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免疫小鼠中,IgE受体阳性的非B/非T细胞主导白细胞介素4和白细胞介素6的产生。

IgE receptor-positive non-B/non-T cells dominate the production of interleukin 4 and interleukin 6 in immunized mice.

作者信息

Aoki I, Kinzer C, Shirai A, Paul W E, Klinman D M

机构信息

Retroviral Immunology Section, Food and Drug Administration, Bethesda, MD 20892, USA.

出版信息

Proc Natl Acad Sci U S A. 1995 Mar 28;92(7):2534-8. doi: 10.1073/pnas.92.7.2534.

DOI:10.1073/pnas.92.7.2534
PMID:7708680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC42252/
Abstract

The phenotype and antigenic specificity of cells secreting interleukin (IL) 4, IL-6, and interferon gamma was studied in mice during primary and secondary immune responses. T lymphocytes were the major source of interferon gamma, whereas non-B/non-T cells were the dominant source of IL-4 and IL-6 in the spleens of immunized animals. Cytokine-secreting non-B/non-T cells expressed surface receptors for IgE and/or IgG types II/III. Exposing these cells to antigen-specific IgE or IgG in vivo (or in vitro) "armed" them to release IL-4 and IL-6 upon subsequent antigenic challenge. These findings suggest that non-B/non-T cells may represent the "natural immunity" analogue of CD4+ T helper type 2 cells and participate in a positive feedback loop involved in the perpetuation of T helper type 2 cell responses.

摘要

在初次和二次免疫反应期间,对小鼠体内分泌白细胞介素(IL)-4、IL-6和干扰素γ的细胞的表型和抗原特异性进行了研究。T淋巴细胞是干扰素γ的主要来源,而在免疫动物的脾脏中,非B/非T细胞是IL-4和IL-6的主要来源。分泌细胞因子的非B/非T细胞表达IgE和/或II/III型IgG的表面受体。在体内(或体外)将这些细胞暴露于抗原特异性IgE或IgG会“武装”它们,使其在随后受到抗原攻击时释放IL-4和IL-6。这些发现表明,非B/非T细胞可能代表CD4 + 2型辅助性T细胞的“天然免疫”类似物,并参与了与2型辅助性T细胞反应持续存在有关的正反馈回路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa0b/42252/c3d57af5517b/pnas01485-0129-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa0b/42252/c3d57af5517b/pnas01485-0129-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa0b/42252/c3d57af5517b/pnas01485-0129-a.jpg

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Interleukin-4 (IL-4) enhances and soluble interleukin-4 receptor (sIL-4R) inhibits histamine release from peripheral blood basophils and mast cells in vitro and in vivo.白细胞介素-4(IL-4)增强,可溶性白细胞介素-4 受体(sIL-4R)抑制体外和体内外周血嗜碱性粒细胞和肥大细胞释放组胺。
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