IgM anti-GM2 antibodies in patients with multifocal motor neuropathy target Schwann cells and are associated with early onset

Background Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of MMN is the presence of IgM antibodies against gangliosides, in particular GM1 and less often GM2. Antibodies against GM1 bind to mo...

Full description

Saved in:

Bibliographic Details
Published in:	Journal of neuroinflammation Vol. 21; no. 1; pp. 100 - 14
Main Authors:	Budding, Kevin, Bos, Jeroen W., Dijkxhoorn, Kim, de Zeeuw, Elisabeth, Bloemenkamp, Lauri M., Zekveld, Eva M., Groen, Ewout J.N., Jacobs, Bart C., Huizinga, Ruth, Goedee, H. Stephan, Cats, Elisabeth A., Leusen, Jeanette H.W., van den Berg, Leonard H., Hack, C. Erik, van der Pol, W. Ludo
Format:	Journal Article
Language:	English
Published:	London BioMed Central 17.04.2024 BioMed Central Ltd BMC
Subjects:	Analysis Anti-ganglioside antibodies Antibodies Biomedical and Life Sciences Biomedicine Complement IgM anti-GM2 Immunology Multifocal motor neuropathy Neurobiology Neurology Neurosciences Puncture Schwann cells Spine Testing Viral antibodies Netherlands Multifocal motor neuropathy Complement Anti-ganglioside antibodies IgM anti-GM2 Schwann cells
ISSN:	1742-2094, 1742-2094
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Abstract	Background Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of MMN is the presence of IgM antibodies against gangliosides, in particular GM1 and less often GM2. Antibodies against GM1 bind to motor neurons (MNs) and cause damage through complement activation. The involvement of Schwann cells (SCs), expressing GM1 and GM2, in the pathogenesis of MMN is unknown. Methods Combining the data of our 2007 and 2015 combined cross-sectional and follow-up studies in Dutch patients with MMN, we evaluated the presence of IgM antibodies against GM1 and GM2 in serum from 124 patients with MMN and investigated their binding to SCs and complement-activating properties. We also assessed the relation of IgM binding and complement deposition with clinical characteristics. Results Thirteen out of 124 patients (10%) had a positive ELISA titer for IgM anti-GM2. Age at onset of symptoms was significantly lower in MMN patients with anti-GM2 IgM. IgM binding to SCs correlated with IgM anti-GM2 titers. We found no correlation between IgM anti-GM2 titers and MN binding or with IgM anti-GM1 titers. IgM binding to SCs decreased upon pre-incubation of serum with soluble GM2, but not with soluble GM1. IgM anti-GM2 binding to SCs correlated with complement activation, as reflected by increased C3 fixation on SCs and C5a formation in the supernatant. Conclusion Circulating IgM anti-GM2 antibodies define a subgroup of patients with MMN that has an earlier onset of disease. These antibodies probably target SCs specifically and activate complement, similarly as IgM anti-GM1 on MNs. Our data indicate that complement activation by IgM antibodies bound to SCs and MNs underlies MMN pathology.
AbstractList	Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of MMN is the presence of IgM antibodies against gangliosides, in particular GM1 and less often GM2. Antibodies against GM1 bind to motor neurons (MNs) and cause damage through complement activation. The involvement of Schwann cells (SCs), expressing GM1 and GM2, in the pathogenesis of MMN is unknown.BACKGROUNDMultifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of MMN is the presence of IgM antibodies against gangliosides, in particular GM1 and less often GM2. Antibodies against GM1 bind to motor neurons (MNs) and cause damage through complement activation. The involvement of Schwann cells (SCs), expressing GM1 and GM2, in the pathogenesis of MMN is unknown.Combining the data of our 2007 and 2015 combined cross-sectional and follow-up studies in Dutch patients with MMN, we evaluated the presence of IgM antibodies against GM1 and GM2 in serum from 124 patients with MMN and investigated their binding to SCs and complement-activating properties. We also assessed the relation of IgM binding and complement deposition with clinical characteristics.METHODSCombining the data of our 2007 and 2015 combined cross-sectional and follow-up studies in Dutch patients with MMN, we evaluated the presence of IgM antibodies against GM1 and GM2 in serum from 124 patients with MMN and investigated their binding to SCs and complement-activating properties. We also assessed the relation of IgM binding and complement deposition with clinical characteristics.Thirteen out of 124 patients (10%) had a positive ELISA titer for IgM anti-GM2. Age at onset of symptoms was significantly lower in MMN patients with anti-GM2 IgM. IgM binding to SCs correlated with IgM anti-GM2 titers. We found no correlation between IgM anti-GM2 titers and MN binding or with IgM anti-GM1 titers. IgM binding to SCs decreased upon pre-incubation of serum with soluble GM2, but not with soluble GM1. IgM anti-GM2 binding to SCs correlated with complement activation, as reflected by increased C3 fixation on SCs and C5a formation in the supernatant.RESULTSThirteen out of 124 patients (10%) had a positive ELISA titer for IgM anti-GM2. Age at onset of symptoms was significantly lower in MMN patients with anti-GM2 IgM. IgM binding to SCs correlated with IgM anti-GM2 titers. We found no correlation between IgM anti-GM2 titers and MN binding or