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Graves' disease (GD) is one of the most common autoimmune conditions, but the mechanisms underlying the associated induction of autoimmunity are not known. We explored the role of peripheral lymphocyte subpopulations in disease pathogenesis.In total, 32 patients and 40 age- and sex-matched healthy controls were recruited in this study. Peripheral levels of T, B, NK, CD4The absolute numbers of circulating Th17 cells (0.45 ± 1.16, p 0.05) between GD patients and healthy controls were not significantly different. However, the percentage of Th17 cells was significantly increased (0.25 ± 0.11, p 0.05). The absolute numbers and percentages of circulating Tregs in GD patients were significantly decreased compared with those in healthy participants (11.61 ± 2.75, p 0.05). There was a significant difference in Treg absolute numbers between the untreated and drug-treated groups. Furthermore, we found that the Treg percentage in untreated patients (mean=4.78) was not significantly different from that in the drug-treated group (mean=4.81). In addition, circulating Treg absolute numbers in GD patients with exophthalmos were significantly lower than those in GD patients without exophthalmos (9.96 ± 4.16, p 0.05). A similar trend was observed in GD patients with weight loss (11.97 ± 3.28, p 0.05).GD pathogenesis was associated with a lower Treg population and an increased Th17/Treg ratio (T helper cell 17/ regulatory T cells). Th17 cells in this study were not related to the disease. Furthermore, anti-thyroid drug therapy improved immune-mediated system disorders. Finally, we found lower absolute numbers of circulating Tregs in GD patients with certain positive signs, such as exophthalmos and/or weight loss. Thus, immune changes are correlated with partial clinical manifestations.

Although amyloid β protein (Aβ) has been recognized as one of the main pathological characteristics in the brain of Alzheimer's disease (AD), the effective strategies against Aβ neurotoxicity are still deficient up to now. Glucagon-like peptide 1 (GLP-1), a natural gut hormone, was found to be effective in modulating insulin signaling and neural protection, but short half-life limited its clinical application in AD treatment. CJC-1131, a newly designed GLP-1 analogue with very longer half-life, has shown good effectiveness in the treatment of type 2 diabetes mellitus (T2DM). However, it is unclear whether CJC-1131 could alleviate Aβ-induced neurotoxicity in cognitive behavior and electrophysiological property. The present study investigated the effects of CJC-1131 on the Aβ-induced impairments in spatial memory and synaptic plasticity of rats by using Morris water maze test and in vivo field potential recording. The results showed that Aβ1-42-induced increase in the escape latency of rats in hidden platform test and decrease in swimming time percent in target quadrant were effectively reversed by CJC-1131 pretreatment. Further, CJC-1131 prevented against Aβ1-42-induced suppression of hippocampal long term potentiation (LTP). In addition, Aβ1-42 injection resulted in a significant decrease of p-PKA in the hippocampus, which was effectively prevented by CJC-1131 treatment. These results indicated that CJC-1131 protected the cognitive function and synaptic plasticity of rats against Aβ-induced impairments, suggesting that GLP-1 analogue CJC-1131 might be potentially beneficial to the prevention and treatment of AD, especially those with T2DM or blood glucose abnormality.

Background T helper (Th17) cells play an important role in many autoimmune diseases. In this meta-analysis, we aimed to specify the proportion of Th17 cells and the levels of Th17-related cytokines in neuromyelitis optica spectrum disorders (NMOSD) patients, we did this meta-analysis. Methods Using previously reported data from PubMed, EMBASE, and Web of Science and Cochrane, we explored the proportion of Th17 cells in CD4+ T cells in peripheral blood (PB) and the level of Th17-related cytokines, such as interleukin (IL)1β, IL6, IL17, IL21, IL22, IL23 and transforming growth factor -beta (TGFβ), in cerebrospinal fluid (CSF), plasma, and serum in NMOSD patients compared to control group and multiple sclerosis (MS) patients. Results In total, 38 trials were included for our analysis. Results showed that the proportion of Th17 cells was higher in NMOSD patients than in the control and MS groups. The levels of IL1β, IL6, IL17 and IL21 in CSF and plasma, and IL6, IL21, IL22, and IL23 in the serum were higher in NMOSD patients than in the control group. The levels of IL6 in CSF and serum and IL17 in plasma and serum were higher in NMOSD patients than in MS patients. Conclusion The proportion of Th17 cells and the levels of Th17-related cytokines was increased in NMOSD patients compared with the control group and MS patients. The results of this meta-analysis indicated that Th17 cells and Th17-associated cytokines may play an essential role in the pathogenesis of NMOSD. PROSPERO registration: CRD42019128785.