The Neuroimmunology of Guillain-Barré Syndrome and the Potential Role of an Aging Immune System

Overview

Journal Front Aging Neurosci

Specialty Geriatrics

Date 2021 Feb 15

PMID 33584245

Citations 13

Authors

Kathleen M Hagen

Shalina S Ousman

Affiliations

Soon will be listed here.

Abstract

Guillain-Barré syndrome (GBS) is a paralyzing autoimmune condition affecting the peripheral nervous system (PNS). Within GBS there are several variants affecting different aspects of the peripheral nerve. In general, there appears to be a role for T cells, macrophages, B cells, and complement in initiating and perpetuating attacks on gangliosides of Schwann cells and axons. Of note, GBS has an increased prevalence and severity with increasing age. In addition, there are alterations in immune cell functioning that may play a role in differences in GBS with age alongside general age-related declines in reparative processes (e.g., delayed de-differentiation of Schwann cells and decline in phagocytic ability of macrophages). The present review will explore the immune response in GBS as well as in animal models of several variants of the disorder. In addition, the potential involvement of an aging immune system in contributing to the increased prevalence and severity of GBS with age will be theorized.

Citing Articles

Anti-sulfatide antibody-positive Guillain-Barré syndrome in adults following off-craniotomy for cerebellar contusion: A case report.

Min X, Feng H, Zhao R, Guo Z, Su H Medicine (Baltimore). 2025; 103(52):e40970.

PMID: 39969334 PMC: 11688002. DOI: 10.1097/MD.0000000000040970.

The Role of Phytochemicals in Managing Neuropathic Pain: How Much Progress Have We Made?.

Sic A, Manzar A, Knezevic N Nutrients. 2025; 16(24.

PMID: 39770963 PMC: 11678138. DOI: 10.3390/nu16244342.

Hernandez E, Dominguez D, Medina-Rioja R, Martinez-Angeles V, Carlos Lopez-Hernandez J Cureus. 2024; 16(7):e65201.

PMID: 39176336 PMC: 11340779. DOI: 10.7759/cureus.65201.

A retrospective analysis of the clinical profile and factors associated with mortality and poor hospital outcomes in adult Guillain-Barre syndrome patients.

Tewedaj Z, Huluka D, Kebede Y, Abebe A, Hussen M, Mohammed B Sci Rep. 2024; 14(1):15520.

PMID: 38969647 PMC: 11226644. DOI: 10.1038/s41598-024-65265-0.

Guillain-Barre syndrome and link with COVID-19 infection and vaccination: a review of literature.

Valaparla V, Rane S, Patel C, Li X Front Neurol. 2024; 15:1396642.

PMID: 38899056 PMC: 11185933. DOI: 10.3389/fneur.2024.1396642.

References

Rampoldi F, Ullrich L, Prinz I . Revisiting the Interaction of γδ T-Cells and B-Cells. Cells. 2020; 9(3). PMC: 7140609. DOI: 10.3390/cells9030743. View

Ho T, Willison H, Nachamkin I, Li C, Veitch J, Ung H . Anti-GD1a antibody is associated with axonal but not demyelinating forms of Guillain-Barré syndrome. Ann Neurol. 1999; 45(2):168-73. DOI: 10.1002/1531-8249(199902)45:2<168::aid-ana6>3.0.co;2-6. View

DeFrancesco-Lisowitz A, Lindborg J, Niemi J, Zigmond R . The neuroimmunology of degeneration and regeneration in the peripheral nervous system. Neuroscience. 2014; 302:174-203. PMC: 4366367. DOI: 10.1016/j.neuroscience.2014.09.027. View

Kracun I, Rosner H, Drnovsek V, Heffer-Lauc M, Cosovic C, Lauc G . Human brain gangliosides in development, aging and disease. Int J Dev Biol. 1991; 35(3):289-95. View

Hartung H, Schafer B, Heininger K, Stoll G, Toyka K . The role of macrophages and eicosanoids in the pathogenesis of experimental allergic neuritis. Serial clinical, electrophysiological, biochemical and morphological observations. Brain. 1988; 111 ( Pt 5):1039-59. DOI: 10.1093/brain/111.5.1039. View

