Human Vaccines & Immunotherapeutics

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Progress in Guillain–Barré syndrome

immunotherapy—A narrative review of new
strategies in recent years

Jiajia Yao, Rumeng Zhou, Yue Liu & Zuneng Lu

To cite this article: Jiajia Yao, Rumeng Zhou, Yue Liu & Zuneng Lu (2023) Progress
in Guillain–Barré syndrome immunotherapy—A narrative review of new strategies
in recent years, Human Vaccines & Immunotherapeutics, 19:2, 2215153, DOI:
10.1080/21645515.2023.2215153

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HUMAN VACCINES & IMMUNOTHERAPEUTICS
2023, VOL. 19, NO. 2, 2215153
https://doi.org/10.1080/21645515.2023.2215153

REVIEW

Progress in Guillain–Barré syndrome immunotherapy—A narrative review of new

strategies in recent years
Jiajia Yao, Rumeng Zhou, Yue Liu, and Zuneng Lu
Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China

ABSTRACT ARTICLE HISTORY

Guillain – Barré syndrome (GBS) is an immune-mediated neuropathy, the pathology of which is not clear. Received 12 March 2023
Both cellular and humoral immunity are involved in the occurrence of the disease, and molecular mimicry Revised 3 May 2023
is currently the most widely recognized pathogenesis. Intravenous immunoglobulin (IVIg) and plasma Accepted 15 May 2023
exchange (PE) have been proven to be effective in improving the prognosis of patients with GBS, but KEYWORDS
there has been no progress in the treatment of the disease or strategies to improve the prognosis. New Guillain–Barré syndrome;
treatment strategies for GBS are mostly immunotherapies, including treatment against antibodies, treatment; complement
complement pathways, immune cells and cytokines. Some of the new strategies are being investigated pathway; immunotherapy
in clinical trials, but none of them have been approved for the treatment of GBS. Here, we summarized
the current therapies for GBS, and new immunotherapies for GBS according to pathogenesis.

Introduction
Guillain–Barré syndrome (GBS) is an immune-mediated neu­
ropathy that is the most common cause of acute flaccid paraly­
sis and affects approximately 100,000 people per year
worldwide. Antecedent events are often found 4 weeks before
clinical syndromes appear in GBS patients, such as surgery or
infection and Campylobacter jejuni, Haemophilus influenzae,
cytomegalovirus, Zika virus and Japanese encephalitis virus are
widely discussed.1–7
Depending on the different sites of the immune response,
GBS is generally divided into demyelinating and axonal sub­
types. Acute inflammatory demyelinating polyradiculoneuropa­
thy (AIDP) is characterized by the demyelination of peripheral
nerves and infiltration of inflammatory cells, with subsequent
axonal damage. Antibodies can be detected on Schwann cells,
and AIDP is the most common subtype in Western countries.8,9
Antigenic epitopes of bacteria and viruses are presented to
T cells by activated macrophages, causing the cross reactivity
of T cells. Activated T cells promote the release of cytokines and
free radicals, disrupt the blood nerve barrier and damage mye­
lin, ultimately leading to acute demyelination syndrome.10
Experimental autoimmune neuritis (EAN) is an animal model
of AIDP that uses myelin epitopes P0 or P2 as major antigens to
induce T-cell-mediated neuritis.1,11
Acute motor axonal neuropathy (AMAN) is the second
most common subtype of GBS. AMAN presents as primary
axonal injury with antibody and membrane attack complex
(MAC) deposition in nodes of Ranvier without obvious
inflammatory cell infiltration or demyelination.1,12–14
Antibodies related to AMAN include anti-GM1 and anti-
GD1a antibodies.14–17 In AMAN patients related to
Campylobacter jejuni, the gangliosides of the peripheral nerves
are similar in structure to the lipo-oligosaccharides of
Campylobacter jejuni. This suggests that the pathogenic
mechanism of AMAN may be the cross-reaction of homolo­
gous epitopes between bacterial lipo-oligosaccharides and per­
ipheral motor axon gangliosides.18–21
Miller-Fisher syndrome (MFS) is a variation of GBS, and
the clinical features of MFS are facial muscle weakness and
ataxia. Most MFS patients have anti-GQ1b antibodies, imply­
ing a potential role for ganglioside antibodies in disease patho­
genesis or as reliable diagnostic biomarkers.22–24 Anti-GQ1b
antibodies have been proven to activate complement at the
neuromuscular junction in vitro, and complement activation is
thought to be the primary pathogenic mechanism of MFS.25
Inflammatory cells and inflammatory factors play an impor­
tant role in the pathogenesis of GBS. Macrophages play a dual
role in the pathogenesis of GBS. Proinflammatory macrophages
(M1) and anti-inflammatory macrophages (M2) play a decisive
role in the initiation and development of GBS and EAN. M1
macrophages can promote the destruction of the blood-nerve
barrier, induce the production of cytokines and chemokines,
promote Th1 polarization, and eventually lead to demyelination
of peripheral nerves. M2 macrophages play a protective role in
the course of disease; they can promote T-cell apoptosis, remove
myelin and axon fragments, inhibit inflammation, and promote
the regeneration of axons and myelin.26,27
T-cell subtypes are also involved in the pathogenesis of
GBS. The imbalance between Th1 and Th2 responses contri­
butes to the pathogenesis of GBS.28–30 Th1 responses are
thought to provoke disease by activating and recruiting macro­
phages to sites in peripheral nerves, subsequently leading to
nerve damage induced by the direct action of macrophages or
by toxic and inflammatory substances released in situ. On the
other hand, the Th2 response acts as a suppressor and regu­
lator of the Th1 pathway and therefore may have the resolving

