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20231224223044.0 |
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cr uuu---uuuuu |
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231224s2017 xx |||||o 00| ||eng c |
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7 |
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|a 10.1016/j.clim.2017.01.014
|2 doi
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2 |
|a pubmed24n0895.xml
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|a (DE-627)NLM268660379
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|a (NLM)28161408
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|a (PII)S1521-6616(17)30086-4
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Sato, Yohei
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a Anti-BlyS antibody reduces the immune reaction against enzyme and enhances the efficacy of enzyme replacement therapy in Fabry disease model mice
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| 264 |
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1 |
|c 2017
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| 336 |
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|a Text
|b txt
|2 rdacontent
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| 337 |
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 14.08.2017
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|a Date Revised 06.02.2018
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2017 Elsevier Inc. All rights reserved.
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|a Formation of antibodies against a therapeutic enzyme is an important complication during enzyme replacement therapy (ERT) for lysosomal storage diseases. Fabry disease (FD) is caused by a deficiency of alpha-galactosidase (GLA), which results in the accumulation of globotriaosylceramide (GL-3). We have shown immune tolerance induction (ITI) during ERT in FD model mice by using an anti-B lymphocyte stimulator (anti-BlyS) antibody (belimumab). A single dose of the anti-BlyS antibody temporarily lowered the percentage of B cells and IgG antibody titer against recombinant human GLA. Administration of a low maintenance dose of the anti-BlyS antibody suppressed the B cell population and immunotolerance was induced in 20% of mice, but antibody formation could not be prevented. We then increased the maintenance dose of the anti-BlyS antibody and immunotolerance was induced in 50% of mice. Therapeutic enzyme distribution and clearance of GL-3 were also enhanced by a high maintenance dose of the anti-BlyS antibody
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| 650 |
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, Non-U.S. Gov't
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| 650 |
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4 |
|a Anti-BlyS antibody
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| 650 |
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4 |
|a Enzyme replacement therapy
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| 650 |
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4 |
|a Fabry disease
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| 650 |
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4 |
|a Immune tolerance induction
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| 650 |
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4 |
|a Neutralizing antibody
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| 650 |
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7 |
|a Antibodies, Monoclonal, Humanized
|2 NLM
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| 650 |
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7 |
|a Immunoglobulin G
|2 NLM
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| 650 |
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7 |
|a Immunosuppressive Agents
|2 NLM
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| 650 |
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7 |
|a Recombinant Proteins
|2 NLM
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| 650 |
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7 |
|a Trihexosylceramides
|2 NLM
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| 650 |
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7 |
|a globotriaosylceramide
|2 NLM
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| 650 |
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7 |
|a 71965-57-6
|2 NLM
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| 650 |
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7 |
|a belimumab
|2 NLM
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| 650 |
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7 |
|a 73B0K5S26A
|2 NLM
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| 650 |
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7 |
|a alpha-Galactosidase
|2 NLM
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| 650 |
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7 |
|a EC 3.2.1.22
|2 NLM
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| 700 |
1 |
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|a Ida, Hiroyuki
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ohashi, Toya
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 178(2017) vom: 05. Mai, Seite 56-63
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
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|g volume:178
|g year:2017
|g day:05
|g month:05
|g pages:56-63
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2017.01.014
|3 Volltext
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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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| 912 |
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|a GBV_ILN_24
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| 912 |
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|a GBV_ILN_350
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| 951 |
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|a AR
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| 952 |
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|d 178
|j 2017
|b 05
|c 05
|h 56-63
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