Publikation: Modulation of murine complement receptor type 2 (CR2/CD21) ectodomain shedding by its cytoplasmic domain
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Ectodomain shedding is a mechanism that regulates numerous functions of cell surface proteins. The extracellular domain of the human complement receptor 2 (CR2/CD21) is released by proteolytic cleavage as a soluble protein through a variety of stimuli including the thiol antioxidants N-acetylcysteine (NAC) and glutathione (GSH), and the oxidant pervanadate (PV). In addition, PV mimics B cell antigen receptor (BCR) signaling. Here, we show that murine CD21 is shed upon those stimuli and that the cytoplasmic domain is an important modulator for CD21-shedding. B cells expressing a mutant CD21 cytoplasmic domain with only three amino acids (KHR) showed increased CD21-shedding and required lower stimuli concentrations. At lower PV concentrations, wildtype CD21 was up-regulated on the cell surface, whereas at higher PV concentrations the ectodomain was shed. These findings further indicate that GSH and NAC utilize different pathways than PV to activate CD21-shedding. Altogether, as pre-activated B cells express higher CD21 levels than resting mature B cells or fully activated and antigen-experienced B cells, we suggest CD21-shedding to be a mechanism to fine-tune B cell activation.
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HOEFER, Melanie M., Annette AICHEM, Andrew M. KNIGHT, Harald ILLGES, 2008. Modulation of murine complement receptor type 2 (CR2/CD21) ectodomain shedding by its cytoplasmic domain. In: Molecular Immunology. Elsevier. 2008, 45(8), pp. 2127-2137. ISSN 0161-5890. eISSN 1872-9142. Available under: doi: 10.1016/j.molimm.2007.12.015BibTex
@article{Hoefer2008-04Modul-49713,
year={2008},
doi={10.1016/j.molimm.2007.12.015},
title={Modulation of murine complement receptor type 2 (CR2/CD21) ectodomain shedding by its cytoplasmic domain},
number={8},
volume={45},
issn={0161-5890},
journal={Molecular Immunology},
pages={2127--2137},
author={Hoefer, Melanie M. and Aichem, Annette and Knight, Andrew M. and Illges, Harald}
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<dcterms:abstract xml:lang="eng">Ectodomain shedding is a mechanism that regulates numerous functions of cell surface proteins. The extracellular domain of the human complement receptor 2 (CR2/CD21) is released by proteolytic cleavage as a soluble protein through a variety of stimuli including the thiol antioxidants N-acetylcysteine (NAC) and glutathione (GSH), and the oxidant pervanadate (PV). In addition, PV mimics B cell antigen receptor (BCR) signaling. Here, we show that murine CD21 is shed upon those stimuli and that the cytoplasmic domain is an important modulator for CD21-shedding. B cells expressing a mutant CD21 cytoplasmic domain with only three amino acids (KHR) showed increased CD21-shedding and required lower stimuli concentrations. At lower PV concentrations, wildtype CD21 was up-regulated on the cell surface, whereas at higher PV concentrations the ectodomain was shed. These findings further indicate that GSH and NAC utilize different pathways than PV to activate CD21-shedding. Altogether, as pre-activated B cells express higher CD21 levels than resting mature B cells or fully activated and antigen-experienced B cells, we suggest CD21-shedding to be a mechanism to fine-tune B cell activation.</dcterms:abstract>
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