with IgM anti-GM1 titers. IgM binding to SCs decreased upon pre-incubation of serum with soluble GM2, but not with soluble GM1. IgM anti-GM2 binding to SCs correlated with complement activation, as reflected by increased C3 fixation on SCs and C5a formation in the supernatant.Circulating IgM anti-GM2 antibodies define a subgroup of patients with MMN that has an earlier onset of disease. These antibodies probably target SCs specifically and activate complement, similarly as IgM anti-GM1 on MNs. Our data indicate that complement activation by IgM antibodies bound to SCs and MNs underlies MMN pathology.CONCLUSIONCirculating IgM anti-GM2 antibodies define a subgroup of patients with MMN that has an earlier onset of disease. These antibodies probably target SCs specifically and activate complement, similarly as IgM anti-GM1 on MNs. Our data indicate that complement activation by IgM antibodies bound to SCs and MNs underlies MMN pathology. Abstract Background Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of MMN is the presence of IgM antibodies against gangliosides, in particular GM1 and less often GM2. Antibodies against GM1 bind to motor neurons (MNs) and cause damage through complement activation. The involvement of Schwann cells (SCs), expressing GM1 and GM2, in the pathogenesis of MMN is unknown. Methods Combining the data of our 2007 and 2015 combined cross-sectional and follow-up studies in Dutch patients with MMN, we evaluated the presence of IgM antibodies against GM1 and GM2 in serum from 124 patients with MMN and investigated their binding to SCs and complement-activating properties. We also assessed the relation of IgM binding and complement deposition with clinical characteristics. Results Thirteen out of 124 patients (10%) had a positive ELISA titer for IgM anti-GM2. Age at onset of symptoms was significantly lower in MMN patients with anti-GM2 IgM. IgM binding to SCs correlated with IgM anti-GM2 titers. We found no correlation between IgM anti-GM2 titers and MN binding or with IgM anti-GM1 titers. IgM binding to SCs decreased upon pre-incubation of serum with soluble GM2, but not with soluble GM1. IgM anti-GM2 binding to SCs correlated with complement activation, as reflected by increased C3 fixation on SCs and C5a formation in the supernatant. Conclusion Circulating IgM anti-GM2 antibodies define a subgroup of patients with MMN that has an earlier onset of disease. These antibodies probably target SCs specifically and activate complement, similarly as IgM anti-GM1 on MNs. Our data indicate that complement activation by IgM antibodies bound to SCs and MNs underlies MMN pathology. Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of MMN is the presence of IgM antibodies against gangliosides, in particular GM1 and less often GM2. Antibodies against GM1 bind to motor neurons (MNs) and cause damage through complement activation. The involvement of Schwann cells (SCs), expressing GM1 and GM2, in the pathogenesis of MMN is unknown. Combining the data of our 2007 and 2015 combined cross-sectional and follow-up studies in Dutch patients with MMN, we evaluated the presence of IgM antibodies against GM1 and GM2 in serum from 124 patients with MMN and investigated their binding to SCs and complement-activating properties. We also assessed the relation of IgM binding and complement deposition with clinical characteristics. Thirteen out of 124 patients (10%) had a positive ELISA titer for IgM anti-GM2. Age at onset of symptoms was significantly lower in MMN patients with anti-GM2 IgM. IgM binding to SCs correlated with IgM anti-GM2 titers. We found no correlation between IgM anti-GM2 titers and MN binding or with IgM anti-GM1 titers. IgM binding to SCs decreased upon pre-incubation of serum with soluble GM2, but not with soluble GM1. IgM anti-GM2 binding to SCs correlated with complement activation, as reflected by increased C3 fixation on SCs and C5a formation in the supernatant. Circulating IgM anti-GM2 antibodies define a subgroup of patients with MMN that has an earlier onset of disease. These antibodies probably target SCs specifically and activate complement, similarly as IgM anti-GM1 on MNs. Our data indicate that complement activation by IgM antibodies bound to SCs and MNs underlies MMN pathology. Background Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of MMN is the presence of IgM antibodies against gangliosides, in particular GM1 and less often GM2. Antibodies against GM1 bind to motor neurons (MNs) and cause damage through complement activation. The involvement of Schwann cells (SCs), expressing GM1 and GM2, in the pathogenesis of MMN is unknown. Methods Combining the data of our 2007 and 2015 combined cross-sectional and follow-up studies in Dutch patients with MMN, we evaluated the presence of IgM antibodies against GM1 and GM2 in serum from 124 patients with MMN and investigated their binding to SCs and complement-activating properties. We also assessed the relation of IgM binding and complement deposition with clinical characteristics. Results Thirteen out of 124 patients (10%) had a positive ELISA titer for IgM anti-GM2. Age at onset of symptoms was significantly lower in MMN patients with anti-GM2 IgM. IgM binding to SCs correlated with IgM anti-GM2 titers. We found no correlation between IgM anti-GM2 titers and MN binding or with IgM anti-GM1 titers. IgM binding to SCs decreased upon pre-incubation of serum with soluble GM2, but not with soluble GM1. IgM anti-GM2 binding to SCs correlated with complement activation, as reflected by increased C3 fixation on SCs and C5a formation in the supernatant. Conclusion Circulating IgM anti-GM2 antibodies define a subgroup of patients with MMN that has an earlier onset of disease. These antibodies probably target SCs specifically and activate complement, similarly as IgM anti-GM1 on MNs. Our data indicate that complement activation by IgM antibodies bound to SCs and MNs underlies MMN pathology. Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of MMN is the presence of IgM antibodies against gangliosides, in particular GM1 and less often GM2. Antibodies against GM1 bind to motor neurons (MNs) and cause damage through complement activation. The involvement of Schwann cells (SCs), expressing GM1 and GM2, in the pathogenesis of MMN is unknown. Combining the data of our 2007 and 2015 combined cross-sectional and follow-up studies in Dutch patients with MMN, we evaluated the presence of IgM antibodies against GM1 and GM2 in serum from 124 patients with MMN and investigated their binding to SCs and complement-activating properties. We also assessed the relation of IgM binding and complement deposition with clinical characteristics. Thirteen out of 124 patients (10%) had a positive ELISA titer for IgM anti-GM2. Age at onset of symptoms was significantly lower in MMN patients with anti-GM2 IgM. IgM binding to SCs correlated with IgM anti-GM2 titers. We found no correlation between IgM anti-GM2 titers and MN binding or with IgM anti-GM1 titers. IgM binding to SCs decreased upon pre-incubation of serum with soluble GM2, but not with soluble GM1. IgM anti-GM2 binding to SCs correlated with complement activation, as reflected by increased C3 fixation on SCs and C5a formation in the supernatant. Circulating IgM anti-GM2 antibodies define a subgroup of patients with MMN that has an earlier onset of disease. These antibodies probably target SCs specifically and activate complement, similarly as IgM anti-GM1 on MNs. Our data indicate that complement activation by IgM antibodies bound to SCs and MNs underlies MMN pathology. Background Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of MMN is the presence of IgM antibodies against gangliosides, in particular GM1 and less often GM2. Antibodies against GM1 bind to motor neurons (MNs) and cause damage through complement activation. The involvement of Schwann cells (SCs), expressing GM1 and GM2, in the pathogenesis of MMN is unknown. Methods Combining the data of our 2007 and 2015 combined cross-sectional and follow-up studies in Dutch patients with MMN, we evaluated the presence of IgM antibodies against GM1 and GM2 in serum from 124 patients with MMN and investigated their binding to SCs and complement-activating properties. We also assessed the relation of IgM binding and complement deposition with clinical characteristics. Results Thirteen out of 124 patients (10%) had a positive ELISA titer for IgM anti-GM2. Age at onset of symptoms was significantly lower in MMN patients with anti-GM2 IgM. IgM binding to SCs correlated with IgM anti-GM2 titers. We found no correlation between IgM anti-GM2 titers and MN binding or with IgM anti-GM1 titers. IgM binding to SCs decreased upon pre-incubation of serum with soluble GM2, but not with soluble GM1. IgM anti-GM2 binding to SCs correlated with complement activation, as reflected by increased C3 fixation on SCs and C5a formation in the supernatant. Conclusion Circulating IgM anti-GM2 antibodies define a subgroup of patients with MMN that has an earlier onset of disease. These antibodies probably target SCs specifically and activate complement, similarly as IgM anti-GM1 on MNs. Our data indicate that complement activation by IgM antibodies bound to SCs and MNs underlies MMN pathology. Keywords: Multifocal motor neuropathy, Complement, Anti-ganglioside antibodies, IgM anti-GM2, Schwann cells
ArticleNumber	100
Audience	Academic
Author	Bos, Jeroen W. Groen, Ewout J.N. Zekveld, Eva M. Goedee, H. Stephan Huizinga, Ruth van der Pol, W. Ludo Leusen, Jeanette H.W. de Zeeuw, Elisabeth Hack, C. Erik Budding, Kevin van den Berg, Leonard H. Dijkxhoorn, Kim Cats, Elisabeth A. Bloemenkamp, Lauri M. Jacobs, Bart C.
Author_xml	– sequence: 1 givenname: Kevin surname: Budding fullname: Budding, Kevin organization: Center for Translational Immunology, University Medical Center Utrecht – sequence: 2 givenname: Jeroen W. surname: Bos fullname: Bos, Jeroen W. organization: Department of Neurology and Neurosurgery, University Medical Center Utrecht Brain Center – sequence: 3 givenname: Kim surname: Dijkxhoorn fullname: Dijkxhoorn, Kim organization: Center for Translational Immunology, University Medical Center Utrecht – sequence: 4 givenname: Elisabeth surname: de Zeeuw fullname: de Zeeuw, Elisabeth organization: Center for Translational Immunology, University Medical Center Utrecht – sequence: 5 givenname: Lauri M. surname: Bloemenkamp fullname: Bloemenkamp, Lauri M. organization: Center for Translational Immunology, University Medical Center Utrecht, Department of Neurology and Neurosurgery, University Medical Center Utrecht Brain Center – sequence: 6 givenname: Eva M. surname: Zekveld fullname: Zekveld, Eva M. organization: Center for Translational