COVID-19-induced autoimmune thyroiditis: Exploring molecular mechanisms.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) damages multiple organs, including the thyroid, by direct invasion and cell entry via angiotensin-converting enzyme 2 or indirectly by promoting excessive inflammation in the body. The immune system is a critical factor in antiviral immunity and disease progression. In the context of SARS-CoV-2 infection, the immune system may become overly activated, resulting in a shift from regulatory to effector responses, which may subsequently promote the development and progression of autoimmune diseases. The incidence of autoimmune thyroid diseases, such as subacute thyroiditis, Graves' disease, and Hashimoto's thyroiditis, increases in individuals with COVID-19 infection. This phenomenon may be attributed to aberrant responses of T-cell subtypes, the presence of autoantibodies, impaired regulatory cell function, and excessive production of inflammatory cytokines, namely interleukin (IL)-6, IL-1ß, interferon-γ, and tumor necrosis factor-α. Therefore, insights into the immune responses involved in the development of autoimmune thyroid disease according to COVID-19 can help identify potential therapeutic approaches and guide the development of effective interventions to alleviate patients' symptoms.

The association between MUC5AC and MUC5B genes expression and remodeling progression in severe neutrophilic asthma: A direct relationship.

BACKGROUND: MUC5 dysregulation is a hallmark of severe neutrophilic asthmatic patients. This study investigates the expression of MUC5AC and MUC5B at mRNA levels on asthma severity and airway wall thickness in severe neutrophilic asthmatic patients. METHOD: In this case-control clinical trial, twenty-five severe neutrophilic asthmatic patients and ten control subjects were enrolled. Subjects underwent ACT, pulmonary functions tests, and fractional exhaled nitric oxide (FENO). Also, induced sputum has been obtained to assess the expression of MUC5AC and MUC5B by the real-time PCR. In addition, the thickness of the airway wall was assessed by high-resolution computed tomography (HRCT), and bioinformatic analysis was implemented to approve the selection of the appropriate genes and for further investigations. RESULT: A significant difference was observed between the asthmatic and control in MUC5AC and MUC5B mRNA expression. Meanwhile, the expression of MUC5AC increased remarkably by asthma severity; also, it is associated with airway wall thickness (WT) (both P-value <0.05). The expression of MUC5B in asthmatic patients was lower than in control. There is no significant correlation between MUC5B mRNA level and WT and asthma severity. Notably, MUC5AC transcription level was correlated to sputum neutrophil percentage, while MUC5B transcription level had a positive correlation with sputum macrophages and a negative one with sputum neutrophils. CONCLUSION: In severe neutrophilic asthma, airway wall thickness increases with MUC5AC mRNA overexpression, which is probably related to asthma severity and the formation of mucus plugs. However, the expression of MUC5B was decreased, resulting in poor mucociliary clearance in the airways. TRIAL REGISTRATION: IR.IAU.MSHD.REC.1400.124.

The role of tolerogenic dendritic cells in systematic lupus erythematosus progression and remission.

Systematic lupus erythematosus (SLE) is an autoimmune disease reflecting an imbalance between effector and regulatory immune responses. Dendritic cells (DC) are a link between innate and adaptive immunity. Inflammatory DCs (inflDC) can initiate and trigger lymphocyte responses in SLE with over-expression of surface molecules and pro-inflammatory cytokine, including Interferon (IFN) α, Interleukin (IL) 1α, IL-1ß, and IL-6, resulting in the overreaction of T helper cells (Th), and B cells immune responses. On the opposite side, tolerogenic DCs (tolDC) express inhibitory interacting surface molecules and repressive mediators, such as IL-10, Transforming growth factor beta (TGF-ß), and Indoleamine 2, 3-dioxygenase (IDO), which can maintain self-tolerance in SLE by induction of regulatory T cells (Treg), T cells deletion and anergy. Hence, tolDCs can be a therapeutic candidate for patients with SLE to suppress their systematic inflammation. Recent pre-clinical and clinical studies showed the efficacy of tolDCs therapy in autoimmune diseases. In this review, we provide a wide perspective on the effect of inflDCs in promoting inflammation and the role of tolDC in the suppression of immune cells' overreaction in SLE. Furthermore, we reviewed the finding of clinical trials and experimental studies related to autoimmune diseases, particularly SLE.