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|a pubmed24n0386.xml
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|a (DE-627)NLM115779205
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|a (NLM)11683571
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Enyedy, E J
|e verfasserin
|4 aut
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|a Defective FcgammaRIIb1 signaling contributes to enhanced calcium response in B cells from patients with systemic lupus erythematosus
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|c 2001
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|a Text
|b txt
|2 rdacontent
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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|a Band
|b nc
|2 rdacarrier
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|a Date Completed 07.12.2001
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|a Date Revised 24.11.2016
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|a published: Print
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|a Citation Status MEDLINE
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|a Copyright 2001 Academic Press.
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|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
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|a Journal Article
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|a Research Support, U.S. Gov't, Non-P.H.S.
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|a Research Support, U.S. Gov't, P.H.S.
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|a Immunoglobulin G
|2 NLM
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|a Immunoglobulin M
|2 NLM
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|a Receptors, Antigen, B-Cell
|2 NLM
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|a Receptors, IgG
|2 NLM
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|a Phosphoric Monoester Hydrolases
|2 NLM
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|a EC 3.1.3.2
|2 NLM
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|a INPPL1 protein, human
|2 NLM
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|a EC 3.1.3.86
|2 NLM
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|a Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases
|2 NLM
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|a EC 3.1.3.86
|2 NLM
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1 |
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|a Mitchell, J P
|e verfasserin
|4 aut
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1 |
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|a Nambiar, M P
|e verfasserin
|4 aut
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1 |
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|a Tsokos, G C
|e verfasserin
|4 aut
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773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 101(2001), 2 vom: 01. Nov., Seite 130-5
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
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|g volume:101
|g year:2001
|g number:2
|g day:01
|g month:11
|g pages:130-5
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 101
|j 2001
|e 2
|b 01
|c 11
|h 130-5
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