Lactobacillus in autoimmune thyroid diseases: benefit or risk?

Impact of dermatology targeted immunotherapies on autoimmune thyroid diseases: cytokine-network crosstalk and thyroid safety

Autoimmune thyroid diseases (AITDs), including Hashimoto’s thyroiditis (HT) and Graves’ disease (GD), affect approximately 2–5% of the global population. They are the most common organ-specific autoimmune disorders worldwide. Growing epidemiological and immunological evidence indicates that AITDs frequently coexist with immune-mediated dermatological diseases. These include atopic dermatitis (AD), psoriasis, alopecia areata (AA), vitiligo, and chronic spontaneous urticaria (CSU). Targeted immunotherapies have become central to the treatment of many immune-mediated skin diseases. Although these therapies are designed to act on specific immune pathways, they may also exert broader systemic immunomodulatory effects. However, thyroid function and thyroid autoantibodies are not routinely assessed in patients with immune-mediated dermatological conditions. This is also true for some patients with known or suspected AITDs. In this narrative review, we summarize the immunological overlap between cutaneous inflammation and autoimmune thyroid disease. We also discuss thyroid-related evidence for IL-4Rα inhibitors, IL-17 inhibitors, JAK inhibitors, IL-12/23 inhibitors, and immune checkpoint inhibitors (ICIs). Current evidence suggests that ICIs have the strongest established association with thyroid dysfunction. In contrast, the thyroid-related effects of dupilumab and ustekinumab are supported mainly by rare case reports. IL-17 inhibitors and selective IL-23p19 inhibitors may theoretically attenuate thyroid inflammatory pathways. However, this possibility has not yet been confirmed in clinical studies. Based on the available evidence, we propose a risk-stratified approach to thyroid surveillance across targeted immunotherapies. Routine thyroid monitoring is most strongly supported for ICIs. For patients at increased thyroid risk, selective assessment of thyroid function and thyroid autoantibodies may also be considered during treatment with dupilumab or ustekinumab. For oral JAK inhibitors, monitoring may be particularly relevant before treatment, during therapy, and after discontinuation because of the potential for immune rebound. Prospective studies are needed to define which patient subgroups would benefit most from thyroid surveillance during targeted immunotherapy.

Gut microbiota dysbiosis and immune responses: insights from IgA nephropathy and inflammatory bowel disease

IgA nephropathy (IgAN) is the most common glomerulonephritis worldwide, and inflammatory bowel disease (IBD) comprises a group of chronic, relapsing inflammatory bowel disorders. Although IgAN and IBD differ in clinical manifestations, both involve interactions among genetic susceptibility, epigenetic abnormalities, and gut microbiota dysbiosis, ultimately pointing to mucosal immune dysregulation and chronic inflammation. They share similar alterations in gut microecology, characterized by a reduction in short-chain fatty acid-producing protective commensals and an increase in pathogenic symbionts. This leads to intestinal barrier disruption and aberrant microbial metabolites, promoting the production of galactose-deficient IgA1 (Gd-IgA1), activating intestinal mucosal immune cells, and driving both local and systemic inflammation. Notably, glucocorticoids (GC) and immunomodulators are common therapeutic agents for both diseases, and effective treatment is accompanied by restoration of the gut microbiota and improvement of immune imbalance. The four currently marketed budesonide enteric-coated capsules employ pH-dependent targeted-release technology and act on different sites ranging from the terminal ileum to the colon to modulate B-cell activation and attenuate local inflammation. IgAN and IBD may be closely related mucosal immune disorders, with immune inflammation associated with gut microbiota dysbiosis may represent a key link between them. Furthermore, upper respiratory tract infection may participate in the development of IgAN through mucosal immunity. The efficacy of tonsillectomy as a therapeutic intervention suggests the existence of crosstalk between the respiratory tract and the kidneys.

Probiotics in Autoimmune Disease: Strain-specific Mechanisms and Therapeutic Perspectives

Inflammatory bowel disease treatment: Mechanisms to clinical translation (Review)

Inflammatory bowel disease (IBD) is a group of chronic, relapsing and systemic inflammatory disorders primarily affecting the gastrointestinal tract, including Crohn's disease, ulcerative colitis and rarer distinct subtypes such as indeterminate colitis. IBD has shown a marked shift in global epidemiology, with increasing incidence in newly industrialized regions across Africa, Asia and Latin America. The pathogenesis of IBD reflects a complex interplay between genetic susceptibility, mucosal immune dysregulation, intestinal barrier dysfunction, microbial dysbiosis and environmental exposures. Clinically, conventional therapy, including 5-aminosalicylic acid, corticosteroids and conventional immunosuppressants, is limited by incomplete efficacy and safety concerns. Alternative therapeutic strategies included biological agents (anti-tumor necrosis factor α, anti-integrin, anti-IL-12/23 and anti-tumor necrosis factor-like ligand 1A), small-molecule inhibitors (JAK inhibitors, tyrosine kinase 2 inhibitors, sphingosine-1-phosphate receptor modulators and NLRP3 inhibitors), microbiome-based interventions (fecal microbiota transplantation, probiotics and engineered microbes) and regenerative approaches (mesenchymal stem cells and intestinal organoids). The present review aimed to summarize mechanistic insights and clinical evidence for established and emerging therapies and discusses current challenges and future directions for individualized, disease-modifying treatment of IBD.

Extracellular vesicles at the immune–metabolic crossroads of Hashimoto’s thyroiditis and diabetes mellitus

This review compares how EVs remodel the immune microenvironment in HT, type 2 diabetes mellitus (T2DM), and related disease contexts, with attention to donor cells, cargo, recipient pathways, biomarkers, and therapeutic implications.

Hepatic control of immunometabolism: implications for the pathogenesis, diagnosis and treatment of rheumatic diseases.