Li S, Jin T, Zhang H, Yu H, Meng F, Quezada H . Circulating Th17, Th22, and Th1 cells are elevated in the Guillain-Barré syndrome and downregulated by IVIg treatments. Mediators Inflamm. 2014; 2014:740947. PMC: 4036596. DOI: 10.1155/2014/740947. View

Lim M, Lee J, Park J, Jhun J, Moon Y, Cho M . Increased Th17 differentiation in aged mice is significantly associated with high IL-1β level and low IL-2 expression. Exp Gerontol. 2013; 49:55-62. DOI: 10.1016/j.exger.2013.10.006. View

Terryberry J, Thor G, Peter J . Autoantibodies in neurodegenerative diseases: antigen-specific frequencies and intrathecal analysis. Neurobiol Aging. 1998; 19(3):205-16. DOI: 10.1016/s0197-4580(98)00049-9. View

Griffin J, Li C, Ho T, Xue P, Macko C, Gao C . Guillain-Barré syndrome in northern China. The spectrum of neuropathological changes in clinically defined cases. Brain. 1995; 118 ( Pt 3):577-95. DOI: 10.1093/brain/118.3.577. View

10.

McGonigal R, Cunningham M, Yao D, Barrie J, Sankaranarayanan S, Fewou S . C1q-targeted inhibition of the classical complement pathway prevents injury in a novel mouse model of acute motor axonal neuropathy. Acta Neuropathol Commun. 2016; 4:23. PMC: 4776408. DOI: 10.1186/s40478-016-0291-x. View

11.

OHanlon G, Humphreys P, Goldman R, Halstead S, Bullens R, Plomp J . Calpain inhibitors protect against axonal degeneration in a model of anti-ganglioside antibody-mediated motor nerve terminal injury. Brain. 2003; 126(Pt 11):2497-509. DOI: 10.1093/brain/awg254. View

12.

Yoshii F, Shinohara Y . Impaired interleukin-2 response of mononuclear cells in Guillain-Barré syndrome. Eur J Neurol. 2000; 7(3):303-7. DOI: 10.1046/j.1468-1331.2000.00072.x. View

13.

Phongsisay V, Susuki K, Matsuno K, Yamahashi T, Okamoto S, Funakoshi K . Complement inhibitor prevents disruption of sodium channel clusters in a rabbit model of Guillain-Barré syndrome. J Neuroimmunol. 2008; 205(1-2):101-4. DOI: 10.1016/j.jneuroim.2008.09.016. View

14.

Chiba A, Kusunoki S, Shimizu T, Kanazawa I . Serum IgG antibody to ganglioside GQ1b is a possible marker of Miller Fisher syndrome. Ann Neurol. 1992; 31(6):677-9. DOI: 10.1002/ana.410310619. View

15.

Azuma T, Matsubara T, Shima Y, Haeno S, Fujimoto T, Tone K . Neurosteroids in cerebrospinal fluid in neurologic disorders. J Neurol Sci. 1993; 120(1):87-92. DOI: 10.1016/0022-510x(93)90030-3. View

16.

Aliprantis A, Mulder L, Zychlinsky A, Lang R . Do macrophages kill through apoptosis?. Immunol Today. 1996; 17(12):573-6. DOI: 10.1016/s0167-5699(96)10071-2. View

17.

Scheib J, Hoke A . An attenuated immune response by Schwann cells and macrophages inhibits nerve regeneration in aged rats. Neurobiol Aging. 2016; 45:1-9. DOI: 10.1016/j.neurobiolaging.2016.05.004. View

18.

Haynes L, Eaton S, Swain S . The defects in effector generation associated with aging can be reversed by addition of IL-2 but not other related gamma(c)-receptor binding cytokines. Vaccine. 2000; 18(16):1649-53. DOI: 10.1016/s0264-410x(99)00501-0. View

19.

Pilartz M, Jess T, Indefrei D, Schroder J . Adoptive transfer-experimental allergic neuritis in newborn Lewis rats results in inflammatory infiltrates, mast cell activation, and increased Ia expression with only minor nerve fiber degeneration. Acta Neuropathol. 2002; 104(5):513-24. DOI: 10.1007/s00401-002-0586-9. View

20.

Buttner R, Schulz A, Reuter M, Akula A, Mindos T, Carlstedt A . Inflammaging impairs peripheral nerve maintenance and regeneration. Aging Cell. 2018; 17(6):e12833. PMC: 6260910. DOI: 10.1111/acel.12833. View