CONTACT Zuneng Lu lzn196480@126.com Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
© 2023 The Author(s). Published with license by Taylor & Francis Group, LLC.
This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/),
which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way. The
terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.
2 J. YAO ET AL.

Table 1. New therapies used for treatment of GBS in recent years.

Species Therapy Type Pathway or approach Year/author
Rat PR-957 Original article T cell and cytokine regulation 2017/Liu H 67
Rabbit IdeS Original article Cleaved antibodies 2017/Wang Y 51
Rat Fingolimod Original article Inflammatory cells (macrophages and T cells) 2017/Ambrosius B 74
Rat cyclo-DPAKKR Original article p75NTR pathway 2017/Gonsalvez DG 77
Rat 4-AP Original article Not clear 2017/Moriguchi K 78
Human Eculizumab Clinical trial Complement pathway 2018/Misawa S 54
Rat Decitabine (DAC) Original article Treg cell induction 2018/Fagone P 59
Rat 2-deoxy-D glucose (2-DG) Original article glycolytic pathway 2018/Liu RT 60
Rat Bifidobacterium Original article T cell regulation 2018/Shi P 62
Rat ZSTK474 Original article T cell and cytokine regulation 2018/Chen X 69
Rat Vasoactive intestinal peptide (VIP) Original article Inflammatory cells regulation 2018/Jiao H 73
Rat Dimethyl fumarate(DMF) Original article Inflammatory cells (macrophages and T cells) 2019/Pitarokoili K 58
Rat TLCK Original article Thrombin-PAR1 pathway 2019/Shavit-Stein E 75
Human Second course of IVIg Retrospective study Immune regulation 2020/Verboon C 42
Mouse Fasudil Original article Inflammatory cells (macrophages and T cells) 2020/Zhao Y 61
Human Second course of IVIg Clinical trial Immune regulation 2021/Walgaard C 43
Mouse Ginkgolide Original article T cell and cytokine regulation 2021/Li C 68
Rat Ginsenoside Rd Original article Monocyte modulation 2021/Ren K 72
Rat Nanoparticles (NPs) Original article Inflammatory cells regulation 2022/Elahi E 71
Rat Bifidobacterium Original article PD-1 signaling 2023/Shi P 63