Immunology, University Medical Center Utrecht – sequence: 7 givenname: Ewout J.N. surname: Groen fullname: Groen, Ewout J.N. organization: Department of Neurology and Neurosurgery, University Medical Center Utrecht Brain Center – sequence: 8 givenname: Bart C. surname: Jacobs fullname: Jacobs, Bart C. organization: Department of Neurology, Erasmus MC, University Medical Center, Department of Immunology, Erasmus MC, University Medical Center – sequence: 9 givenname: Ruth surname: Huizinga fullname: Huizinga, Ruth organization: Department of Immunology, Erasmus MC, University Medical Center – sequence: 10 givenname: H. Stephan surname: Goedee fullname: Goedee, H. Stephan organization: Department of Neurology and Neurosurgery, University Medical Center Utrecht Brain Center – sequence: 11 givenname: Elisabeth A. surname: Cats fullname: Cats, Elisabeth A. organization: Department of Neurology, Gelre Hospital – sequence: 12 givenname: Jeanette H.W. surname: Leusen fullname: Leusen, Jeanette H.W. organization: Center for Translational Immunology, University Medical Center Utrecht – sequence: 13 givenname: Leonard H. surname: van den Berg fullname: van den Berg, Leonard H. organization: Department of Neurology and Neurosurgery, University Medical Center Utrecht Brain Center – sequence: 14 givenname: C. Erik surname: Hack fullname: Hack, C. Erik organization: Center for Translational Immunology, University Medical Center Utrecht – sequence: 15 givenname: W. Ludo surname: van der Pol fullname: van der Pol, W. Ludo email: w.l.vanderpol@umcutrecht.nl organization: Department of Neurology and Neurosurgery, University Medical Center Utrecht Brain Center
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/38632654$$D View this record in MEDLINE/PubMed
BookMark	eNp9kktv1DAUhSNURB_wB1ggS2zYpPgRO8kKVRWUkVqxANbWteNkPErsYjutZsF_xzNpUQehyrJsXZ_zydc-p8WR884UxVuCzwlpxMdIaFtXJaZ5MtzicvuiOCF1RUuK2-royf64OI1xgzGjXNBXxTFrBKOCVyfF79Vwg8AlW17d0P1G-c6aiKxDt5CscSmie5vWaJrHZHuvYUSTTz4gZ-bgs2a9RQnCYBL6rtf34BzSZhxjhnUIgkEQo9cWkukWkIEwbpF30aTXxcsexmjePKxnxc8vn39cfi2vv12tLi-uS80bnEpKwUDV8Z40BlRLGYaemK4XTFOiuGj7VoCohQZsalUT1SijNeOMaqYEEHZWrBZu52Ejb4OdIGylByv3BR8GCSFZPRopgNdcdTVjrK2IblTXaNwajlutlOjrzPq0sG5nNZlO5xcKMB5AD0-cXcvB30lCMOX5SzLhwwMh-F-ziUlONu7eDJzxc5QMV4QyjjHP0veLdIB8N-t6n5F6J5cXdYt5Q6t2Bzz_jyqPzkxW59D0NtcPDO-e9vD38o-5yIJmEejgYwyml9qmHAe_a8mOkmC5i6BcIihzBOU-gnKbrfQf6yP9WRNbTDGL3WCC3Pg5uJyJ51x_AEU18GM
CitedBy_id	crossref_primary_10_1016_j_neurol_2024_09_002 crossref_primary_10_1016_j_smim_2025_101956 crossref_primary_10_1097_WCO_0000000000001406 crossref_primary_10_3390_cells14171336 crossref_primary_10_1111_ene_16541
Cites_doi	10.1212/WNL.0000000000010369 10.1111/jns5.12046 10.3233/JND-150080 10.1212/WNL.0b013e3181f0738e 10.1016/j.jns.2007.09.020 10.1002/mus.25266 10.1038/nrneurol.2011.175 10.1093/brain/awf272 10.4103/0028-3886.86549 10.1002/(SICI)1098-1136(199905)26:3<201::AID-GLIA2>3.0.CO;2-M 10.4049/jimmunol.155.6.3049 10.1002/mus.26051 10.1136/jnnp-2013-305755 10.1002/ana.24680 10.1016/S0165-5728(98)00245-8 10.3988/jcn.2018.14.3.401 10.1212/NXG.0000000000000598 10.1016/S0165-5728(01)00266-1 10.1016/S0006-8993(96)01123-7 10.1212/WNL.0b013e3181ff94c2 10.1002/mus.25391 10.1016/0005-2760(94)90034-5 10.1016/j.pediatrneurol.2016.03.017 10.1136/jnnp.2009.202796 10.1016/j.braindev.2019.08.013 10.1212/WNL.45.8.1570 10.1093/brain/123.10.2020 10.1111/jns.12529 10.1016/j.nbd.2013.03.005 10.1007/s00415-014-7354-3 10.1097/WCO.0000000000000607 10.1136/jnnp-2019-321532 10.1002/mus.10122 10.1186/s12974-023-02920-9 10.1136/jnnp.62.6.641 10.1002/mus.21163 10.1212/WNL.0000000000010538 10.1016/j.jneuroim.2010.08.023 10.1111/j.1529-8027.2010.00290.x 10.1016/j.jns.2005.07.009 10.1002/mus.20893 10.1097/WCO.0000000000000605 10.3109/08916930008994083 10.1111/jns5.12011 10.1212/NXI.0000000000000119 10.1046/j.1471-4159.1996.66010303.x 10.1136/jnnp.2005.064816 10.1212/NXI.0000000000001107
ContentType	Journal Article
Copyright	The Author(s) 2024 2024. The Author(s). COPYRIGHT 2024 BioMed Central Ltd.
Copyright_xml	– notice: The Author(s) 2024 – notice: 2024. The Author(s). – notice: COPYRIGHT 2024 BioMed Central Ltd.
DBID	C6C AAYXX CITATION NPM 7X8 5PM DOA
DOI	10.1186/s12974-024-03090-y
DatabaseName	Springer Nature OA Free Journals CrossRef PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals
DatabaseTitle	CrossRef PubMed MEDLINE - Academic
DatabaseTitleList	MEDLINE - Academic PubMed
Database_xml	– sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Medicine
EISSN	1742-2094
EndPage	14
ExternalDocumentID	oai_doaj_org_article_6a575bd7333941c8bd8c09e509cbb6f7 PMC11025174 A790582494 38632654 10_1186_s12974_024_03090_y
Genre	Journal Article
GeographicLocations	Netherlands
GeographicLocations_xml	– name: Netherlands
GroupedDBID	--- 0R~ 29L 2WC 53G 5GY 5VS 7X7 88E 8FI 8FJ AAFWJ AAJSJ AASML AAWTL ABDBF ABUWG ACGFO ACGFS ACIHN ACPRK ACUHS ADBBV ADRAZ ADUKV AEAQA AENEX AFKRA AFPKN AHBYD AHMBA AHYZX ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIJS BAPOH BAWUL BCNDV BENPR BFQNJ BMC BPHCQ BVXVI C6C CCPQU CS3 DIK DU5 E3Z EBD EBLON EBS ESX F5P FYUFA GROUPED_DOAJ GX1 HMCUK HYE IAO IHR INH INR ITC KQ8 M1P M48 M~E O5R O5S OK1 OVT P2P PGMZT PHGZM PHGZT PIMPY PJZUB PPXIY PQQKQ PROAC PSQYO PUEGO RBZ RNS ROL RPM RSV SBL SOJ TR2 TUS UKHRP WOQ WOW XSB ~8M AAYXX AFFHD CITATION ALIPV NPM 7X8 5PM
ID	FETCH-LOGICAL-c580t-22aea4d5f18eab9230af1edf63c21b569f96a676ca0e7b71b8becc3532c3b6a13
