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用新城疫病毒感染小鼠会抑制调节对苦味酸氯接触敏感性的T抑制传入细胞回路。

Infection of mice with Newcastle disease virus inhibits the T suppressor afferent cell circuit which regulates contact sensitivity to picryl chloride.

作者信息

Dieli F, Colonna Romano G, Abrignani S, Colizzi V, Salerno A

出版信息

Cell Immunol. 1985 Aug;94(1):225-30. doi: 10.1016/0008-8749(85)90099-1.

Abstract

The interaction between Newcastle disease virus (NDV) and the suppressor cell circuit which regulates the induction phase of contact sensitivity reaction to picryl chloride (Pcl) was investigated. NDV infection impairs the activity of the T suppressor afferent cells (Ts-aff) which inhibit DNA synthesis in the draining lymph nodes of mice specifically sensitized with Pcl and the development of contact sensitivity. The inhibitory effect of NDV was evident when the virus was administered up to 2 days before or at the same time as the injection of picrylsulfonic acid; this effect required infectious virus, as NDV inactivated by ultraviolet irradiation failed to inhibit Ts-aff activity. Taken together with the previous finding that the T suppressor efferent cell is unaffected by NDV, the present results support the view that contact sensitivity reaction to picryl chloride is regulated by two distinct T-suppressor-cell circuits.

摘要

研究了新城疫病毒(NDV)与调节对苦味酸氯(Pcl)接触敏感性反应诱导阶段的抑制细胞回路之间的相互作用。NDV感染会损害T抑制传入细胞(Ts-aff)的活性,这些细胞可抑制在用Pcl特异性致敏的小鼠引流淋巴结中的DNA合成以及接触敏感性的发展。当在注射苦味磺酸前2天或同时给予病毒时,NDV的抑制作用很明显;这种作用需要感染性病毒,因为经紫外线照射灭活的NDV无法抑制Ts-aff活性。结合先前发现T抑制传出细胞不受NDV影响这一结果,目前的结果支持这样一种观点,即对苦味酸氯的接触敏感性反应由两个不同的T抑制细胞回路调节。

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