effect observed in the recovery phase of GBS and EAN.31–33
Recently, IL-17 and Th17 cells have been found to play an
important role in many immune diseases, and Treg cells have
a suppressive effect on inflammation.34 In the acute phase of
the clinical course of GBS, the number and ratio of CD4+CD25
+ T cells decrease, but this decrease is reversible.35 Another
study found that regulatory T cells (Tregs) from GBS patients
and Tregs from healthy controls showed equal expression of
FoxP-3 mRNA, and their ability to suppress the proliferation
and cytokine secretion of CD4+ effector T cells was unim­
paired in GBS patients.36 Furthermore, adoptive infusion of
autologous CD4+CD25+ Treg cells can reduce inflammatory
cell infiltration of the sciatic nerve in EAN rats.37
Cytokines are small active proteins secreted by immune
cells and some nonimmune cells that have several functions,
such as regulating cell growth and differentiation, modulating
the immune response, and participating in the inflammatory
response. Proinflammatory cytokines such as interleukin (IL)-
1β, IL-6, IL-12, tumor necrosis factor (TNF)-α, interferon
(IFN)-γ, etc., damage myelin by recruiting effector cells to
peripheral nerves and promoting the in situ release of toxic
substances. Anti-inflammatory cytokines, such as IL-4 and IL-
10, inhibit disease progression or promote myelin repair by
exerting anti-inflammatory effects.38
Along with more studies on the pathogenesis of GBS, new
strategies targeting at different points in the treatment of the
disease have emerged. In this narrative review, we summarize
the new approaches of classical therapies and new strategies in
both animal models and clinical practice to identify potential
therapies for GBS patients.
Materials and methods
Articles published between 2017 and 2022 were included in
our research, and clinical trials, original articles, retrospective
studies and systematic reviews in MEDLINE via PubMed
interface and Cochrane Library were all carefully examined.
Both animal experiments and human studies were included.
Key words for searching included Guillain – Barré syndrome,
treatment/therapy, experimental autoimmune neuritis, Miller-
Fisher syndrome, etc. Clinical trials that were not completed
were excluded. Titles and abstracts of papers were screened by
reviewers to identify whether they met the criteria of the
review. All references were examined for background informa­
tion and potentially relevant articles.
Results
Classical therapies for GBS
Intravenous immunoglobulin (IVIg) and plasma exchange
(PE) have been proven to be effective in improving the prog­
nosis of patients with GBS and should be applied before the
occurrence of irreversible axonal injury as soon as possible.1
These two therapies have equal effects.1,39 Patients undergo
five sessions of PE with 50 ml/kg plasma each session, admi­
nistered over 1–2 weeks. The typical dose for IVIg is 0.4 g/kg
body weight per day for five consecutive days.39–41 The
mechanism by which IVIg and PE are effective for GBS is
still unclear but mostly involves removing the antibodies and
MAC in plasma and regulating immune cells.
A single course of IVIg is effective for GBS patients, but
some patients still have poor outcomes. A possible cause for this
may be the rapid consumption of immunoglobulin, and
a second course of IVIg may benefit these patients.
A retrospective study in 2020 and a prospective study in 2021
both showed that patients with poor outcomes after the first
course of IVIg could not benefit from the repeated use of IVIg,
and research suggested that other immunomodulatory treat­
ments should be used for GBS patients with poor prognosis.42,43
Although IVIg and PE are the most effective therapies for
GBS, it has been proven that neither IVIg nor PE can prevent
the disease course or nerve damage.6 PE requires specific equip­
ment, and hypocalcemia, thrombosis, pneumothorax, compli­
cations from central venous access and allergic reactions are the
main complications. Moreover, PE should be avoided in
patients with severe autonomic dysfunction.44 IVIg is more
likely to be completed than PE but is much more expensive,

