Memory B cells in Guillain-Barré syndrome

Wang, Qian; Xing, Chunye; Hao, Yanlei; Shi, Qiguang; Qi, Ziyou; Lv, Zhanyun; Song, Yan; Peng, Xu; Feng, Xungang; Zhang, Lili; Zhang, Yong; Wang, Yu‐Zhong; Yuki, Nobuhiro

doi:10.1016/j.jneuroim.2017.01.004

Cited by 6 publications

(6 citation statements)

References 19 publications

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“…The peripheral blood B-cell subset did not alter in GBS (42). However, increase in memory B-cell ratio in GBS patients with IgG antiganglioside antibodies suggested the antibody-initiated immune chain reaction (57). In our study, only case 3 had a before-after change of BAFF concentration, but not significant (Figure 1).…”

Section: B-cell Immunity In Gbscontrasting

confidence: 54%

Case Report: Plasma Biomarkers Reflect Immune Mechanisms of Guillain–Barré Syndrome

Chao

Lin

et al. 2021

Front. Neurol.

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This case series reported a group of patients with Guillain–Barré syndrome (GBS) and their plasma cytokine changes before and after immunotherapy. We aimed to understand GBS's pathogenesis and pathophysiology through observing the interval differences of the representative cytokines, which were the thymus and activation regulated chemokine (TARC) for T-cell chemotaxis, CD40 ligand (CD40L) for cosimulation of B and T cells, activated complement component C5/C5a, and brain-derived neurotrophic factor (BDNF) for survival and regenerative responses to nerve injuries. The fluorescence magnetic bead-based multiplexing immunoassay simultaneously quantified the five cytokines in a single sample. From June 2018 to December 2019, we enrolled five GBS patients who had completed before–after blood cytokine measurements. One patient was diagnosed with paraneoplastic GBS and excluded from the following cytokine analysis. The BDNF level decreased consistently in all the patients and made it a potential biomarker for the acute stage of GBS. Interval changes of the other four cytokines were relatively inconsistent and possibly related to interindividual differences in the immune response to GBS triggers, types of GBS variants, and classes of antiganglioside antibodies. In summary, utilizing the multiplexing immunoassay helps in understanding the complex immune mechanisms of GBS and the variation of immune responses in GBS subtypes; this method is feasible for identifying potential biomarkers of GBS.

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Section: B-cell Immunity In Gbscontrasting

confidence: 54%

Case Report: Plasma Biomarkers Reflect Immune Mechanisms of Guillain–Barré Syndrome

Chao

Lin

et al. 2021

Front. Neurol.

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“…Given the high production of IgG against myelin peptides, it has been proposed that memory B cells play a key role in the pathogenesis of GBS. 71 Wang et al 72 found that patients with GBS portrayed higher percentage of memory B cells than healthy controls, and were positively correlated with clinical severity. The humoral immune response is driven by γδ T cells that promotes class switching and enhancement of GM1 antibodies secretion by B cells in patients with GBS associated with C. jejuni infection.…”

Section: Bacterial Infections and Gbsmentioning

confidence: 99%

Guillain–Barré syndrome, transverse myelitis and infectious diseases

et al. 2018

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Guillain-Barré syndrome (GBS) and transverse myelitis (TM) both represent immunologically mediated polyneuropathies of major clinical importance. Both are thought to have a genetic predisposition, but as of yet no specific genetic risk loci have been clearly defined. Both are considered autoimmune, but again the etiologies remain enigmatic. Both may be induced via molecular mimicry, particularly from infectious agents and vaccines, but clearly host factor and co-founding host responses will modulate disease susceptibility and natural history. GBS is an acute inflammatory immune-mediated polyradiculoneuropathy characterized by tingling, progressive weakness, autonomic dysfunction, and pain. Immune injury specifically takes place at the myelin sheath and related Schwann-cell components in acute inflammatory demyelinating polyneuropathy, whereas in acute motor axonal neuropathy membranes on the nerve axon (the axolemma) are the primary target for immune-related injury. Outbreaks of GBS have been reported, most frequently related to Campylobacter jejuni infection, however, other agents such as Zika Virus have been strongly associated. Patients with GBS related to infections frequently produce antibodies against human peripheral nerve gangliosides. In contrast, TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. There is interruption of ascending and descending neuroanatomical pathways on the transverse plane of the spinal cord similar to GBS. It has been suggested to be triggered by infectious agents and molecular mimicry. In this review, we will focus on the putative role of infectious agents as triggering factors of GBS and TM.

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“…In this previous study, memory B cells were positively correlated with clinical severity in AIDP patients. Furthermore, the percentage of memory B cells in patients with AIDP gradually decreased during the recovery phase [ 26 ]. In our study, memory B cells were not directly correlated with disability scores whereas they were negatively correlated with IENDs in distal leg.…”

Section: Discussionmentioning

confidence: 99%

Disease activity in chronic inflammatory demyelinating polyneuropathy: association between circulating B-cell subsets, cytokine levels, and clinical outcomes

Ozdag Acarli,

Tuzun,

Sanli

et al. 2023

Clinical and Experimental Immunology

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Chronic inflammatory demyelinating polyneuropathy (CIDP), a common and treatable autoimmune neuropathy, is frequently misdiagnosed. The aim of this study is to evaluate the relationship between immunological markers and clinical outcome measures in a mixed cohort of patients with typical CIDP and CIDP variants at different disease stages. Twenty-three typical, 16 multifocal and five distal CIDP patients were included. Twenty-five sex and age-matched healthy controls and 12 patients with Charcot–Marie–Tooth type 1A (CMT1A) disease served as controls. Peripheral B-cell populations were analyzed by flow cytometry. IL6, IL10, TNFA mRNA and mir-21, mir-146a, and mir-155-5p expression levels were evaluated by real-time polymerase chain reaction in peripheral blood mononuclear cells (PBMC) and/or skin biopsy specimens. Results were then assessed for a possible association with clinical disability scores and intraepidermal nerve fiber densities (IENFD) in the distal leg. We detected a significant reduction in naive B cells (P ≤ 0.001), plasma cells (P ≤ 0.001) and regulatory B cells (P < 0.05), and an elevation in switched memory B cells (P ≤ 0.001) in CIDP compared to healthy controls. CMT1A and CIDP patients had comparable B-cell subset distribution. CIDP cases had significantly higher TNFA and IL10 gene expression levels in PBMC compared to healthy controls (P < 0.05 and P ≤ 0.01, respectively). IENFDs in the distal leg showed a moderate negative correlation with switched memory B-cell ratios (r = –0.51, P < 0.05) and a moderate positive correlation with plasma cell ratios (r = 0.46, P < 0.05). INCAT sum scores showed a moderate positive correlation with IL6 gene expression levels in PBMC (r = 0.54, P < 0.05). Altered B-cell homeostasis and IL10 and TNFA gene expression levels imply chronic antigen exposure and overactivity in the humoral immune system, and seem to be a common pathological pathway in both typical CIDP and CIDP variants.

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Memory B cells in Guillain-Barré syndrome

Cited by 6 publications

References 19 publications

Case Report: Plasma Biomarkers Reflect Immune Mechanisms of Guillain–Barré Syndrome

Case Report: Plasma Biomarkers Reflect Immune Mechanisms of Guillain–Barré Syndrome

Guillain–Barré syndrome, transverse myelitis and infectious diseases

Disease activity in chronic inflammatory demyelinating polyneuropathy: association between circulating B-cell subsets, cytokine levels, and clinical outcomes

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