IEDL.DBID	DOA
ISICitedReferencesCount	6
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=001204817400002&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	1742-2094
IngestDate	Fri Oct 03 12:50:38 EDT 2025 Tue Nov 04 02:05:47 EST 2025 Sun Nov 09 11:06:12 EST 2025 Tue Nov 11 11:05:40 EST 2025 Tue Nov 04 18:23:42 EST 2025 Mon Jul 21 06:01:38 EDT 2025 Sat Nov 29 04:11:22 EST 2025 Tue Nov 18 21:52:00 EST 2025 Sat Sep 06 07:29:52 EDT 2025
IsDoiOpenAccess	true
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	1
Keywords	Multifocal motor neuropathy Complement Anti-ganglioside antibodies IgM anti-GM2 Schwann cells
Language	English
License	2024. The Author(s). Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
LinkModel	DirectLink
MergedId	FETCHMERGED-LOGICAL-c580t-22aea4d5f18eab9230af1edf63c21b569f96a676ca0e7b71b8becc3532c3b6a13
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
OpenAccessLink	https://doaj.org/article/6a575bd7333941c8bd8c09e509cbb6f7
PMID	38632654
PQID	3041235005
PQPubID	23479
PageCount	14
ParticipantIDs	doaj_primary_oai_doaj_org_article_6a575bd7333941c8bd8c09e509cbb6f7 pubmedcentral_primary_oai_pubmedcentral_nih_gov_11025174 proquest_miscellaneous_3041235005 gale_infotracmisc_A790582494 gale_infotracacademiconefile_A790582494 pubmed_primary_38632654 crossref_citationtrail_10_1186_s12974_024_03090_y crossref_primary_10_1186_s12974_024_03090_y springer_journals_10_1186_s12974_024_03090_y
PublicationCentury	2000
PublicationDate	2024-04-17
PublicationDateYYYYMMDD	2024-04-17
PublicationDate_xml	– month: 04 year: 2024 text: 2024-04-17 day: 17
PublicationDecade	2020
PublicationPlace	London
PublicationPlace_xml	– name: London – name: England
PublicationTitle	Journal of neuroinflammation
PublicationTitleAbbrev	J Neuroinflammation
PublicationTitleAlternate	J Neuroinflammation
PublicationYear	2024
Publisher	BioMed Central BioMed Central Ltd BMC
Publisher_xml	– name: BioMed Central – name: BioMed Central Ltd – name: BMC
References	G Meyer zu Horste (3090_CR49) 2008; 37 C Vedeler (3090_CR45) 1994; 82 JK Kim (3090_CR34) 2018; 14 L Vlam (3090_CR16) 2015; 2 U Rodella (3090_CR52) 2017; 10 B Cavanna (3090_CR44) 1999; 94 I Herraets (3090_CR4) 2020; 95 3090_CR14 IN van Schaik (3090_CR18) 1995; 45 JW Bos (3090_CR25) 2021; 7 EA Cats (3090_CR24) 2010; 75 L Svennerholm (3090_CR29) 1994; 1214 A Pestronk (3090_CR19) 2010; 81 A Chiba (3090_CR28) 1997; 745 Joint Task Force of the E, the PNS (3090_CR23) 2010; 15 GM O’Hanlon (3090_CR20) 2000; 32 AF Hahn (3090_CR6) 2013; 18 H Ishigaki (3090_CR42) 2016; 62 ML Kuijf (3090_CR26) 2005; 239 WZ Yeh (3090_CR12) 2020; 91 AC Stork (3090_CR38) 2014; 261 CL Koski (3090_CR46) 1996; 66 H Maeda (3090_CR41) 2020; 42 L Vlam (3090_CR13) 2011; 8 O Harschnitz (3090_CR10) 2016; 80 I Van Rhijn (3090_CR51) 2000; 123 BA Jongbloed (3090_CR9) 2016; 54 A Pestronk (3090_CR5) 1998; 51 G Lopate (3090_CR37) 2002; 25 MA Kannan (3090_CR35) 2011; 59 E Nobile-Orazio (3090_CR21) 2014; 85 K Beadon (3090_CR1) 2018; 31 DS Regier (3090_CR30) 2016; 13 E Ydens (3090_CR50) 2013; 55 F Galban-Horcajo (3090_CR33) 2015; 2 SK Halstead (3090_CR39) 2023; 28 HJ Willison (3090_CR11) 2002; 125 A Rupp (3090_CR27) 2013; 18 G Paterson (3090_CR31) 1995; 155 EA Cats (3090_CR3) 2010; 75 BC Jacobs (3090_CR40) 1997; 62 N Karbian (3090_CR47) 2023; 20 IJT Herraets (3090_CR8) 2020; 95 E Nobile-Orazio (3090_CR32) 2008; 266 E Nobile-Orazio (3090_CR2) 2001; 115 JM Martinez-Thompson (3090_CR22) 2018; 57 V Lambrecq (3090_CR43) 2009; 39 HS Goedee (3090_CR7) 2018; 31 N Davoust (3090_CR48) 1999; 26 JT Van Asseldonk (3090_CR15) 2006; 77 S Piepers (3090_CR17) 2010; 229 C Fan (3090_CR36) 2017; 55
References_xml	– volume: 95 start-page: e1745 issue: 12 year: 2020 ident: 3090_CR8 publication-title: Neurology doi: 10.1212/WNL.0000000000010369 – volume: 18 start-page: 321 issue: 4 year: 2013 ident: 3090_CR6 publication-title: J Peripher Nerv Syst doi: 10.1111/jns5.12046 – volume: 13 start-page: 663 issue: 1Suppl 1 year: 2016 ident: 3090_CR30 publication-title: Pediatr Endocrinol Rev – volume: 2 start-page: 157 issue: 2 year: 2015 ident: 3090_CR33 publication-title: J Neuromuscul Dis doi: 10.3233/JND-150080 – volume: 51 start-page: S22 issue: 6 Suppl 5 year: 1998 ident: 3090_CR5 publication-title: Neurology – volume: 75 start-page: 818 issue: 9 year: 2010 ident: 3090_CR24 publication-title: Neurology doi: 10.1212/WNL.0b013e3181f0738e – volume: 266 start-page: 156 issue: 1–2 year: 2008 ident: 3090_CR32 publication-title: J Neurol Sci doi: 10.1016/j.jns.2007.09.020 – volume: 55 start-page: 470 issue: 4 year: 2017 ident: 3090_CR36 publication-title: Muscle Nerve doi: 10.1002/mus.25266 – volume: 8 start-page: 48 issue: 1 year: 2011 ident: 3090_CR13 publication-title: Nat Rev Neurol doi: 10.1038/nrneurol.2011.175 – volume: 125 start-page: 2591 issue: Pt 12 year: 2002 ident: 3090_CR11 publication-title: Brain doi: 10.1093/brain/awf272 – volume: 59 start-page: 727 issue: 5 year: 2011 ident: 3090_CR35 publication-title: Neurol India doi: 10.4103/0028-3886.86549 – volume: 26 start-page: 201 issue: 3 year: 1999 ident: 3090_CR48 publication-title: Glia doi: 10.1002/(SICI)1098-1136(199905)26:3<201::AID-GLIA2>3.0.CO;2-M – volume: 155 start-page: 3049 issue: 6 year: 1995 ident: 3090_CR31 publication-title: J Immunol doi: 10.4049/jimmunol.155.6.3049 – volume: 57 start-page: 1000 issue: 6 year: 2018 ident: 