and liver dysfunction and thromboembolic events are rare but
severe adverse events of IVIg.1 More research on classical
treatments is needed for patients with mild disease and patients
whose treatment starts more than 2 weeks after disease onset,
and new strategies are also needed for patients with poor out­
comes after treatment with PE or IVIg.
Neither oral nor intravenous use of glucocorticoids in GBS
can accelerate recovery, nor can they affect the long-term
outcome of patients.45 The combination of glucocorticoids
and IVIg does not have a better effect than IVIg alone,46,47
but in the early phase of the disease, the combination of
glucocorticoids and IVIg has a better effect in GBS patients.47
New strategies in GBS treatment
Therapies for antibodies
Neonatal Fc receptor (FcRn) can adjust the concentration of
endogenous IgG. Inhibiting FcRn can reduce the level of IgG
in the body, and it has been proven effective in animal experi­
ments. Anti-ganglioside antibody levels in mice lacking FcRn
are significantly reduced. The use of FcRn inhibitors signifi­
cantly reduces the antibody levels in mice, reducing nerve
damage and clinical symptoms. This suggests that FcRn inhi­
bitors can be used to treat GBS in the future.48
Immunoglobulin G-degrading enzyme of Streptococcus
pyogenes (IdeS) is secreted by Streptococcus pyogenes and can
cleave IgG antibodies into F(ab’)2 and Fc fragments, thereby
inhibiting the killing of S. pyogenes by the immune response of
hosts.49 Ryo Takahashi found that IdeS efficiently cleaved IgG
and blocked complement activation in vitro.50 A further study
showed that IdeS could reduce complement deposition in the
spinal nerve heel and significantly facilitate the clinical recov­
ery process in the rabbit model of AMAN, and axonal degen­
eration of the anterior spinal nerve root was significantly
reduced in IdeS-treated rabbits.51
Therapies for the complement pathway
Anti-GQ1b antibodies bind and destroy neuromuscular junc­
tions, causing muscle paralysis. This damage activates comple­
ment and ultimately leads to the deposition of membrane
attack complex (MAC) C5b-9. Susan K. Halstead and collea­
gues conducted a study to block the role of C5b-9 in auto­
immune peripheral neuropathy using eculizumab to treat
MFS. Studies have shown that the application of eculizumab
in MFS mice can effectively prevent respiratory failure and
neurological symptoms.52 Furthermore, they conducted
a randomized trial to investigate the effect of eculizumab in
GBS patients. The clinical trial included 28 patients diagnosed
with GBS on the basis of a functioning score greater than 2
points, and 8 subjects were finally recruited. Four weeks after
recruitment, 2 out of 2 patients received placebo, and 2 out of 5
patients received eculizumab and had decreased functioning
scores of more than one point. The results indicated the need
for further studies on eculizumab.53 A prospective study was
carried out on the application of eculizumab in GBS patients.
The study included patients with a GBS disability score of 3–5.
After 4 weeks of treatment, the proportion of patients in the
eculizumab and placebo groups who were able to walk inde­
pendently was 61% and 45%, respectively, but both groups had
HUMAN VACCINES & IMMUNOTHERAPEUTICS 3
adverse events. However, because the outcome indicators did
not meet expectations, the researchers suggested that further
large-scale prospective studies were needed to prove the effect
of eculizumab.54 The 2020 Cochrane Database of Systematic
Reviews also pointed out that the current level of evidence for
eculizumab in the treatment of GBS is low.46
Previous studies showed that C5 inhibition could mitigate
nerve injuries, but Rhona McGonigal determined that the early
stage of complement activation could also cause immune cell
recruitment. C1q is the first complement cascade molecule in
the classical pathway. Two animal models were used to evalu­
ate the efficacy of the anti-C1q antibody (M1). Studies have
shown that anti-C1q treatment reduces axonal injury, and
improves respiratory function in mouse models.55 ANX005 is
a humanized immunoglobulin G4 (IgG4) recombinant anti­
body against C1q that blocks the initiation of the classical
complement cascade. Inhibition of C1q can be used in acute
immune-mediated diseases such as GBS, and the pharmacoki­
netics and pharmacology are currently under study.56 ANX005
has not been used to treat in GBS patients or animal models,
and it may be a promising treatment option.
Therapies inhibiting inflammatory cells and inflammatory
factors
A study by Ranran Han et al. found that dimethyl fumarate
(DMF) improved the demyelination and inflammatory cell
infiltration of the sciatic nerve when used in the treatment of
EAN rats. DMF reduces the level of M1 macrophages and
increases the level of M2 macrophages in the spleen and sciatic
nerve. In the sciatic nerve, DMF treatment increases the level of
nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and its
target gene hemooxygenase-1 (HO-1), which can promote the
transfer of macrophages to M2-type polarization. In addition,
DMF also improves the inflammatory environment of the
spleen of EAN rats, characterized by the downregulation of
IFN-γ, TNF-α, IL-6 and IL-17 messenger RNA (mRNA) and
upregulation of IL-4 and IL-10 mRNA levels.57 Another study
showed that DMF regulated T-cell proliferation and differentia­
tion through different regions and layers of the small intestine,58
indicating that DMF protects EAN rats from nerve damage
through multiple mechanisms.
A preventive and therapeutic study of decitabine (DAC) in
EAN suggests that DAC can increase the number of thymic
Tregs and reduce the production of proinflammatory cyto­
kines, thereby improving the clinical symptoms of EAN.59
Ru-Tao Liu’s research found that 2-deoxy-D glucose
(2-DG) inhibits the initiation and development of EAN at
the same time by inhibiting the glycolytic pathway, simulta­
neously inhibiting the differentiation of Th1 and Th17 cells
and enhancing the development of Treg cells. The enhance­
ment of the glycolysis pathway can promote the pathogenesis
of EAN, and inhibiting glycolysis may be a new treatment for
GBS.60
A study of fasudil for EAN found that Th1 cell and Th17
cell proportions were decreased in mice treated with fasudil,
the proportion of Th2 cells was similar, and the proportion of
Treg cells in splenocytes was increased. Fasudil has a good
