Deciphering immune mechanisms in chronic inflammatory demyelinating polyneuropathies

Wolbert, Jolien; Cheng, Mandy I.; Hörste, Gerd Meyer zu; Su, Maureen A.

doi:10.1172/jci.insight.132411

Cited by 21 publications

(12 citation statements)

References 102 publications

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“…The antibodies are able to penetrate into the paranodes and disrupt the CNTN1/Caspr/NF155 complex [ 35 ]. The axonal loss was associated with the inflammatory infiltrate, mainly composed of macrophages and, to a lesser extent, CD3+ T cells and CD19+ B cells with more diffuse instances of demyelination within mice nerves [ 9 , 34 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

Correlations between Electrophysiological Parameters, Lymphocyte Distribution and Cytokine Levels in Patients with Chronic Demyelinating Inflammatory Polyneuropathy

Dziadkowiak

Moreira

Wieczorek

et al. 2021

JPM

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The goal of this study was to analyse, in relation to electrophysiological results, the distribution of lymphocyte subpopulations and the level of cytokines in patients with the typical form of chronic demyelinating inflammatory polyneuropathy (CIDP) before immunoglobulin treatment. The study group consisted of 60 patients (52 men, eight women), with a mean age 64.8 ± 11.2, who fulfilled the diagnostic criteria for the typical variant of CIDP, with (23 patients) and without (37 patients) diabetes mellitus. We analysed the results of the neurophysiological tests, and correlated them with the leukocyte subpopulations, and cytokine levels. In CIDP patients, IL-6, IL-2, IL-4 and TNF-α levels were significantly increased compared to the control group. Fifty patients had decreased levels of T CD8+ lymphocytes, and 51 patients had increased levels of CD4+ lymphocytes. An increased CD4+/CD8+ ratio was also found. Negative correlations were observed mainly between compound muscle action potential (CMAP) amplitudes and cytokine levels. The study enabled the conclusion that electrophysiological parameters in CIDP patients are closely related to the autoimmune process, but without any clear differences between patients with and without diabetes mellitus. Correlations found in the study indicated that axonal degeneration might be independent of the demyelinating process and might be caused by direct inflammatory infiltration.

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Section: Discussionmentioning

confidence: 99%

Correlations between Electrophysiological Parameters, Lymphocyte Distribution and Cytokine Levels in Patients with Chronic Demyelinating Inflammatory Polyneuropathy

Dziadkowiak

Moreira

Wieczorek

et al. 2021

JPM

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“…A proportion of CIDP patients have antibodies against CNTN1 and NF155. In the peripheral nervous system (PNS) of this subgroup of CIDP patients, the function as adhesion receptors are severely disrupted (Wolbert et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

A Systematic Review and Meta-Analysis of Autoantibodies for Diagnosis and Prognosis in Patients With Chronic Inflammatory Demyelinating Polyradiculoneuropathy

et al. 2021

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Objectives: To review the available evidence on sensitivity and specificity of anti-NF155 antibody detection in diagnosing a specific subset of patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and to calculate the frequencies of different autoantibodies to paranodal proteins.Background: Diagnosis of CIDP relies on clinical and neurophysiologic criteria and lacks useful diagnostic biomarkers. A subset of CIDP patients exhibit atypical clinical phenotypes and impaired response to conventional treatments. These patients were reported as having autoantibodies targeting paranodal protein neurofascin isoform 155 (NF155), contactin-1 (CNTN1), and contactin-associated protein-1 (CASPR1). Here, we conducted a meta-analysis to summarize evidence on the diagnostic and prognostic value of these autoantibodies, especially for anti-NF155 antibody.Methods: We searched the following electronic bibliographic databases: PubMed, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), and Web of Science. Eligible studies provided information to calculate the frequencies of anti-NF155 antibody and anti-CNTN1 antibody, the sensitivity and specificity of anti-NF155 antibody, and the incidence of improvement and deterioration among anti-NF155 antibody seropositive CIDP patients. Heterogeneity was assessed using Q and I2 statistics.Results: The pooled frequency of anti-NF155 autoantibody across 14 studies was 7% [95% confidence interval (CI): 0.05–0.10] with high heterogeneity; the overall pooled sensitivity and specificity of anti-NF155 antibody for the diagnosis of a specific subgroup of CIDP patients were 0.45 (95% CI: 0.29–0.63) and 0.93 (95% CI: 0.86–0.97), respectively.Conclusions: For diagnosing of a specific subset of CIDP characterized by poor response to intravenous immunoglobulin (IVIg), we found a moderate sensitivity and a high specificity. The anti-NF155 antibody test should be used as a confirmatory test rather than a screening test.Systematic Review Registration: PROSPERO, identifier: CRD42020203385 and CRD42020190789.

