State-of-the-Art Review on the Treatment of Axial SpondyloarthritisKaltsonoudis, Karagianni, Memi
et alMed Sci (Basel) (2025) 13 (1)
Abstract: The term axial spondyloarthritis (axSpA) encompasses patients with both radiographic (r-axSpA) and non-radiographic (nr-axSpA) forms of the disease. These are two entities within the same family that share many genetic and pathogenic factors, but they also have significant differences. For example, the male-to-female ratio is 2:1 in r-axSpA and 1:1 in nr-axSpA. Additionally, the prevalence of the HLA-B27 gene is notably higher in r-axSpA. Early diagnosis remains an unmet need, with magnetic resonance imaging (MRI) being the most important tool for diagnosis and disease monitoring. Early detection is crucial, as it allows for timely treatment, increasing the chances of preventing new bone formation and long-term structural bone damage. Various cytokines, such as tumor necrosis factor (TNF)-α and interleukin-17, play active roles in the disease's pathogenesis, although the exact mechanisms of interaction are not yet fully understood. Clarifying these mechanisms will be key to developing new classification criteria, screening methods, and more personalized, targeted therapies. Non-steroidal anti-inflammatory drugs (NSAIDs), TNF inhibitors, interleukin-17 blockers, and, more recently, Janus kinase (JAK) inhibitors, are the most effective treatments for both radiographic and non-radiographic axial spondyloarthritis.
Cardiometabolic Risk in Psoriatic Arthritis: A Hidden Burden of Inflammation and Metabolic DysregulationRadić, Belančić, Đogaš
et alMetabolites (2025) 15 (3)
Abstract: Psoriatic arthritis (PsA) is a chronic inflammatory disease that extends beyond musculoskeletal and dermatologic involvement to elevate cardiometabolic risk. Emerging evidence highlights the critical role of systemic inflammation in metabolic dysregulation, accelerating insulin resistance, dyslipidemia, and oxidative stress, all of which contribute to the increased burden of cardiovascular disease in PsA. This review explores the intricate interplay between inflammatory mediators-such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-17 (IL-17),-adipokine imbalances, and lipid metabolism abnormalities, all of which foster endothelial dysfunction and atherosclerosis. The dysregulation of adipokines, including leptin, adiponectin, and resistin, further perpetuates inflammatory cascades, exacerbating cardiovascular risk. Additionally, the metabolic alterations seen in PsA, particularly insulin resistance and lipid dysfunction, not only contribute to cardiovascular comorbidities but also impact disease severity and therapeutic response. Understanding these mechanistic links is imperative for refining risk stratification strategies and tailoring interventions. By integrating targeted immunomodulatory therapies with metabolic and cardiovascular risk management, a more comprehensive approach to PsA treatment can be achieved. Future research must focus on elucidating shared inflammatory and metabolic pathways, enabling the development of innovative therapeutic strategies to mitigate both systemic inflammation and cardiometabolic complications in PsA.
Biological Disease-Modifying Antirheumatic Drugs Decrease Uric Acid Levels in the Sera of Patients with Psoriatic ArthritisPerković, Petrić, Maleš
et alCurr Issues Mol Biol (2025) 47 (3)
Abstract: There are many explanations for increased levels of serum uric acid (SUA) in patients with psoriatic arthritis (PsA), but correlation with different treatment options in PsA is not well elucidated. Our aim was to determine the effects of biological disease-modifying antirheumatic drugs (bDMARDs) on SUA levels in patients with PsA.We analyzed the data of PsA patients treated with different bDMARDs from January 2007 to June 2021. Patients treated with interleukin-17 (IL-17) inhibitors (secukinumab and ixekizumab) and tumor necrosis factor α (TNFα) inhibitors (golimumab, infliximab, adalimumab, certolizumab pegol, and etanercept) were included.A total of 87 patients were included. The SUA levels decreased in 60 (69%) patients after a 3-6-month-long follow-up, and in 25 (28.7%), we noticed an increase. The average decrease in SUA levels was 9.4 ± 49.5 µmol/L (p = 0.039); for TNFα patients, it was 7.3 ± 59.8 µmol/L (p = 0.386), and for IL-17 patients, it was 12.6 ± 28.4 µmol/L (p = 0.013). The levels of SUA decreased in 81.8% of patients treated with infliximab, as well as in 76% of those treated with secukinumab and in 72.7% of those treated with etanercept. The largest average decrease in SUA levels was recorded in the group treated with golimumab (23 µmol/L).A significant decrease in SUA levels was noticed, especially in patients treated with IL-17 inhibitors. Further studies should identify which bDMARD is the most potent in the lowering of SUA levels. bDMARDs were efficient in PsA disease activity.
Phenotypic and functional dysregulations of CD8 + T Cells in myasthenia gravisLiu, Zhang, Zhai
et alClin Exp Med (2025) 25 (1), 96
Abstract: Myasthenia Gravis (MG) is a heterogeneous autoimmune disorder characterized by fluctuating muscle weakness caused by autoantibodies targeting neuromuscular junction components. While the role of CD4 + T cells in MG is well established, the contribution of CD8 + T cells remains poorly understood. In this study, we analyze CD8 + T cells in 36 MG patients and 38 age- and gender-matched controls using flow cytometry to evaluate subset distribution, granzyme expression, and cytokine production. MG patients exhibit an altered CD4 + /CD8 + T cell ratio and significant changes in CD8 + T cell subsets, including increased central memory CD8 + T cell (Tcm) proportions and decreased effector memory CD8 + T cell (Tem) proportions. Granzyme B expression in Tcm cells is significantly elevated in MG patients, whereas no significant changes are observed in other subsets or GZMK expression. Cytokine analysis reveals increased IL-21, GM-CSF, and IL-17A production by CD8 + T cells in MG patients. These phenotypic and functional alterations of CD8 + T cells persist during the acute phase of the disease, regardless of immunotherapy usage, and vary between ocular and generalized MG. Subgroup and correlation analyses further identify age-dependent and age-independent dysregulations of CD8 + T cells, indicating complex and subtype-specific roles of CD8 + T cells in the immunopathological processes underlying MG. Our findings provide novel insights into the involvement of CD8 + T cells in MG pathogenesis, laying a foundation for future research and potential therapeutic strategies targeting CD8 + T cells.© 2025. The Author(s).
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