Guillain-Barré syndrome: expanding the concept of molecular mimicry

Jon D. Laman; Ruth Huizinga; Geert-Jan Boons; Bart C. Jacobs

doi:10.1016/j.it.2022.02.003

Guillain-Barré syndrome: expanding the concept of molecular mimicry

Jon D. Laman, Ruth Huizinga, Geert-Jan Boons, Bart C. Jacobs

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

Guillain-Barré syndrome (GBS) is a rapidly progressive, monophasic, and potentially devastating immune-mediated neuropathy in humans. Preceding infections trigger the production of cross-reactive antibodies against gangliosides concentrated in human peripheral nerves. GBS is elicited by at least five distinct common bacterial and viral pathogens, speaking to the notion of polymicrobial disease causation. This opinion emphasizes that GBS is the best-supported example of true molecular mimicry at the B cell level. Moreover, we argue that mechanistically, single and multiplexed microbial carbohydrate epitopes induce IgM, IgA, and IgG subclasses in ways that challenge the classic concept of thymus-dependent (TD) versus thymus-independent (TI) antibody responses in GBS. Finally, we discuss how GBS can be exemplary for driving innovation in diagnostics and immunotherapy for other antibody-driven neurological diseases.

Original language	English
Pages (from-to)	296-308
Number of pages	13
Journal	Trends in Immunology
Volume	43
Issue number	4
DOIs	https://doi.org/10.1016/j.it.2022.02.003
Publication status	Published - 1 Apr 2022

Bibliographical note

Funding Information:
This work was supported by the Dutch MS Research Foundation (J.D.L.) and the Zabawas Foundation (J.D.L.). B.C.J. was supported by Prinses Beatrix Spierfonds , GBS-CIDP Foundation International , Annexon, CSL-Behring, Grifols, and Hansa Biopharma. R.H. was funded by GBS-CIDP Foundation International and the T2B collaboration project funded by a PPP Allowance made available by Top Sector Life Sciences & Health to Samenwerkende Gezondheidsfondsen (SGF) under project number LSHM18055-SGF to stimulate public-private partnerships and cofinancing by health foundations that are part of the SGF. G.J.B. was funded by the National Institute of General Medical Sciences, National Institutes of Health (grant U01GM120408). The authors thank Margot van der Maarel for a first version of Table 1 and Anna Sieben for artwork in several figures.

Publisher Copyright:
© 2022 Elsevier Ltd

Keywords

Antibody Formation
Autoantibodies
Gangliosides
Guillain-Barre Syndrome/etiology
Humans
Immunoglobulin G
Molecular Mimicry

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.it.2022.02.003

PIIS147149062200028XFinal published version, 1.91 MBLicence: Taverne

Cite this

@article{377f46f3331948c3903dbf7aba5ce43b,

title = "Guillain-Barr{\'e} syndrome: expanding the concept of molecular mimicry",

abstract = "Guillain-Barr{\'e} syndrome (GBS) is a rapidly progressive, monophasic, and potentially devastating immune-mediated neuropathy in humans. Preceding infections trigger the production of cross-reactive antibodies against gangliosides concentrated in human peripheral nerves. GBS is elicited by at least five distinct common bacterial and viral pathogens, speaking to the notion of polymicrobial disease causation. This opinion emphasizes that GBS is the best-supported example of true molecular mimicry at the B cell level. Moreover, we argue that mechanistically, single and multiplexed microbial carbohydrate epitopes induce IgM, IgA, and IgG subclasses in ways that challenge the classic concept of thymus-dependent (TD) versus thymus-independent (TI) antibody responses in GBS. Finally, we discuss how GBS can be exemplary for driving innovation in diagnostics and immunotherapy for other antibody-driven neurological diseases.",

keywords = "Antibody Formation, Autoantibodies, Gangliosides, Guillain-Barre Syndrome/etiology, Humans, Immunoglobulin G, Molecular Mimicry",

author = "Laman, {Jon D.} and Ruth Huizinga and Geert-Jan Boons and Jacobs, {Bart C.}",

