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脂多糖作为揭示自身反应性B细胞的工具。

Lipopolysaccharide as a tool to reveal autoreactive B cells.

作者信息

Möller G

机构信息

Department of Immunology, University of Stockholm, Sweden.

出版信息

APMIS. 1988 Feb;96(2):93-100. doi: 10.1111/j.1699-0463.1988.tb05274.x.

Abstract

It has been found in several different test systems that LPS is competent to induce autoantibodies of different specificities. As a rule only IgM autoantibodies have been found. The presence of autoreactive B cells in healthy individuals indicate that autoreactive B cells have not been not eliminated by the induction of immunological tolerance. This result is to expected according to the concept of the one non-specific signal hypothesis for B cell activation, which only ascribes a passive focussing role to the immunoglobulin receptors, whereas activation and tolerogenic signals are delivered via non-clonally distributed receptors for polyclonal B cell activators and T cell interleukins. The induction of autoantibodies by LPS in mice does not result in detectable disease or symptoms. Therefore, the ability of LPS to induce IgM autoantibodies does not constitute a model for induction of autoimmune diseases. The main importance of these findings is that the self-non-self distinction is not carried out by B cells. Presumably T cells alone are responsible for the self-non-self distinction.

摘要

在几种不同的测试系统中发现,脂多糖(LPS)能够诱导不同特异性的自身抗体。通常只发现了IgM自身抗体。健康个体中自身反应性B细胞的存在表明,自身反应性B细胞并未因免疫耐受的诱导而被清除。根据B细胞激活的单非特异性信号假说的概念,这一结果在意料之中,该假说仅将免疫球蛋白受体的作用归为被动聚焦,而激活和致耐受性信号则通过多克隆B细胞激活剂和T细胞白细胞介素的非克隆分布受体传递。LPS在小鼠中诱导自身抗体不会导致可检测到的疾病或症状。因此,LPS诱导IgM自身抗体的能力并不构成自身免疫性疾病诱导模型。这些发现的主要重要性在于,B细胞并不进行自我与非自我的区分。推测仅T细胞负责自我与非自我的区分。

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