Assessment of IL-38 Levels in Patients with Acquired Immune-Mediated Polyneuropathies.

Acute and chronic inflammatory demyelinating polyneuropathy (AIDP and CIDP) are two types of immune-mediated neuropathies in which abnormal cellular or humoral immune responses have been observed. Although dysregulation of several cytokines has been detected in these disorders, expression of interleukin 38 (IL-38) has not yet been assessed in AIDP and CIDP. In the current study, we evaluated serum concentrations of this member of the IL-1 family of cytokines in 24 patients with CIDP, 13 patients with AIDP and 27 healthy subjects. We detected higher levels of IL-38 in CIDP patients compared with controls. When assessing study subgroups based on gender, there were no significant differences in IL-38 levels among the three female subgroups (P = 0.14). However, the difference among male subgroups was significant (P = 0.010). A Tukey test showed significant differences between male CIDP patients and male controls (P = 0.014). Considering the proposed anti-inflammatory role of IL-38, higher levels of this cytokine in CIDP might reflect the presence of a compensatory mechanism to reduce inflammatory processes in these patients. Further longitudinal assessment of this cytokine is need to test this hypothesis.

Evaluation of Expression of STAT Genes in Immune-Mediated Polyneuropathies.

Immune-mediated polyneuropathies are acquired conditions that can be categorized to acute and chronic forms based on the disease course. Although the basic mechanism of these conditions has not been clarified yet, genes that regulate immune responses are putative contributors in their development. In the current study, we assessed expression of signal transducer and activator of transcription (STAT)1-3 and STAT5a genes in peripheral blood of 51 patients and 40 healthy subjects. Expression of STAT1 was higher in female patients compared with female controls (Posterior Beta = 3.622, P = 0.044). The gender*group interaction was significant for this gene which indicates different direction of association in males and females. Expressions of other STAT genes were not different between cases and controls. The diagnostic power of STAT1 in female subjects was estimated to be 0.72 with sensitivity of 68.75% and specificity of 84.62%. There was no significant correlation either between expression of different STAT genes or between their expression and age of study participants. The current study potentiates STAT1 as a putative factor in the pathophysiology of acquired immune-mediated polyneuropathies in females and suggests conduction of further functional studies to elaborate the molecular mechanism of this contribution.