note = "Funding Information: This work was supported by the Dutch MS Research Foundation (J.D.L.) and the Zabawas Foundation (J.D.L.). B.C.J. was supported by Prinses Beatrix Spierfonds , GBS-CIDP Foundation International , Annexon, CSL-Behring, Grifols, and Hansa Biopharma. R.H. was funded by GBS-CIDP Foundation International and the T2B collaboration project funded by a PPP Allowance made available by Top Sector Life Sciences & Health to Samenwerkende Gezondheidsfondsen (SGF) under project number LSHM18055-SGF to stimulate public-private partnerships and cofinancing by health foundations that are part of the SGF. G.J.B. was funded by the National Institute of General Medical Sciences, National Institutes of Health (grant U01GM120408). The authors thank Margot van der Maarel for a first version of Table 1 and Anna Sieben for artwork in several figures. Publisher Copyright: {\textcopyright} 2022 Elsevier Ltd",

year = "2022",

month = apr,

day = "1",

doi = "10.1016/j.it.2022.02.003",

language = "English",

volume = "43",

pages = "296--308",

journal = "Trends in Immunology",

issn = "1471-4906",

publisher = "Elsevier Ltd",

number = "4",

}

TY - JOUR

T1 - Guillain-Barré syndrome

T2 - expanding the concept of molecular mimicry

AU - Laman, Jon D.

AU - Huizinga, Ruth

AU - Boons, Geert-Jan

AU - Jacobs, Bart C.

N1 - Funding Information: This work was supported by the Dutch MS Research Foundation (J.D.L.) and the Zabawas Foundation (J.D.L.). B.C.J. was supported by Prinses Beatrix Spierfonds , GBS-CIDP Foundation International , Annexon, CSL-Behring, Grifols, and Hansa Biopharma. R.H. was funded by GBS-CIDP Foundation International and the T2B collaboration project funded by a PPP Allowance made available by Top Sector Life Sciences & Health to Samenwerkende Gezondheidsfondsen (SGF) under project number LSHM18055-SGF to stimulate public-private partnerships and cofinancing by health foundations that are part of the SGF. G.J.B. was funded by the National Institute of General Medical Sciences, National Institutes of Health (grant U01GM120408). The authors thank Margot van der Maarel for a first version of Table 1 and Anna Sieben for artwork in several figures. Publisher Copyright: © 2022 Elsevier Ltd

PY - 2022/4/1

Y1 - 2022/4/1

N2 - Guillain-Barré syndrome (GBS) is a rapidly progressive, monophasic, and potentially devastating immune-mediated neuropathy in humans. Preceding infections trigger the production of cross-reactive antibodies against gangliosides concentrated in human peripheral nerves. GBS is elicited by at least five distinct common bacterial and viral pathogens, speaking to the notion of polymicrobial disease causation. This opinion emphasizes that GBS is the best-supported example of true molecular mimicry at the B cell level. Moreover, we argue that mechanistically, single and multiplexed microbial carbohydrate epitopes induce IgM, IgA, and IgG subclasses in ways that challenge the classic concept of thymus-dependent (TD) versus thymus-independent (TI) antibody responses in GBS. Finally, we discuss how GBS can be exemplary for driving innovation in diagnostics and immunotherapy for other antibody-driven neurological diseases.

AB - Guillain-Barré syndrome (GBS) is a rapidly progressive, monophasic, and potentially devastating immune-mediated neuropathy in humans. Preceding infections trigger the production of cross-reactive antibodies against gangliosides concentrated in human peripheral nerves. GBS is elicited by at least five distinct common bacterial and viral pathogens, speaking to the notion of polymicrobial disease causation. This opinion emphasizes that GBS is the best-supported example of true molecular mimicry at the B cell level. Moreover, we argue that mechanistically, single and multiplexed microbial carbohydrate epitopes induce IgM, IgA, and IgG subclasses in ways that challenge the classic concept of thymus-dependent (TD) versus thymus-independent (TI) antibody responses in GBS. Finally, we discuss how GBS can be exemplary for driving innovation in diagnostics and immunotherapy for other antibody-driven neurological diseases.

KW - Antibody Formation

KW - Autoantibodies

KW - Gangliosides

KW - Guillain-Barre Syndrome/etiology

KW - Humans

KW - Immunoglobulin G

KW - Molecular Mimicry

UR - http://www.scopus.com/inward/record.url?scp=85125646795&partnerID=8YFLogxK

U2 - 10.1016/j.it.2022.02.003

DO - 10.1016/j.it.2022.02.003

M3 - Article

C2 - 35256276

SN - 1471-4906

VL - 43

SP - 296

EP - 308

JO - Trends in Immunology

JF - Trends in Immunology

IS - 4

ER -

Guillain-Barré syndrome: expanding the concept of molecular mimicry

Abstract

Bibliographical note

Keywords

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this