3090_CR22 publication-title: Muscle Nerve doi: 10.1002/mus.26051 – volume: 85 start-page: 754 issue: 7 year: 2014 ident: 3090_CR21 publication-title: J Neurol Neurosurg Psychiatry doi: 10.1136/jnnp-2013-305755 – volume: 80 start-page: 71 issue: 1 year: 2016 ident: 3090_CR10 publication-title: Ann Neurol doi: 10.1002/ana.24680 – volume: 94 start-page: 157 issue: 1–2 year: 1999 ident: 3090_CR44 publication-title: J Neuroimmunol doi: 10.1016/S0165-5728(98)00245-8 – volume: 14 start-page: 401 issue: 3 year: 2018 ident: 3090_CR34 publication-title: J Clin Neurol doi: 10.3988/jcn.2018.14.3.401 – volume: 7 start-page: e598 issue: 4 year: 2021 ident: 3090_CR25 publication-title: Neurol Genet doi: 10.1212/NXG.0000000000000598 – volume: 115 start-page: 4 issue: 1–2 year: 2001 ident: 3090_CR2 publication-title: J Neuroimmunol doi: 10.1016/S0165-5728(01)00266-1 – volume: 745 start-page: 32 issue: 1–2 year: 1997 ident: 3090_CR28 publication-title: Brain Res doi: 10.1016/S0006-8993(96)01123-7 – volume: 75 start-page: 1961 issue: 22 year: 2010 ident: 3090_CR3 publication-title: Neurology doi: 10.1212/WNL.0b013e3181ff94c2 – volume: 54 start-page: 1133 issue: 6 year: 2016 ident: 3090_CR9 publication-title: Muscle Nerve doi: 10.1002/mus.25391 – volume: 1214 start-page: 115 issue: 2 year: 1994 ident: 3090_CR29 publication-title: Biochim Biophys Acta doi: 10.1016/0005-2760(94)90034-5 – volume: 62 start-page: 51 year: 2016 ident: 3090_CR42 publication-title: Pediatr Neurol doi: 10.1016/j.pediatrneurol.2016.03.017 – volume: 81 start-page: 726 issue: 7 year: 2010 ident: 3090_CR19 publication-title: J Neurol Neurosurg Psychiatry doi: 10.1136/jnnp.2009.202796 – volume: 42 start-page: 88 issue: 1 year: 2020 ident: 3090_CR41 publication-title: Brain Dev doi: 10.1016/j.braindev.2019.08.013 – volume: 45 start-page: 1570 issue: 8 year: 1995 ident: 3090_CR18 publication-title: Neurology doi: 10.1212/WNL.45.8.1570 – volume: 123 start-page: 2020 issue: Pt 10 year: 2000 ident: 3090_CR51 publication-title: Brain doi: 10.1093/brain/123.10.2020 – volume: 28 start-page: 32 issue: 1 year: 2023 ident: 3090_CR39 publication-title: J Peripher Nerv Syst doi: 10.1111/jns.12529 – volume: 55 start-page: 95 year: 2013 ident: 3090_CR50 publication-title: Neurobiol Dis doi: 10.1016/j.nbd.2013.03.005 – volume: 261 start-page: 1398 issue: 7 year: 2014 ident: 3090_CR38 publication-title: J Neurol doi: 10.1007/s00415-014-7354-3 – volume: 31 start-page: 526 issue: 5 year: 2018 ident: 3090_CR7 publication-title: Curr Opin Neurol doi: 10.1097/WCO.0000000000000607 – volume: 91 start-page: 140 issue: 2 year: 2020 ident: 3090_CR12 publication-title: J Neurol Neurosurg Psychiatry doi: 10.1136/jnnp-2019-321532 – volume: 25 start-page: 828 issue: 6 year: 2002 ident: 3090_CR37 publication-title: Muscle Nerve doi: 10.1002/mus.10122 – volume: 20 start-page: 245 issue: 1 year: 2023 ident: 3090_CR47 publication-title: J Neuroinflammation doi: 10.1186/s12974-023-02920-9 – volume: 62 start-page: 641 issue: 6 year: 1997 ident: 3090_CR40 publication-title: J Neurol Neurosurg Psychiatry doi: 10.1136/jnnp.62.6.641 – volume: 39 start-page: 131 issue: 2 year: 2009 ident: 3090_CR43 publication-title: Muscle Nerve doi: 10.1002/mus.21163 – volume: 95 start-page: e1979 issue: 14 year: 2020 ident: 3090_CR4 publication-title: Neurology doi: 10.1212/WNL.0000000000010538 – volume: 229 start-page: 256 issue: 1–2 year: 2010 ident: 3090_CR17 publication-title: J Neuroimmunol doi: 10.1016/j.jneuroim.2010.08.023 – volume: 15 start-page: 295 issue: 4 year: 2010 ident: 3090_CR23 publication-title: J Peripher Nerv Syst doi: 10.1111/j.1529-8027.2010.00290.x – volume: 239 start-page: 37 issue: 1 year: 2005 ident: 3090_CR26 publication-title: J Neurol Sci doi: 10.1016/j.jns.2005.07.009 – volume: 37 start-page: 3 issue: 1 year: 2008 ident: 3090_CR49 publication-title: Muscle Nerve doi: 10.1002/mus.20893 – volume: 31 start-page: 559 issue: 5 year: 2018 ident: 3090_CR1 publication-title: Curr Opin Neurol doi: 10.1097/WCO.0000000000000605 – volume: 82 start-page: 542 issue: 4 year: 1994 ident: 3090_CR45 publication-title: Immunology – volume: 32 start-page: 133 issue: 2 year: 2000 ident: 3090_CR20 publication-title: Autoimmunity doi: 10.3109/08916930008994083 – volume: 18 start-page: 75 issue: 1 year: 2013 ident: 3090_CR27 publication-title: J Peripher Nerv Syst doi: 10.1111/jns5.12011 – volume: 2 start-page: e119 issue: 4 year: 2015 ident: 3090_CR16 publication-title: Neurol Neuroimmunol Neuroinflamm doi: 10.1212/NXI.0000000000000119 – volume: 66 start-page: 303 issue: 1 year: 1996 ident: 3090_CR46 publication-title: J Neurochem doi: 10.1046/j.1471-4159.1996.66010303.x – volume: 77 start-page: 743 issue: 6 year: 2006 ident: 3090_CR15 publication-title: J Neurol Neurosurg Psychiatry doi: 10.1136/jnnp.2005.064816 – ident: 3090_CR14 doi: 10.1212/NXI.0000000000001107 – volume: 10 start-page: 597 issue: 5 year: 2017 ident: 3090_CR52 publication-title: Dis Model Mech
SSID	ssj0032562
Score	2.42985
Snippet	Background Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important... Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important feature of... Background Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An important... Abstract Background Multifocal motor neuropathy (MMN) is a rare, chronic immune-mediated polyneuropathy characterized by asymmetric distal limb weakness. An...
