Ly6G-mediated depletion of neutrophils is dependent on macrophages

Kevin W. Bruhn , Ken Dekitani , Travis B. Nielsen , Paul Pantapalangkoor , Brad Spellberg
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引用次数: 55

Abstract

Antibody-mediated depletion of neutrophils is commonly used to study neutropenia. However, the mechanisms by which antibodies deplete neutrophils have not been well defined. We noticed that mice deficient in complement and macrophages had blunted neutrophil depletion in response to anti-Ly6G monoclonal antibody (MAb) treatment. In vitro, exposure of murine neutrophils to anti-Ly6G MAb in the presence of plasma did not result in significant depletion of cells, either in the presence or absence of complement. In vivo, anti-Ly6G-mediated neutrophil depletion was abrogated following macrophage depletion, but not complement depletion, indicating a requirement for macrophages to induce neutropenia by this method. These results inform the use and limitations of anti-Ly6G antibody as an experimental tool for depleting neutrophils in various immunological settings.

ly6g介导的中性粒细胞耗竭依赖于巨噬细胞
抗体介导的中性粒细胞耗竭通常用于研究中性粒细胞减少症。然而,抗体消耗中性粒细胞的机制尚未明确。我们注意到,补体和巨噬细胞缺乏的小鼠在抗ly6g单克隆抗体(MAb)治疗后,中性粒细胞耗竭减弱。在体外实验中,小鼠中性粒细胞在血浆存在的情况下暴露于抗ly6g单抗,无论在补体存在或不存在的情况下,都不会导致细胞的显著消耗。在体内,巨噬细胞耗竭后,抗ly6g介导的中性粒细胞耗竭被消除,但补体耗竭未被消除,这表明巨噬细胞需要通过这种方法诱导中性粒细胞减少。这些结果告知使用和局限性抗ly6g抗体作为一个实验工具消耗中性粒细胞在各种免疫设置。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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