Redox regulation of CD21 shedding involves signaling via PKC and indicates the formation of a juxtamembrane stalk

Aichem, Annette; Masilamani, Madhan; Illges, Harald

doi:10.1242/jcs.02984

Cited by 17 publications

(10 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CD21 exists also in a soluble form as the receptor can be shed from the plasma membrane by proteolytic cleavage in the short consensus repeat 16 . It has been shown that CD21 is constantly shed from peripheral blood B cells , and that the levels in blood are increased after B cell activation .…”

Section: Introductionmentioning

confidence: 99%

CD21^−/low B cells: A Snapshot of a Unique B Cell Subset in Health and Disease

et al. 2015

View full text Add to dashboard Cite

a These authors contributed equally. AbstractB cells represent one of the cellular components of the immune system that protects the individual from invading pathogens. In response to the invader, these cells differentiate into plasma cells and produce large amounts of antibodies that bind to and eliminate the pathogen. A hallmark of autoimmune diseases is the production of autoantibodies i.e. antibodies that recognize self. Those that are considered pathogenic can damage tissues and organs, either by direct binding or when deposited as immune complexes. For decades, B cells have been considered to play a major role in autoimmune diseases by antibody production. However, as pathogenic autoantibodies appear to derive mainly from T cell dependent responses, T cells have been the focus for many years. The successful treatment of patients with autoimmune diseases with either B cell depletion therapy (rituximab) or inhibition of B cell survival (belimumab), suggested that not only the autoantibodies but also other B cell features are important. This has caused a surge of interest in B cells and their biology resulting in the identification of various subsets e.g. regulatory B cells, several memory B cell subsets etc. Also, in other conditions such as chronic viral infections and primary immunodeficiency, several B cell subsets with unique characteristics have been identified. In this review, we will discuss one of these subsets, a subset that is expanded in conditions characterized by chronic immune stimulation. This B cell subset lacks, or expresses low, surface levels of the complement receptor 2 (CD21) and has therefore been termed CD21 À/low B cells.

show abstract

Section: Introductionmentioning

confidence: 99%

CD21^−/low B cells: A Snapshot of a Unique B Cell Subset in Health and Disease

et al. 2015

View full text Add to dashboard Cite

show abstract

“…ES is known to take place in a constitutive or regulated manner by different stimuli that include: ligand binding, PKC activation [22,60,160,166,203], Ca ++ dynamics [50,72,94,160,166,204], oxidative stress [60,205,206], cell density [24,115,141] and pH [185], and depends upon actin dynamics [207,208], dynamin function [209] or GTPase activation [160,210]. Posttranslational modifications such as glycosilation [38] and extracellular phosphorylation [211], as well as, target molecule structural conformation that preclude accessibility to sheddases [174] are also known to regulate ES (Fig.…”

Section: Discussionmentioning

confidence: 99%

Ectodomain Shedding and Regulated Intracellular Proteolysis in the Central Nervous System

Oca-B¹

2010

CNSAMC

View full text Add to dashboard Cite

The term Ectodomain Shedding (ES) refers to extracellular domain proteolytic release from cell membrane molecules. This proteolysis is mediated mainly by matrix metalloproteases (MMP) or disintegrin and metalloproteases (ADAM), although some other proteases may mediate it. Virtually, all functional categories of cell membrane molecules are subject of this kind of proteolysis, for this reason ES is involved in different cellular processes such as proliferation, apoptosis, migration, differentiation or pathologies such as inflammation, cancer and degeneration among others. ES releases membrane molecule's extracellular domain (or ectodomain) to the extracellular milieu where it can play different biological functions. ES of transmembrane molecules also generates membrane attached terminal fragments comprising transmembrane and intracellular domains that enable their additional processing by intracellular proteases known as Regulated Intracellular Proteolysis (RIP). This second proteolytic cleavage delivers molecule's intracellular domain (ICD) that carry out intracellular functions. RIP is mediated by the group of intracellular cleaving proteases (i-CLiPs) that include presenilin from the γ-secretase complex. In the CNS the best well known ES is that of the Amyloid Precursor Protein, although many other membrane molecules expressed by cells of the CNS are also subject to ES and RIP. In this review, these molecules are summarized, and some meaningful examples are highlighted and described. In addition, ES and RIP implications in the context of cell biology are discussed. Finally, some considerations that rise from the study of ES and RIP are formulated in view of the unexpected roles of intracellular fragments.

show abstract

“…The mechanism by which this process occurs remains unknown. CD21 shedding is a redox-regulated process involving oxidation of a tyrosine kinase pathway and reduction of metalloproteases [30]. Thus, the possibility remains that ATP-induced reactive oxygen species (ROS) formation may be involved in P2X7-induced CD21 shedding.…”

Section: Cd21 (C3d Receptor)mentioning

confidence: 99%

Roles of extracellular nucleotides and P2 receptors in ectodomain shedding

Pupovac

Sluyter

2016

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Ectodomain shedding of integral membrane receptors results in the release of soluble molecules and modification of the transmembrane portions to mediate or modulate extracellular and intracellular signalling. Ectodomain shedding is stimulated by a variety of mechanisms, including the activation of P2 receptors by extracellular nucleotides. This review describes in detail the roles of extracellular nucleotides and P2 receptors in the shedding of various cell surface molecules, including amyloid precursor protein, CD23, CD62L, and members of the epidermal growth factor, immunoglobulin and tumour necrosis factor families. This review discusses the mechanisms involved in P2 receptor-mediated shedding, demonstrating central roles for the P2 receptors, P2X7 and P2Y2, and the sheddases, ADAM10 and ADAM17, in this process in a number of cell types.

show abstract

Redox regulation of CD21 shedding involves signaling via PKC and indicates the formation of a juxtamembrane stalk

Cited by 17 publications

References 54 publications

CD21^−/low B cells: A Snapshot of a Unique B Cell Subset in Health and Disease

CD21^−/low B cells: A Snapshot of a Unique B Cell Subset in Health and Disease

Ectodomain Shedding and Regulated Intracellular Proteolysis in the Central Nervous System

Roles of extracellular nucleotides and P2 receptors in ectodomain shedding

Contact Info

Product

Resources

About

Redox regulation of CD21 shedding involves signaling via PKC and indicates the formation of a juxtamembrane stalk

Cited by 17 publications

References 54 publications

CD21−/low B cells: A Snapshot of a Unique B Cell Subset in Health and Disease

CD21−/low B cells: A Snapshot of a Unique B Cell Subset in Health and Disease

Ectodomain Shedding and Regulated Intracellular Proteolysis in the Central Nervous System

Roles of extracellular nucleotides and P2 receptors in ectodomain shedding

Contact Info

Product

Resources

About

CD21^−/low B cells: A Snapshot of a Unique B Cell Subset in Health and Disease

CD21^−/low B cells: A Snapshot of a Unique B Cell Subset in Health and Disease