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B细胞活化导致II型补体受体(CR2/CD21)脱落。

B cell activation leads to shedding of complement receptor type II (CR2/CD21).

作者信息

Masilamani Madhan, Kassahn Daniela, Mikkat Stefan, Glocker Michael O, Illges Harald

机构信息

Faculty of Sciences, Department of Biology, Immunology, University of Konstanz, Konstanz, Germany.

出版信息

Eur J Immunol. 2003 Sep;33(9):2391-7. doi: 10.1002/eji.200323843.

DOI:10.1002/eji.200323843
PMID:12938215
Abstract

Complement receptor type II (CR2/CD21) is the major receptor for C3d fragments on immune complexes. CD21 also serves as the receptor for Epstein-Barr virus in humans. On mature B cells, CD21 reduces the threshold of BCR signaling together with CD81, Leu13 and CD19, but it also occurs on other cells of the immune system where it performs unknown functions. A soluble form of CD21 (sCD21) is shed from the cell surface and is found in human blood plasma. An as-yet-unknown protease is thought to be responsible for this shedding. Altered levels of sCD21 occur in plasma in certain clinical conditions. We show here by mass spectrometry that sCD21 in human plasma of healthy donors is predominantly a short form of CD21 without the exon-11-encoded sequences. Whereas the N terminus of sCD21 was found unmodified, the C terminus is truncated, implying that only the extracellular portion of CD21 is shed. Peripheral blood B cells, but not T cells, contribute to the plasma CD21-pool. CD21 shedding is induced by stimulation with PMA plus Ca(2+) ionophore, or by stimulation of the BCR with anti-IgM+anti-CD40.

摘要

补体II型受体(CR2/CD21)是免疫复合物上C3d片段的主要受体。CD21也是人类Epstein-Barr病毒的受体。在成熟B细胞上,CD21与CD81、Leu13和CD19一起降低BCR信号传导的阈值,但它也存在于免疫系统的其他细胞上,其功能尚不清楚。一种可溶性形式的CD21(sCD21)从细胞表面脱落,存在于人类血浆中。一种尚未明确的蛋白酶被认为负责这种脱落过程。在某些临床情况下,血浆中sCD21的水平会发生改变。我们通过质谱分析表明,健康供体人血浆中的sCD21主要是一种不含外显子11编码序列的CD21短形式。虽然发现sCD21的N末端未被修饰,但其C末端被截断,这意味着只有CD21的细胞外部分被脱落。外周血B细胞而非T细胞对血浆CD21池有贡献。用PMA加Ca(2+)离子载体刺激,或用抗IgM+抗CD40刺激BCR可诱导CD21的脱落。

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