Defective FcgammaRIIb1 signaling contributes to enhanced calcium response in B cells from patients with systemic lupus erythematosus

Copyright 2001 Academic Press.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 101(2001), 2 vom: 01. Nov., Seite 130-5
1. Verfasser: Enyedy, E J (VerfasserIn)
Weitere Verfasser: Mitchell, J P, Nambiar, M P, Tsokos, G C
Format: Aufsatz
Sprache:English
Veröffentlicht: 2001
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Immunoglobulin G Immunoglobulin M Receptors, Antigen, B-Cell Receptors, IgG Phosphoric Monoester Hydrolases EC 3.1.3.2 INPPL1 protein, human mehr... EC 3.1.3.86 Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases
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100 1 |a Enyedy, E J  |e verfasserin  |4 aut 
245 1 0 |a Defective FcgammaRIIb1 signaling contributes to enhanced calcium response in B cells from patients with systemic lupus erythematosus 
264 1 |c 2001 
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520 |a Copyright 2001 Academic Press. 
520 |a B lymphocytes from patients with systemic lupus erythematosus (SLE) display enhanced B cell antigen receptor (BCR)-mediated early signal transduction events, including increased fluxes of intracytoplasmic calcium ([Ca(2+)](i)). Because crosslinking of FcgammaRIIb1 (CD32) in normal B cells suppresses the BCR-initiated signal transduction process, we investigated whether the increased BCR-initiated [Ca(2+)](i) response in SLE B cells is the consequence of decreased FcgammaRIIb1-mediated suppression. To this end, we used flow cytometry to study the [Ca(2+)](i) responses of indo-1-loaded negatively gated B cells stimulated with F(ab')(2) fragments or whole IgG anti-human micro Ab. We found that the ratio of F(ab')(2) to whole anti-micro Ab [Ca(2+)](i) response was significantly lower in SLE B cells compared to B cells from patients with other systemic rheumatic diseases or normal individuals (P < 0.01). Because the surface expressions of FcgammaRIIb1 and surface IgM were similar in B cells from SLE patients and disease and normal controls, these data indicate a decrease in FcgammaRIIb-mediated suppression in SLE B cells. In addition, the whole IgG anti-micro Ab but not its F(ab')(2) fragment caused increased redistribution of SH2 domain-containing inositol 5'phosphatase in SLE compared to normal and disease control B cells. In conclusion, deficient FcgammaRIIb1-mediated suppression contributes to the augmented [Ca(2+)](i) responses of human SLE B cells 
650 4 |a Journal Article 
650 4 |a Research Support, U.S. Gov't, Non-P.H.S. 
650 4 |a Research Support, U.S. Gov't, P.H.S. 
650 7 |a Immunoglobulin G  |2 NLM 
650 7 |a Immunoglobulin M  |2 NLM 
650 7 |a Receptors, Antigen, B-Cell  |2 NLM 
650 7 |a Receptors, IgG  |2 NLM 
650 7 |a Phosphoric Monoester Hydrolases  |2 NLM 
650 7 |a EC 3.1.3.2  |2 NLM 
650 7 |a INPPL1 protein, human  |2 NLM 
650 7 |a EC 3.1.3.86  |2 NLM 
650 7 |a Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases  |2 NLM 
650 7 |a EC 3.1.3.86  |2 NLM 
700 1 |a Mitchell, J P  |e verfasserin  |4 aut 
700 1 |a Nambiar, M P  |e verfasserin  |4 aut 
700 1 |a Tsokos, G C  |e verfasserin  |4 aut 
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