therapeutic effect on EAN by attenuating Th1/Th17 cells and
promoting Treg activation and M2 macrophage polarization.61
4 J. YAO ET AL.
Shi Peng et al. found that the level of Bifidobacterium in GBS
patients was significantly lower than that in healthy controls
(HCs), and the concentration of Bifidobacterium was negatively
correlated with Th2 and Th17 subgroups. Treatment with
Bifidobacterium significantly reduced the levels of Th2 and
Th17 cells and increased the level of Treg cells in EAN rats.
This finding suggested that Bifidobacterium could alleviate GBS
by regulating Th17 and Treg cells.62 Further study showed that,
the expression level of programmed death (PD)-1 increased in
EAN rats treated with Bifidobacterium. The function of
Bifidobacterium in regulating T cells was partly blocked by
inhibiting the expression of PD-1, suggesting that
Bifidobacterium alleviates GBS in a partial way through PD-1.63
The immunoproteasome plays a critical role in homeostasis
and immunity, especially in processing antigens for presenta­
tion on major histocompatibility complex (MHC) class
I molecules to CD8+ T lymphocytes.64–66 The subunit of the
immunoproteasome, low-MW polypeptide (LMP) 7, has an
important role in cytokine production. PR-957 is a highly
selective inhibitor of LMP7, and previous studies found that
PR-957 can regulate the differentiation of Th cells and reduce
the amount of proinflammatory cytokines. PR-957 reduced the
proportion of Th17 cells in the sciatic nerve and spleen in EAN
rats, decreased the expression of IL-6 and IL-23, and down­
regulated STAT3 phosphorylation, thereby reducing the sever­
ity and duration of EAN.67
Chunrong Li et al. found that ginkgolide can decrease the
score of EAN mice and delay the peak of disease. It can also
downregulate the proportion of Th17 cells in the spleen of
EAN mice and reduce the levels of IFN-γ and IL-12 in GBS
patients, suggesting that ginkgolides have potential therapeutic
effects in GBS patients and the EAN model.68
The class I phosphatidylinositol 3-kinase inhibitor
2-(2-difluoromethylbenzimidazol-1-yl)-4,6-dimorpholino-
1,3,5-triazine (ZSTK474) was also proven to be effective in
alleviating the inflammatory response of sciatic nerves. The
author reported that ZSTK474 could reduce the number of
Th1/Th17 cells and levels of proinflammatory cytokines
through the PI3K/AKT/mTORC1 pathway, suggesting
a possible anti-inflammatory therapy for GBS.69
Nanoparticles (NPs) can bind with monocytes and remove
monocytes from the lesion site to the spleen.70 Ehsan Elahi
et al. used drug-free poly-lactic coglycolic acid (PLGA)-based
NPs to modulate the inflammatory cells of EAN rats and found
that regardless of different treatment approaches, NPs showed
good effects in modulating inflammatory cells in circulation
system, helping to reduce disease severity.71
Kaixi Ren et al. found that ginsenoside Rd (GSRd) could
also protect against nerve damage in EAN rats by modulating
monocyte conversion and increasing resolution-phase macro­
phage infiltration, showing that GSRd may be useful for GBS
patients.72
Furthermore, Hong Jiao et al. found that vasoactive intest­
inal peptide (VIP) can inhibit neural inflammation, reduce
inflammatory cytokine levels and improve body functions in
EAN rats.73
Björn Ambrosius et al. used fingolimod as an immunomo­
dulator for the treatment of EAN rats. A study showed that
low-dose fingolimod could reduce circulating peripheral blood
T cells and infiltrating T cells and macrophages in the sciatic
nerve, and fewer apoptotic Schwann cells were found in rats
treated with fingolimod at disease nadir.74
Therapies targeting other mechanisms
Efrat Shavit-Stein found that thrombin and its protease-
activated receptor 1 (PAR1) participate in the development of
EAN. N-Tosyl-Lys-chloromethylketone (TLCK) and N-alpha 2
naphthalenesulfonylglycyl 4 amidino-phenylalaninepiperidide
(NAPAP) were used as PAR1 inhibitors to block the thrombin-
PAR1 pathway. In vitro studies showed that both TLCK and
NAPAP could inhibit the thrombin-PAR1 pathway in rat sciatic
nerve damage. In vivo studies showed that TLCK- or NAPAP-
treated rats had improved clinical scores, and TLCK treatment
could prevent structural damage to the node of Ranvier in the
sciatic nerve.75
Neurotrophic factors are essential for the development and
damage repair of the peripheral nervous system. The p75
neurotrophic receptor (p75NTR) is fundamental to peripheral
nerve growth.76 Brain-derived neurotrophic factor (BDNF)
promotes peripheral nerve myelination via the p75NTR path­
way. David G. Gonsalvez used the cyclic pentapeptide cyclo-
[DPro-Ala-Lys-Lys-Arg] (cyclo-DPAKKR), a structural
mimetic of BDNF to investigate the therapeutic effect in
EAN rats. The study found that cyclo-DPAKKR administra­
tion limited the extent of inflammatory demyelination and
axonal damage by inhibiting the p75NTR pathway, and the
therapeutic effect of cyclo-DPAKKR was abrogated.77
Kota Moriguchi found that 4-aminopyridine (4-AP) could
reduce the clinical scores of EAN rats and improve the electro­
physiological properties, but the histological assessment
revealed no significant difference between the 4-AP and con­
trol groups.78 The mechanism of 4-AP in the treatment of
EAN is not clear, and further studies are needed to investigate
the therapeutic effect of 4-AP.
Discussion
In 1916, Guillain, Barré and Strohl reported two cases of acute
flaccid paralysis with high cerebrospinal fluid (CSF) protein
levels and normal cell counts, which is now known as GBS. In
the past century, we have made great progress in understanding
the clinical variations, pathology and treatment of GBS.79,80
Until the 1970s, there was no specific and effective treat­
ment for GBS. In the late 1970s, PE was first used to treat
GBS.81 In 1984, two clinical trials showed that PE was efficient
in GBS patients.82,83 A year later, one larger study confirmed
the results and found that PE could benefit patients who were
unable to walk independently, especially when treatment was
started within 2 weeks of disease onset.84 PE was the first
treatment proven to be effective for GBS, but the treatment
also carries risk for patients with autonomic dysfunctions,
which are common in GBS patients.
Ten years after the first report of PE, immunoglobulin
was first reported in the treatment of GBS.85 A randomized
clinical trial (RCT) in 1992 compared the efficiency of PE

