The Low‐Affinity Receptor for IgE

Delespesse, Guy; Sarfati, Marika; Cy, Wu; Fournier, Sylvie; Letellier, Marie-Claude

doi:10.1111/j.1600-065x.1992.tb00626.x

Cited by 159 publications

(80 citation statements)

References 91 publications

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“…Our finding that EBVCS1 decreases the expression of the Fc⑀RII at the surface of B cells and induces the release of fragments, together with the observation that it enhances IgE synthesis by human B cells stimulated in vitro by a combination of IL-4 and CD40 mAb or hydrocortisone (31), further supports this model. It is interesting to point out that among the sCD23 fragments, the 29-kDa species, which is one of the major components produced by EBVCS1-stimulated cells, has a strong stimulatory activity on IgE production (2,23).…”

Section: Fig 5 Effects Of Ige On Ebvcs1-induced Cd23 Cleavagementioning

confidence: 99%

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Binding of Anti-CD23 Monoclonal Antibody to the Leucine Zipper Motif of FcεRII/CD23 on B Cell Membrane Promotes Its Proteolytic Cleavage

Munoz

Brignone

Grenier-Brossette³

et al. 1998

Journal of Biological Chemistry

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In the present study we have compared the binding of two monoclonal antibodies to CD23, EBVCS1 and mAb25, which recognize the stalk and the lectin domain, respectively, on the CD23 molecule. At 4°C, EBVCS1 binds to about 10% of the receptors recognized by mAb25 on the B cell surface. At 37°C, whereas mAb25 reaches its maximal binding within a few seconds, EB-VCS1 requires 60 min to bind to the same extent. Stabilization of the oligomeric structure of CD23 with IgE strongly affects in a dose-dependent fashion the number of binding sites seen by EBVCS1 but not the t 1/2 to reach them, suggesting that EBVCS1 binds to the coiled coil region through an allosteric mechanism. EBVCS1 rapidly down-modulates the membrane CD23 expression with a coincident increase of CD23-soluble fragments in the culture medium, an effect that is inhibited by IgE. In contrast, mAb25, as well as IgE, protects CD23 from proteolytic cleavage and stimulates its endocytosis. These results suggest that EBVCS1 unravels the coiled coil structure of CD23, rendering it more susceptible to proteolytic attack. This supports the oligomeric model proposed previously (Gould, H., Sutton, B., Edmeades, R., and Beavil, A. (1991) Monogr. Allergy 29, 28 -49). The biological significance of these observations is discussed.

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Section: Fig 5 Effects Of Ige On Ebvcs1-induced Cd23 Cleavagementioning

confidence: 99%

“…CD23 at the cell surface is turned over to yield a series of soluble fragments (sCD23) 1 (10,11) by a mechanism stimulated by triggering of CD20 (12,13). In vitro experiments have shown that sCD23 has a variety of biological activities (2).…”

mentioning

confidence: 99%

Binding of Anti-CD23 Monoclonal Antibody to the Leucine Zipper Motif of FcεRII/CD23 on B Cell Membrane Promotes Its Proteolytic Cleavage

Munoz

Brignone

Grenier-Brossette³

et al. 1998

Journal of Biological Chemistry

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“…Since production of autoantibodies to muscle is pathognomonic for juvenile DM (29,30), we examined the differentiation state of the infiltrating B cells. In normal B cells, CD23, the low-affinity IgE receptor, indicates B cell maturation and differentiation to plasma cells (31). Hence, we examined costaining for CD23 and CD20.…”

mentioning

confidence: 99%

Extranodal lymphoid microstructures in inflamed muscle and disease severity of new‐onset juvenile dermatomyositis

Padilla¹,

Vallejo²,

Lacomis³

et al. 2009

Arthritis & Rheumatism

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Objective. Juvenile dermatomyositis (DM) is an autoimmune disease of childhood characterized by lesions in skin and muscle that are populated by plasmacytoid dendritic cells (PDCs) and lymphocyte infiltrates. We undertook this study to examine the cellular composition, organization, and molecular milieu of the cellular infiltrates in muscle in juvenile DM and to correlate the infiltrates with clinical disease manifestations.Methods. Since PDCs and lymphocyte foci express CCL19 and CCL21, we investigated for in situ formation of lymphoid microstructures that could be sites of extranodal immune activation.Results. Analyses of muscle biopsy samples from children with new-onset juvenile DM showed 3 categories of lesions: diffuse infiltrates, lymphocytic aggregates lacking follicle-like organization, and follicle-like structures. The last of these exhibited elements of classic lymphoid follicles, including networks of follicular dendritic cells and high endothelial venules. They also expressed high levels of CXCL13 and lymphotoxins known to support lymphoid organogenesis. There were also resident naive CD45RA؉ T cells and maternally derived B cells and PDCs. Patients with diffuse infiltrates or lymphocytic aggregates were responsive to standard therapy with steroids and methotrexate, but those with follicle-like structures tended to have severe disease that required additional agents such as intravenous Ig or rituximab.Conclusion. These data suggest that lymphoneogenesis is a component of the early disease process in juvenile DM. Ectopic lymphoid structures could indicate a severe course of disease; their early detection could be a tool for disease management.

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“…[1][2][3] In the human, CD23 is encoded by a single, eleven-exon gene spanning 13 Kb located at chromosome 19p13 adjacent to the DC-SIGN and DC-SIGNR genes. 4,5 The gene gives rise to two protein isoforms, CD23a and CD23b, which differ by only six or seven amino acids in their extreme cytoplasmic Ntermini.…”

Section: Introductionmentioning

confidence: 99%

The CD23a and CD23b proximal promoters display different sensitivities to exogenous stimuli in B lymphocytes

Cushley

2002

Genes Immun

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The Low‐Affinity Receptor for IgE

Cited by 159 publications

References 91 publications

Binding of Anti-CD23 Monoclonal Antibody to the Leucine Zipper Motif of FcεRII/CD23 on B Cell Membrane Promotes Its Proteolytic Cleavage

Binding of Anti-CD23 Monoclonal Antibody to the Leucine Zipper Motif of FcεRII/CD23 on B Cell Membrane Promotes Its Proteolytic Cleavage

Extranodal lymphoid microstructures in inflamed muscle and disease severity of new‐onset juvenile dermatomyositis

The CD23a and CD23b proximal promoters display different sensitivities to exogenous stimuli in B lymphocytes

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