B-cells expressing NgR1 and NgR3 are localized to EAE-induced inflammatory infiltrates and are stimulated by BAFF
Abstract We have previously reported evidence that Nogo-A activation of Nogo-receptor 1 (NgR1) can drive axonal dystrophy during the neurological progression of experimental autoimmune encephalomyelitis (EAE). However, the B-cell activating factor (BAFF/BlyS) may also be an important ligand of NgR d...
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2021
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oai:doaj.org-article:7f98d0d0bafb467bb50ba3cdc0460e712021-12-02T14:06:56ZB-cells expressing NgR1 and NgR3 are localized to EAE-induced inflammatory infiltrates and are stimulated by BAFF10.1038/s41598-021-82346-62045-2322https://doaj.org/article/7f98d0d0bafb467bb50ba3cdc0460e712021-02-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-82346-6https://doaj.org/toc/2045-2322Abstract We have previously reported evidence that Nogo-A activation of Nogo-receptor 1 (NgR1) can drive axonal dystrophy during the neurological progression of experimental autoimmune encephalomyelitis (EAE). However, the B-cell activating factor (BAFF/BlyS) may also be an important ligand of NgR during neuroinflammation. In the current study we define that NgR1 and its homologs may contribute to immune cell signaling during EAE. Meningeal B-cells expressing NgR1 and NgR3 were identified within the lumbosacral spinal cords of ngr1 +/+ EAE-induced mice at clinical score 1. Furthermore, increased secretion of immunoglobulins that bound to central nervous system myelin were shown to be generated from isolated NgR1- and NgR3-expressing B-cells of ngr1 +/+ EAE-induced mice. In vitro BAFF stimulation of NgR1- and NgR3-expressing B cells, directed them into the cell cycle DNA synthesis phase. However, when we antagonized BAFF signaling by co-incubation with recombinant BAFF-R, NgR1-Fc, or NgR3 peptides, the B cells remained in the G0/G1 phase. The data suggest that B cells express NgR1 and NgR3 during EAE, being localized to infiltrates of the meninges and that their regulation is governed by BAFF signaling.Maha M. BakhuraysahPaschalis TheotokisJae Young LeeAmani A. AlrehailiPei-Mun AuiWilliam A. FiggettMichael F. AzariJohn-Paul Abou-AfechFabienne MackayChristopher SiatskasFrank AlderuccioStephen M. StrittmatterNikolaos GrigoriadisSteven PetratosNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-16 (2021) |
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Medicine R Science Q Maha M. Bakhuraysah Paschalis Theotokis Jae Young Lee Amani A. Alrehaili Pei-Mun Aui William A. Figgett Michael F. Azari John-Paul Abou-Afech Fabienne Mackay Christopher Siatskas Frank Alderuccio Stephen M. Strittmatter Nikolaos Grigoriadis Steven Petratos B-cells expressing NgR1 and NgR3 are localized to EAE-induced inflammatory infiltrates and are stimulated by BAFF |
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Abstract We have previously reported evidence that Nogo-A activation of Nogo-receptor 1 (NgR1) can drive axonal dystrophy during the neurological progression of experimental autoimmune encephalomyelitis (EAE). However, the B-cell activating factor (BAFF/BlyS) may also be an important ligand of NgR during neuroinflammation. In the current study we define that NgR1 and its homologs may contribute to immune cell signaling during EAE. Meningeal B-cells expressing NgR1 and NgR3 were identified within the lumbosacral spinal cords of ngr1 +/+ EAE-induced mice at clinical score 1. Furthermore, increased secretion of immunoglobulins that bound to central nervous system myelin were shown to be generated from isolated NgR1- and NgR3-expressing B-cells of ngr1 +/+ EAE-induced mice. In vitro BAFF stimulation of NgR1- and NgR3-expressing B cells, directed them into the cell cycle DNA synthesis phase. However, when we antagonized BAFF signaling by co-incubation with recombinant BAFF-R, NgR1-Fc, or NgR3 peptides, the B cells remained in the G0/G1 phase. The data suggest that B cells express NgR1 and NgR3 during EAE, being localized to infiltrates of the meninges and that their regulation is governed by BAFF signaling. |
format |
article |
author |
Maha M. Bakhuraysah Paschalis Theotokis Jae Young Lee Amani A. Alrehaili Pei-Mun Aui William A. Figgett Michael F. Azari John-Paul Abou-Afech Fabienne Mackay Christopher Siatskas Frank Alderuccio Stephen M. Strittmatter Nikolaos Grigoriadis Steven Petratos |
author_facet |
Maha M. Bakhuraysah Paschalis Theotokis Jae Young Lee Amani A. Alrehaili Pei-Mun Aui William A. Figgett Michael F. Azari John-Paul Abou-Afech Fabienne Mackay Christopher Siatskas Frank Alderuccio Stephen M. Strittmatter Nikolaos Grigoriadis Steven Petratos |
author_sort |
Maha M. Bakhuraysah |
title |
B-cells expressing NgR1 and NgR3 are localized to EAE-induced inflammatory infiltrates and are stimulated by BAFF |
title_short |
B-cells expressing NgR1 and NgR3 are localized to EAE-induced inflammatory infiltrates and are stimulated by BAFF |
title_full |
B-cells expressing NgR1 and NgR3 are localized to EAE-induced inflammatory infiltrates and are stimulated by BAFF |
title_fullStr |
B-cells expressing NgR1 and NgR3 are localized to EAE-induced inflammatory infiltrates and are stimulated by BAFF |
title_full_unstemmed |
B-cells expressing NgR1 and NgR3 are localized to EAE-induced inflammatory infiltrates and are stimulated by BAFF |
title_sort |
b-cells expressing ngr1 and ngr3 are localized to eae-induced inflammatory infiltrates and are stimulated by baff |
publisher |
Nature Portfolio |
publishDate |
2021 |
url |
https://doaj.org/article/7f98d0d0bafb467bb50ba3cdc0460e71 |
work_keys_str_mv |
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