SourceID	doaj pubmedcentral proquest gale pubmed crossref springer
SourceType	Open Website Open Access Repository Aggregation Database Index Database Enrichment Source Publisher
StartPage	100
SubjectTerms	Analysis Anti-ganglioside antibodies Antibodies Biomedical and Life Sciences Biomedicine Complement IgM anti-GM2 Immunology Multifocal motor neuropathy Neurobiology Neurology Neurosciences Puncture Schwann cells Spine Testing Viral antibodies
SummonAdditionalLinks	– databaseName: SpringerLINK Contemporary 1997-Present dbid: RSV link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3da9UwFA86Rfbi90d1SgTBBw22TZukj1OcCt4hTsfeQpIm2wVpR3un3Af_d89J24udMtC30pyU5OSXc06ak18IeaZs5RwsJVguvWeFTGtmjA0MIl3nPHchjez8hx_l_r46Oqo-jYfC-inbfdqSjJY6TmslXvXgmWTBwKcw3BZI2foyuQLuTuGFDZ8PDif7y8GJ59PxmL_Wm7mgyNT_pz3-zSGdT5Y8t2MaHdHejf_rwk1yfQw86e6AlFvkkm9uk2uLcWv9Dvn54XhBQc1L9m6RxwfbYoYhXTZ0JF_tKf61pTEHMaAPpDDObUcjJyZebbymQ2I5PXAnP0zTUNwW6OFjNTWdp2aEgq-HD3kkV6aYzr26S77uvf3y5j0b72ZgrlTpiuW58aaoy5ApbyxEiakJma-D4DDythRVqIQRUjiTemllZhWChZc8d9wKk_F7ZKtpG_-A0NqFwrk6NRxChaBy6yAI8hUvJEorm5BsGi7tRuJyvD_jm44LGCX0oFcNetVRr3qdkBebOqcDbceF0q8RBRtJpNyOL9ruWI8zWAsDka2tJee8KjJoV61cWnlAoLNWBJmQ54ghjYYBmufMeL4BOokUW3oXqdAUrHaLhOzMJGFCu1nx0wmFGoswC67x7VmvOZKj8RIMZ0LuD6jctJkrAZF4CbXVDK-zTs1LmuVJ5BOHCBCJ66Dqywm2erRk_QVae_hv4o_Idh6RX7BM7pCtVXfmH5Or7vtq2XdP4hT-BXXxRWs priority: 102 providerName: Springer Nature
Title	IgM anti-GM2 antibodies in patients with multifocal motor neuropathy target Schwann cells and are associated with early onset
URI	https://link.springer.com/article/10.1186/s12974-024-03090-y https://www.ncbi.nlm.nih.gov/pubmed/38632654 https://www.proquest.com/docview/3041235005 https://pubmed.ncbi.nlm.nih.gov/PMC11025174 https://doaj.org/article/6a575bd7333941c8bd8c09e509cbb6f7
Volume	21
WOSCitedRecordID	wos001204817400002&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText	1
inHoldings	1
isFullTextHit
isPrint
journalDatabaseRights	– providerCode: PRVADU databaseName: Open Access: BioMedCentral Open Access Titles customDbUrl: eissn: 1742-2094 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0032562 issn: 1742-2094 databaseCode: RBZ dateStart: 20040101 isFulltext: true titleUrlDefault: https://www.biomedcentral.com/search/ providerName: BioMedCentral – providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 1742-2094 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0032562 issn: 1742-2094 databaseCode: DOA dateStart: 20040101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVHPJ databaseName: ROAD: Directory of Open Access Scholarly Resources customDbUrl: eissn: 1742-2094 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0032562 issn: 1742-2094 databaseCode: M~E dateStart: 20040101 isFulltext: true titleUrlDefault: https://road.issn.org providerName: ISSN International Centre – providerCode: PRVPQU databaseName: Health & Medical Collection customDbUrl: eissn: 1742-2094 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0032562 issn: 1742-2094 databaseCode: 7X7 dateStart: 20090101 isFulltext: true titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Central customDbUrl: eissn: 1742-2094 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0032562 issn: 1742-2094 databaseCode: BENPR dateStart: 20090101 isFulltext: true titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: Publicly Available Content Database customDbUrl: eissn: 1742-2094 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0032562 issn: 1742-2094 databaseCode: PIMPY dateStart: 20090101 isFulltext: true titleUrlDefault: http://search.proquest.com/publiccontent providerName: ProQuest – providerCode: PRVAVX databaseName: SpringerLINK Contemporary 1997-Present customDbUrl: eissn: 1742-2094 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0032562 issn: 1742-2094 databaseCode: RSV dateStart: 20041201 isFulltext: true titleUrlDefault: https://link.springer.com/search?facet-content-type=%22Journal%22 providerName: Springer Nature
