---

Background and Objective: Immune-mediated polyneuropathy is divided into acute and chronic categories named as Guillain Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy based on the course of the disease. Although the basic mechanism of these conditions has not been yet clarified, genes that regulate immune responses are putative contributors in their development. The aim of this study was to compare the blood expression level of IL-34 gene between patients with GBS and healthy individuals.
Materials and Methods: In this case-control study, blood samples were collected from 53 patients with GBS (i.e., 33 chronic patients and 20 acute patients) and 40 healthy individuals. Gene expression levels in the studied groups were measured using the real-time polymerase chain reaction technique. Finally, statistical analysis was performed using SPSS software (version 16) at a significance level of < 0.05 was.
Results: The patient group consisted of 36 (67.93%) males and 17 (32.07%) females. In addition, the healthy control group included 27 (67.5%) males and 13 (32.5%) females. The results showed a significant increase in IL-34 expression in the GBS patients, compared to that in the control group.
Conclusion: The findings of the present study revealed an increase in IL-34 gene expression in patients with GBS. Accordingly, it seems that IL-34 gene has an important role in the pathogenesis of this disease.
 

---

Background and Objective: The alterations of the adaptive immune system are involved in type 2 diabetes mellitus (T2DM) pathogenesis. T helper 1 (Th1) cells or CD4⁺ T cells are the pro-inflammatory components of adaptive immunity with the main feature of interferon-gamma (IFN-γ) secretion. The aim of this study was to evaluate the percentage of IFN-γ, assess the expression of related-genes in CD4⁺ T cells, including T-bet, IRF1, RUNX3, and NFκB, and determine the correlation between them and clinical parameters in T2DM patients.
Materials and Methods: In this case-control study, peripheral blood CD4⁺ T cells were isolated from 40 patients and 40 healthy controls (HCs). The percentage of IFN-γ secreting CD4⁺ T cells was assessed using flow cytometry, and the related-genes were evaluated using real-time polymerase chain reaction.

Results: The percentage of IFN-γ secreting CD4+ T cells significantly increased in the patients in comparison to that of the HCs (P<0.001). The expression levels of IRF1 and NFκB were higher in the patients in comparison to those of the HCs (P=0.02 and P<0.001, respectively). A significant positive correlation between IFN-γ secreting CD4+ T cells and both IRF1 and NFκB was observed in the patients (P=0.001 and P=0.002, respectively). There was a significant positive correlation between IFN-γ secreting CD4+ T cells, IRF1, and NFκB with fasting plasma glucose and hemoglobin A1c in the patients (P<0.001).

Conclusion: Due to the increased response of Th1 cells (the production of IFN-γ and expression of related genes) in the patients and existing correlation between them and plasma glucose level, it seems that these inflammatory factors are involved in T2DM pathogenesis, and the use of IFN-γ pathway antagonists could be considered a novel therapeutic approach.
 

---

Results:The levels of fasting plasma glucose and hemoglobin A1c diminished in the EMPA+ group after empagliflozin therapy, compared to those reported at the baseline (initiation day; P<0.001 and P=0.04). The gene expression level of IL-22 and production of IL-22 significantly reduced after 6 months of empagliflozin therapy (P=0.011 and P=0.001). A significant positive correlation between IL-22 production and its gene expression with AHR as well as between fasting plasma glucose and hemoglobin A1c was observed in the EMPA+ patients after therapy (P˂0.05).

---

Background and Objective: Cytokine production was shown to be changed in Type 2 diabetes mellitus (T2DM). Nonetheless, the relationship of pro-inflammatory interleukin (IL)-32α with anti-inflammatory IL-35 and transforming growth factor (TGF)-β is unclear in T2DM. The present study aimed to evaluate the IL-32α, IL-35, and TGF-β levels produced by peripheral blood mononuclear cells (PBMCs) in patients compared to healthy controls (HCs). Correlations between the IL-32α and IL-35 and TGF-β, as well as between those cytokines and paraclinical parameters [(fasting plasma glucose (FPG) and hemoglobin A1c (HbA1c), GFR, albumin, and creatinine)] were assessed.
Materials and Methods: Blood samples were taken from 38 patients and 38 HCs. The PBMCs from each donor were isolated with the ficoll method and cultured with in vitro stimulator for four days. The production of IL-32α, IL-35, and TGF-β in culture supernatants was determined with ELISA. Paraclinical parameters were evaluated by standard laboratory methods.
Results: High levels of IL-32α and low levels of IL-35 were found in patients compared to in HCs (P=0.006; P<0.001). A negative correlation between IL-32α and IL-35 was detected in patients (P<0.001). IL-32α was positively correlated with FPG and HbA1c (P=0.002, P=0.005), whereas IL-35 was negatively correlated with them in patients (both P<0.001). No correlations were detected between the cytokines and BMI, GFR, albumin, and creatinine, as well as between the TGF-β levels.
Conclusion: Increased IL-32α but diminished IL-35 production are linked with each other and with the glucose metabolism parameters in T2DM. It seems that IL-32α and IL-35 have a potential role in T2DM pathogenesis.