IL-17 and other cytokines have a number of immunomodulatory effects on thyroid cells. The present study investigated the changes and correlations amongst IL-17, NF-κB, IL-6, IL-10, interferon-γ (IFN-γ), TNF-α, IL-2 and IL-4 in patients with different autoimmune thyroid diseases in order to further clarify the pathogenesis of autoimmune thyroid disease. A total of 82 patients with autoimmune thyroid diseases (41 with Graves' disease and 41 with Hashimoto's thyroiditis) and 53 healthy controls were enrolled. All relevant thyroid hormones were detected by electrochemiluminescence analyzer. The serum levels of IL-17 and other cytokines were detected using flow cytometry, NF-κB was detected by ELISA, reverse transcription-quantitative PCR was used to detect the protein expression of various mRNAs, and the correlations between IL-17 and these factors were analyzed. Significant differences occurred amongst all groups. NF-κB, TNF-α, IL-6, IL-17 and their mRNA levels were significantly higher in the healthy controls compared with those in the patients; whereas IFN-γ and IL-10 levels were significantly lower in the healthy controls compared with those in the patients . Correlation analysis showed that the expression levels of IL-17 and its mRNA were significantly positively correlated with the expression levels of NF-κB, IL-6, thyroid peroxidase antibody, thyroid gland globulin, thyroglobulin antibody, TNF-α and IFN-γ, and were also significantly negatively correlated with IL-10 . These findings suggested that IL-17 was elevated in patients with autoimmune thyroid disease and that IL-17 could activate the NF-κB signaling pathway, stimulate the production and release of inflammatory factors such as TNF-α, IL-6 and IFN-γ and participate in the pathogenesis of autoimmune thyroid injury.

Background: To study the changes and effects of angiotensin-converting enzyme 2 (ACE2)/angiotensin 1-7 (Ang1-7) and ACE/AngII in people with different glucose metabolisms and to explore the possible mechanisms underlying the severity of COVID-19 infection in diabetic patients. Methods: A total of 88 patients with type 2 diabetes, 72 patients with prediabetes (impaired fasting glucose, 30 patients; impaired glucose regulation, 42 patients), and 50 controls were selected. Changes and correlations of ACE2, Ang1-7 and other indicators were detected among the three groups. Patients were divided into four groups according to the course of diabetes: <1 year, 1–5 years, 5–10 years, and >10 years. ACE2 and Ang1-7 levels were compared and analyzed. Results: ACE2 and Ang1-7 increased with the severity of diabetes ( P 0 < .05 or P < .01). The levels of ACE2 and Ang1-7 in the longer course group were lower than those in the shorter course group, whereas the levels of ACE, Ang II, and interleukin-6 (IL-6) gradually increased ( P < .05). Pearson correlation analysis showed that ACE2 was positively correlated with IL-6, FBG, and 2hPBG levels in the prediabetes group. In the diabetic group, ACE2 was positively correlated with Ang1-7 and negatively correlated with ACE, AngII, IL-6, and C-reactive protein levels. Multiple linear regression analysis showed that IL-6 and ACE were the main factors influencing ACE2 in the diabetic group. Conclusion subsections: ACE2/Ang1-7 and ACE/AngII systems are activated, and inflammatory cytokine release increases in prediabetes. With the prolongation of the disease course, the effect of ACE2/Ang1-7 decreased gradually, while the effect of ACE/AngII increased significantly. Dysfunctions of ACE2/Ang1-7 may be one of the important mechanisms underlying the severity of COVID-19 infection in patients with diabetes.

Objective: To analyze the levels and correlation of vitamin D, ACE2, ACE and inflammatory factors in patients with type 2 diabetes,To explore the effect of vitamin D deficiency on ACE2 and inflammatory factors and the mechanism of action on the occurrence and development of diabetes.Methods: Non-diabetic control 87 cases and type 2 diabetes 96 cases,According to the level of serum 25-hydroxyvitamin D, 47 cases of non-diabetic vitamin D normal group and 40 cases of vitamin D deficiency group were divided into two groups.52 patients in the normal vitamin D group and 44 patients in the vitamin D deficient group were tested for ACE, ACE2, IL-6, TNF-a and other inflammatory indexes.The correlation and influencing factors of vitamin D and each index were analyzed.Results: The levels of HOMA-IR, ACE, AngII, IL-6 and TNF-a in vitamin D deficient group were significantly higher than those in vitamin D normal group.ACE2 and IL-10 were significantly decreased (P < 0.05); Compared with non-diabetic vitamin D deficiency group, BMI, waist circumference, blood pressure, blood lipids, blood glucose, INS, HOMA-IR, ACE, AngII, IL-6 and TNF-a were significantly increased with the severity of vitamin D deficiency. Insulin resistance was more severe, ACE2 and IL-10 decreased significantly(P < 0.05); Pearson correlation analysis showed that vitamin D in non-diabetic group was negatively correlated with AngII and IL-6, but positively correlated with IL-10 (P < 0.05 or P < 0.01).Vitamin D in diabetic group was positively correlated with ACE2 and IL-10, and negatively correlated with ACE, AngII, IL-6, TNF-a, HOMA-IR and HbA1c (all P < 0.01).Multiple linear regression analysis showed that IL-10 and AngII were the main influencing factors of vitamin D deficiency in the non-diabetic group (P < 0.05).33.6% of the total variation of regression equation was explained. In diabetic group, ACE2, IL-6, TNF-a, IL-10 and HOMA-IR were the main influencing factors of vitamin D deficiency (P < 0.05), explaining 55.8% of the total variation of regression equation.Conclusion: Vitamin D deficiency may change the improper regulation of ACE2 and ACE/AngII and the release of inflammatory factors, destroy the autoimmune state of the body, and participate in the occurrence and development of diabetes mellitus.The degree of vitamin D deficiency can aggravate insulin resistance by mediating RAS system and inflammatory factors, and increase the potential pathogenic effect of diabetes.ACE2, ACE/AngII and inflammatory factors can be used as markers of diabetes vitamin D deficiency.