and IVIg and found that IVIg was an effective alternative
to PE; patients treated with IVIg showed more improve­
ment after 4 weeks than those with PE.86 Currently, clinical
trials have shown that PE and IVIg have equal effects.1,39
IVIg has become the most popular therapy in most coun­
tries, unless the costs limit its use.
The treatment of GBS is still challenging for neurologists.
Traditional therapies such as PE and IVIg are effective, but the
high price of immunoglobulin and lack of specific equipment and
PE specialists limit their use. New immunotherapies start by
clearing antibodies, reducing membrane attack complexes and
regulating the immune response, and targeting other pathways
are also considered to be effective in EAN models or clinical trials.
New therapies are aimed at the pathology of GBS, which means
they are more specific. Most of the new therapies are drugs that
are easy to produce, transport and store, and the use of new
therapies does not require specific equipment. The combination
of new therapies with classical therapies could help to improve the
prognosis in patients with poor outcomes after treatment with
classical therapies alone. Immunotherapies are still the most
popular methods for GBS treatment. Further clinical and basic
studies are needed to prove the role of these methods in the
treatment of GBS and provide more possibilities for treatment.
New therapies also have limitations. Most therapies have only
been verified in animal models, and only eculizumab and IdeS are
undergoing clinical trials. The Cochrane library also reviewed the
therapeutic effect of methods that have been used in RCTs and
found that IFNβ-1a, CSF filtration and the Chinese herb tripter­
ygium polyglycoside all had a very low level of certainty based on
the evidence.46 Further studies should focus on the translation of
basic research to clinical trials. Nonetheless, it will take a long time
for new strategies to be applied in clinical practice.
In conclusion, IVIg and PE are still the most effective thera­
pies for GBS. Additionally, immunotherapies are still the most
popular methods for GBS treatment (Table 1). Further clinical
and basic studies are needed to prove the role of these methods
in the treatment of GBS and provide more possibilities for
treatment.
Author contributions
JY and ZN provided the idea for the study, RZ, YL, JY collected the
clinical data, JY analyzed the data and wrote the manuscript. All authors
read and approved the final version of the manuscript and agreed with its
submission for publication.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Funding
The author(s) reported there is no funding associated with the work
featured in this article.
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