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Exploring the Role of Nuclear Factor Kappa B in the Immunobiology of Inflammatory Neuropathies.

Created on 14 Sep 2026

Authors

Madhu Nagappa, Sandipan Mondal, B Pradeepkumar, Thrinath Mullapudi, Srinath Rajeevan, Pokala Akhil, Lakshminarayanapuram Gopal Viswanathan, Monojit Debnath

Published in

Annals of Indian Academy of Neurology. Volume 29. Issue 1. Pages 46-51. Jan 01, 2026. Epub Feb 14, 2026.

Abstract

Guillain-Barré 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-κB (NF-κB) 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-κB pathway ( Nfkb1 and Nfkb2 ), together with a prototype inflammatory gene, Tnfα , in inflammatory neuropathies.
Forty-nine patients with inflammatory neuropathies (GBS = 38, CIDP = 11) were recruited prospectively from a single neurology unit. Gene expression levels of Nf κ b1 , Nf κ b2 , and Tnfα were quantified using quantitative real-time polymerase chain reaction.
There were significantly increased expression levels of Nf κ b1 in the inflammatory neuropathy group compared to healthy controls ( P = 0.001), GBS versus healthy controls ( P = 0.03), and CIDP versus healthy controls ( P = 0.003). There were no significant differences in the expression levels of Nf κ b2 and Tnfα genes between cases and controls. There was no correlation between the expression levels of these genes and the clinical severity scores.
The present study provides evidence for NF-κB 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-κB 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.

PMID:
41692694
Bibliographic data and abstract were imported from PubMed on 14 Sep 2026.

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