞的去唾液酸化强烈增加其PWM结合能力,此外,克服了PWM诱导T细胞有丝分裂和IL-2分泌对Mo的需求。这种分泌的IL-2水平甚至高于依赖Mo的PWM激活的T淋巴细胞培养物中的水平,但与后者类似,PWM激活的去唾液酸化纯化T淋巴细胞表现出可忽略不计的高亲和力IL-2结合能力,并且无法利用它们产生的IL-2。这些效应不是由于去唾液酸化本身,如用花生凝集素获得的数据所示,花生凝集素是一种与去唾液酸化T淋巴细胞强烈反应的凝集素。数据清楚地表明存在与PWM相关的事件,这些事件能够损害功能性IL-2R的表达而不影响IL-2分泌,并表明这些事件是由于PWM激活的T细胞自身水平产生的机制所致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bc1/1456722/a8e2e1037073/immunology00023-0068-a.jpg

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