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELagIMQF8SZQVkZC4gBWkzixnWOLWqjErlYtVMvJsh2broSyaLMF7YH_zoyTXTVFKhcuURI_5MyM_Y3j8WdCXitbOQdTCZZL71kh05oZYwMDT9c5z11IIzv_2Sc5majZrJpeOuoLY8I6euBOcHvCgENha8k5r4rMKVsrl1YecM5ZK0LcR57KajOZ6sZgDkCeb7bIKLHXAqrJggEeMVxSSNl6AEORrf_vMfkSKF0NmLyyahrB6Og-udd7kXS_a_0DcsM3D8mdcb9O_oj8Pv42piCzOfswzuONXWC4IJ03tGdSbSn-gqUxoDAgoFFQ2mJJI8ElnlO8pl2UOD11579M01D8x99CZTU1S09Nr1dfdxV5ZEqmGJu9eky-HB1-fv-R9QctMFeqdMXy3HhT1GXIlDcWXL7UhMzXQXBQoy1FFSphhBTOpF5amVmFmuclzx23wmT8CdlpFo1_RmjtQuFcnRoOuB9Ubh14NL7ihcTcyiYk28hdu56FHA_D-K7jbEQJ3elKg6501JVeJ-TttsyPjoPj2twHqM5tTuTPji_AqnRvVfpfVpWQN2gMGns5NM-ZfrMCfCTyZel95DVTMHUtErI7yAm90w2SX23MSWMShrQ1fnHRao5MZ7yEUTAhTzvz2raZKwFudQml1cDwBh81TGnm55EcHNw5ZKGDou82Nqr7Yam9RmrP_4fUXpC7eexjBcvkLtlZLS_8S3Lb_VzN2-WI3JQzGa9qRG4dHE6mJ6PYa-FpejyefoWnk9OzP6juRt0
linkProvider	Directory of Open Access Journals
linkToHtml	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9QwELagIODCmxIoYCQkDtQiiRPbORZEacXuCtFS9WbZjtOuVGVRsgXtgf_OjJOsSEGV4BbF48gez8uZ8WdCXilbOAdbCZZK71km45IZYysGka5znrsqDuj8RxM5m6nj4-JzfyisHardh5RksNRBrZV424JnkhkDn8IwLRCz1VVyLQOPhYj5Xw6OBvvLwYmnw_GYv_YbuaCA1P-nPf7NIV0slryQMQ2OaPfO_03hLrndB550p5OUe-SKr--TG9M-tf6A_Nw_mVJg85x9nKbhwS6wwpDOa9qDr7YU_9rSUINYoQ-ksM6LhgZMTLzaeEW7wnJ64E5_mLqmmBZo4WMlNY2nphcFX3Yf8giuTLGce_mQfN39cPh-j_V3MzCXq3jJ0tR4k5V5lShvLESJsakSX1aCw8rbXBRVIYyQwpnYSysTq1BYeM5Tx60wCX9ENupF7R8TWroqc66MDYdQoVKpdRAE-YJnEqmVjUgyLJd2PXA53p9xpsMGRgnd8VUDX3Xgq15F5M26z7cOtuNS6ncoBWtKhNwOLxbNie41WAsDka0tJee8yBIYV6lcXHgIuJy1opIReY0ypNEwwPCc6c83wCQRYkvvIBSagt1uFpGtESUotBs1vxykUGMTVsHVfnHeao7gaDwHwxmRzU4q12PmSkAknkNvNZLX0aTGLfX8NOCJQwSIwHXQdXsQW91bsvYSrj35N_IX5Obe4XSiJ_uzT0_JrTRoQcYSuUU2ls25f0auu-_Leds8D-r8C7gVSE8
linkToPdf	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3db9MwELdgoIkXvgeFAUZC4gGsJXFiO4_jozCxVpMG094s27G3Siidmg7UB_537pykWgaahHir6nNkX37nO-fOPxPyStnSOdhKsEx6z3KZVMwYGxhEus557kIS2fmP9uV0qo6Py4MLp_hjtXufkmzPNCBLU73cOatCa-JK7DTgpWTOwL8wTBEkbHWd3MixkB7364dH_VrMwaFn_VGZv_YbuKPI2v_n2nzBOV0unLyUPY1OaXzn_6dzl9zuAlK62yLoHrnm6_tkc9Kl3B-QX3snEwrqn7FPkyz-sHOsPKSzmnakrA3Fr7k01iYG9I0U3v98QSNXJl55vKJtwTk9dKc_TV1TTBc08LCKmoWnpoOIr9oHeSRdpljmvXxIvo0_fn3_mXV3NjBXqGTJssx4k1dFSJU3FqLHxITUV0FwQIQtRBlKYYQUziReWplahSDiBc8ct8KkfIts1PPaPya0ciF3rkoMhxAiqMw6CI58yXOJ0sqOSNq_Ou06QnO8V-O7jhsbJXSrVw161VGvejUib9Z9zlo6jyul3yEi1pJIxR3_mC9OdGfZWhiIeG0lOedlnsK4KuWS0kMg5qwVQY7Ia8STxgUDhudMd-4BJonUW3oXKdIU7ILzEdkeSIKhu0Hzyx6RGpuwOq728_NGcyRN4wUsqCPyqEXoesxcCYjQC-itBtgdTGrYUs9OI884RIZIaAdd3_YQ1t0K11yhtSf_Jv6CbB58GOv9vemXp-RWFo0gZ6ncJhvLxbl_Rm66H8tZs3geLfs3dbBRMw
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=IgM+anti-GM2+antibodies+in+patients+with+multifocal+motor+neuropathy+target+Schwann+cells+and+are+associated+with+early+onset&rft.jtitle=Journal+of+neuroinflammation&rft.au=Budding%2C+Kevin&rft.au=Bos%2C+Jeroen+W.&rft.au=Dijkxhoorn%2C+Kim&rft.au=de+Zeeuw%2C+Elisabeth&rft.date=2024-04-17&rft.pub=BioMed+Central&rft.eissn=1742-2094&rft.volume=21&rft_id=info:doi/10.1186%2Fs12974-024-03090-y&rft_id=info%3Apmid%2F38632654&rft.externalDocID=PMC11025174
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1742-2094&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1742-2094&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1742-2094&client=summon