{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T16:20:36Z","timestamp":1787761236332,"version":"build-2784847793"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","license":[{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background and Objectives:<\/jats:title>\n                    <jats:p>\n                      Guillain-Barr\u00e9 syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are inflammatory conditions, representing prototype examples of immune-mediated disorders of the peripheral nervous system. Activation of the nuclear factor-\u03baB (NF-\u03baB) pathway is crucial for generating immune and inflammatory responses and creating an inflammatory milieu; however, this has not been studied in inflammatory neuropathies. We aimed to quantify the expression levels of two critical genes in the NF-\u03baB pathway (\n                      <jats:italic toggle=\"yes\">Nfkb1<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Nfkb2<\/jats:italic>\n                      ), together with a prototype inflammatory gene,\n                      <jats:italic toggle=\"yes\">Tnf\u03b1<\/jats:italic>\n                      , in inflammatory neuropathies.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      Forty-nine patients with inflammatory neuropathies (GBS = 38, CIDP = 11) were recruited prospectively from a single neurology unit. Gene expression levels of\n                      <jats:italic toggle=\"yes\">Nf<\/jats:italic>\n                      \u03ba\n                      <jats:italic toggle=\"yes\">b1<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">Nf<\/jats:italic>\n                      \u03ba\n                      <jats:italic toggle=\"yes\">b2<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">Tnf\u03b1<\/jats:italic>\n                      were quantified using quantitative real-time polymerase chain reaction.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      There were significantly increased expression levels of\n                      <jats:italic toggle=\"yes\">Nf<\/jats:italic>\n                      \u03ba\n                      <jats:italic toggle=\"yes\">b1<\/jats:italic>\n                      in the inflammatory neuropathy group compared to healthy controls (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.001), GBS versus healthy controls (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.03), and CIDP versus healthy controls (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.003). There were no significant differences in the expression levels of\n                      <jats:italic toggle=\"yes\">Nf<\/jats:italic>\n                      \u03ba\n                      <jats:italic toggle=\"yes\">b2<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Tnf\u03b1<\/jats:italic>\n                      genes between cases and controls. There was no correlation between the expression levels of these genes and the clinical severity scores.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>The present study provides evidence for NF-\u03baB pathway activation in inflammatory neuropathies, including both GBS and CIDP, suggesting that this spectrum of disorders may share a common central pathway for immune activation. Thus, the NF-\u03baB pathway plays a critical role in the immunopathogenesis of inflammatory neuropathies; however, the molecular interacting partners within the immune system need to be studied to identify the differential immune trajectories in GBS and CIDP.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.4103\/aian.aian_821_25","type":"journal-article","created":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T04:00:13Z","timestamp":1771214413000},"page":"46-51","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Exploring the Role of Nuclear Factor Kappa B in the Immunobiology of Inflammatory Neuropathies"],"prefix":"10.4103","volume":"29","author":[{"given":"Madhu","family":"Nagappa","sequence":"first","affiliation":[{"name":"Department of Neurology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, 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