Israt Jahan, Rasel Ahmed, Jigishu Ahmed, Nure Alam Afsar, Pritha Promita Biswas, Sarah Khurshid, Quazi Deen Mohammad, Hubert P. Endtz, Ruth Huizinga, Bart C. Jacobs, Zhahirul Islam
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CD4<sup>+</sup>CD25<sup>+</sup>FoxP3<sup>+</sup> Treg percentages, cytokine production (IL-10, TNF-α, IFN-γ, and IL-12), and serum C3 levels were measured using flow cytometry, Luminex assay, and turbidimetric methods, respectively. Treatment response was defined as ≥ 1-point GBS-disability score improvement during evaluation.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>GBS patients exhibited lower CD4<sup>+</sup>CD25<sup>+</sup>FoxP3<sup>+</sup> Tregs frequencies compared to HCs (<i>p</i> = 0.006), which were inversely associated with serum C3 levels (<i>p</i> = 0.003) during the acute phase. At 4 weeks post-onset, patients with normal C3 levels (90–180 mg/dL) exhibited higher Treg frequencies (<i>p</i> = 0.005) compared to acute GBS, whereas patients with persistently elevated C3 levels showed reduced Treg percentage (<i>p</i> = 0.009). Among I VIg-treated patients, Tregs significantly increased at 2 and 4 weeks post-treatment, alongside significantly higher IL-10 and lower TNF-α, IFN-γ, and IL-12 levels at 4 weeks. However, patients with supportive care showed no such changes in Tregs and cytokine levels. Furthermore, Tregs elevated significantly in patients responsive to IVIg at 2 and 4 weeks (<i>p</i> < 0.05), but not in non-responsive or supportive care patients.</p>\n </section>\n \n <section>\n \n <h3> Interpretation</h3>\n \n <p>IVIg treatment modulates immune dysregulation in GBS by expanding CD4<sup>+</sup>CD25<sup>+</sup>FoxP3<sup>+</sup> Tregs and altering cytokines and serum C3 levels, which are associated with clinical improvement. These findings indicate Tregs as potential biomarkers for monitoring initial clinical response to IVIg in GBS.</p>\n </section>\n </div>","PeriodicalId":17451,"journal":{"name":"Journal of the Peripheral Nervous System","volume":"30 3","pages":""},"PeriodicalIF":3.9000,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Intravenous Immunoglobulin Elevates Regulatory T Cells in Guillain-Barré Syndrome: A Potential Biomarker of Therapeutic Response\",\"authors\":\"Israt Jahan, Rasel Ahmed, Jigishu Ahmed, Nure Alam Afsar, Pritha Promita Biswas, Sarah Khurshid, Quazi Deen Mohammad, Hubert P. Endtz, Ruth Huizinga, Bart C. 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Treatment response was defined as ≥ 1-point GBS-disability score improvement during evaluation.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>GBS patients exhibited lower CD4<sup>+</sup>CD25<sup>+</sup>FoxP3<sup>+</sup> Tregs frequencies compared to HCs (<i>p</i> = 0.006), which were inversely associated with serum C3 levels (<i>p</i> = 0.003) during the acute phase. At 4 weeks post-onset, patients with normal C3 levels (90–180 mg/dL) exhibited higher Treg frequencies (<i>p</i> = 0.005) compared to acute GBS, whereas patients with persistently elevated C3 levels showed reduced Treg percentage (<i>p</i> = 0.009). Among I VIg-treated patients, Tregs significantly increased at 2 and 4 weeks post-treatment, alongside significantly higher IL-10 and lower TNF-α, IFN-γ, and IL-12 levels at 4 weeks. However, patients with supportive care showed no such changes in Tregs and cytokine levels. 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Intravenous Immunoglobulin Elevates Regulatory T Cells in Guillain-Barré Syndrome: A Potential Biomarker of Therapeutic Response
Background and Aims
Intravenous immunoglobulin (IVIg) is the primary treatment for Guillain-Barré syndrome (GBS), yet its immunological mechanisms underlying variable clinical outcomes remain unclear. This study investigated the immunomodulatory effect of IVIg on regulatory T cells (Tregs), cytokines, and their association with treatment response and clinical outcomes.
Methods
In this prospective case-controlled study, 57 GBS patients and 57 age- and sex-matched healthy controls (HCs) were investigated. CD4+CD25+FoxP3+ Treg percentages, cytokine production (IL-10, TNF-α, IFN-γ, and IL-12), and serum C3 levels were measured using flow cytometry, Luminex assay, and turbidimetric methods, respectively. Treatment response was defined as ≥ 1-point GBS-disability score improvement during evaluation.
Results
GBS patients exhibited lower CD4+CD25+FoxP3+ Tregs frequencies compared to HCs (p = 0.006), which were inversely associated with serum C3 levels (p = 0.003) during the acute phase. At 4 weeks post-onset, patients with normal C3 levels (90–180 mg/dL) exhibited higher Treg frequencies (p = 0.005) compared to acute GBS, whereas patients with persistently elevated C3 levels showed reduced Treg percentage (p = 0.009). Among I VIg-treated patients, Tregs significantly increased at 2 and 4 weeks post-treatment, alongside significantly higher IL-10 and lower TNF-α, IFN-γ, and IL-12 levels at 4 weeks. However, patients with supportive care showed no such changes in Tregs and cytokine levels. Furthermore, Tregs elevated significantly in patients responsive to IVIg at 2 and 4 weeks (p < 0.05), but not in non-responsive or supportive care patients.
Interpretation
IVIg treatment modulates immune dysregulation in GBS by expanding CD4+CD25+FoxP3+ Tregs and altering cytokines and serum C3 levels, which are associated with clinical improvement. These findings indicate Tregs as potential biomarkers for monitoring initial clinical response to IVIg in GBS.
期刊介绍：
The Journal of the Peripheral Nervous System is the official journal of the Peripheral Nerve Society. Founded in 1996, it is the scientific journal of choice for clinicians, clinical scientists and basic neuroscientists interested in all aspects of biology and clinical research of peripheral nervous system disorders.
The Journal of the Peripheral Nervous System is a peer-reviewed journal that publishes high quality articles on cell and molecular biology, genomics, neuropathic pain, clinical research, trials, and unique case reports on inherited and acquired peripheral neuropathies.
Original articles are organized according to the topic in one of four specific areas: Mechanisms of Disease, Genetics, Clinical Research, and Clinical Trials.
The journal also publishes regular review papers on hot topics and Special Issues on basic, clinical, or assembled research in the field of peripheral nervous system disorders. Authors interested in contributing a review-type article or a Special Issue should contact the Editorial Office to discuss the scope of the proposed article with the Editor-in-Chief.
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