The NF-κB family includes some transcription factors which have important functions in the regulation of immune responses, therefore participating in the pathophysiology of inflammatory conditions such as peripheral neuropathies. We have quantified expression of a number of NF-κB-related transcripts in patients with Guillain-Barré syndrome (GBS) or chronic inflammatory demyelinating polyneuropathy (CIDP) versus healthy subjects. These transcripts have been previously shown to be functionally related with this family of transcription factors. Expressions of ATG5, DICER-AS1, PACER, DILC, NKILA and ADINR have been increased in both CIDP and GBS patients compared with controls. However, expression of ATG5 was not different between female CIDP cases and female controls. Moreover, expression of PACER was not different between male GBS cases and male controls. Expression levels of CHAST and CEBPA were not different between patients and controls. Expression of none of the assessed genes was different between GBS and CIDP cases. Significant correlations have been revealed between expression amounts of NF-κB-related transcripts both among CIDP/ GBS patients and among controls except for NKILA/ATG5, ADINR/ATG5 and PACER/ATG5 and DICER-AS1/ATG5 pairs among controls whose expression levels have not been correlated. In the patient group, CEBPA/PACER, CHAST/PACER and CHAST/DICER-AS1 pairs had the most robust correlations (r = 0.94). Among controls, NKILA/ADINR pair had the most strong correlation (r = 0.78). ADINR and DICER-AS1 levels could differentiate CIDP cases from controls with 100% sensitivity and specificity. In differentiation of GBS cases from controls, these two transcripts had the AUC values of 0.99 and 1. Combination transcript levels of NF-κB-related transcripts similarly detects CIDP and GBS cases from healthy controls with 100% sensitivity and specificity. Therefore, NF-κB-related transcripts are possibly involved in the pathophysiology of inflammatory peripheral nerve disorders and can be used as diagnostic markers for these conditions.

NF-κB 家族包括一些在免疫反应调节中具有重要功能的转录因子，因此参与了周围神经病变等炎症性疾病的病理生理学。我们已经量化了格林-巴利综合征 (GBS) 或慢性炎症性脱髓鞘性多发性神经病 (CIDP) 患者与健康受试者中许多 NF-κB 相关转录物的表达。这些转录本先前已被证明在功能上与该转录因子家族相关。ATG5、DICER -AS1、PACER、DILC、NKILA和ADINR的表达与对照组相比，CIDP 和 GBS 患者的 然而，ATG5的表达在女性 CIDP 病例和女性对照之间没有差异。此外，男性 GBS 病例和男性对照之间PACER的表达没有差异。CHAST和CEBPA的表达水平在患者和对照组之间没有差异。在 GBS 和 CIDP 病例中，所有评估基因的表达均无差异。除NKILA / ATG5、ADINR / ATG5和PACER外，CIDP/GBS 患者和对照组中 NF-κB 相关转录物的表达量之间存在显着相关性/ ATG5和DICER-AS1 / ATG5对在其表达水平尚未相关的对照中。在患者组中， CEBPA / PACER、CHAST / PACER和CHAST / DICER-AS1对的相关性最强（r = 0.94）。在对照组中，NKILA / ADINR对具有最强的相关性（r = 0.78）。ADINR和DICER-AS1水平可以以 100% 的敏感性和特异性将 CIDP 病例与对照区分开来。在将 GBS 病例与对照区分开来时，这两个转录本的 AUC 值为 0.99 和 1。NF-κB 相关转录本的组合转录本水平类似地以 100% 的敏感性和特异性检测来自健康对照的 CIDP 和 GBS 病例。因此，NF-κB 相关转录物可能参与炎症性周围神经疾病的病理生理学，并可用作这些疾病的诊断标志物。