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“…MALAT1 has been shown to induce the expansion of tolerogenic DCs and Tregs through the miR155/DC-SIGN/IL-10 axis ( 21 ). Both mentioned cell populations contribute to the modulation of immune responses during the course of immune-related neuropathies ( 22 , 23 ). Thus, this axis might also mediate the role of MALAT1 in the pathobiology of these conditions.…”

Section: Discussionmentioning

confidence: 99%

A Diagnostic Panel for Acquired Immune-Mediated Polyneuropathies Based on the Expression of lncRNAs

et al. 2021

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Long non-coding RNAs (lncRNAs) have been shown to alter immune responses, thus contributing to the pathobiology of autoimmune conditions. We investigated the expression levels of ANRIL, PICART1, MALAT1, CCAT1, CCAT2, and CCHE1 lncRNAs in acute and chronic inflammatory demyelinating polyneuropathy (AIDP and CIDP). ANRIL, PICART1, MALAT1, CCAT1, CCAT2, and CCHE1 lncRNAs were significantly downregulated in individuals with both AIDP and CIDP compared with unaffected individuals. Gender-based comparisons also verified such downregulations in both male and female subjects compared with sex-matched unaffected controls for all lncRNAs. There was no significant difference in the expression of any of the lncRNAs between cases with AIDP and cases with CIDP. While the expression levels of ANRIL and PICART1 were significantly correlated in healthy subjects (r = 0.86, p = 8.5E-16), similar analysis in cases with AIDP and CIDP revealed no significant correlation. The most robust correlation among patients was detected between ANRIL and MALAT1 lncRNAs (r = 0.59, p = 3.52E-6). ANRIL, MALAT1, and PICART1 had the diagnostic power of 0.96, 0.94, and 0.92 in distinguishing between cases with CIDP and controls, respectively. A combination of all lncRNAs resulted in 0.95 diagnostic power with a sensitivity of 0.85 and specificity of 0.96 for this purpose. Diagnostic power values of these lncRNAs in differentiation between cases with AIDP and controls were 0.98, 0.95, and 0.93, respectively. The combinatorial diagnostic power reached 0.98 for differentiation between cases with AIDP and controls. The six-lncRNA panel could differentiate combined cases with AIDP and CIDP from controls with area under the curve (AUC), sensitivity, and specificity values of 0.97, 0.90, and 0.96, respectively. Collectively, the lncRNA panel is suggested as a sensitive and specific diagnostic panel for acquired immune-mediated polyneuropathies.

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Deciphering immune mechanisms in chronic inflammatory demyelinating polyneuropathies

Cited by 21 publications

References 102 publications

Correlations between Electrophysiological Parameters, Lymphocyte Distribution and Cytokine Levels in Patients with Chronic Demyelinating Inflammatory Polyneuropathy

Correlations between Electrophysiological Parameters, Lymphocyte Distribution and Cytokine Levels in Patients with Chronic Demyelinating Inflammatory Polyneuropathy

A Systematic Review and Meta-Analysis of Autoantibodies for Diagnosis and Prognosis in Patients With Chronic Inflammatory Demyelinating Polyradiculoneuropathy

A Diagnostic Panel for Acquired Immune-Mediated Polyneuropathies Based on the Expression of lncRNAs

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