Background: Gelsolin (GSN) is the most widely expressed actin-severing protein in humans, which could regulate cell morphology, differentiation, movement and apoptosis. This study aims to explore the GSN as a prognostic biomarker of stomach adenocarcinoma (STAD). Methods: In this study, we used several online databases to comprehensively analyze the role of GSN in STAD. Oncomine and HPA databases were used to explore the GSN expression in various cancer, especially in gastric cancer. Then, UALCAN database was used to evaluate the relationship between GSN expression and promoter methylation in clinical characteristics. Finally, we used TIMER to analyze the correlation between GSN expression and immune infiltrates in gastric cancer. Results: GSN was down-regulated in gastric cancer, and decreased expression of GSN was related to worse survival. The GSN expression was significantly related to tumor purity in STAD and significantly correlated with infiltrating level of various immune cells, especially the dendritic cells. Conclusion: Our study proposes that GSN can be served as the biomarker of disease and neoantigen for STAD treatment, which can improve the deficiency of disease-specific targeted therapies currently exist.

Objective: To investigate the expression patterns and clinical significance of specific lymphocyte subsets in the peripheral blood of patients with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection.Methods: Between December 2022 and February 2023, a cohort of 165 patients from the First Affiliated Hospital of Guangzhou University of Chinese Medicine were analyzed. The participants represented various stages of coronavirus infection severity: mild, moderate, severe, and critical. Additionally, 40 healthy individuals constituted the control group. The FC 500MPL flow cytometer and associated reagents for flow cytometry.Results: Compared with the healthy control group, activated B lymphocytes witnessed a pronounced increase (p < .05). A significant decrease was observed in the levels of Breg, Cytotoxic T cells or Suppressor T‐cell (Tc/s), late‐activated T, late‐activated Th, and late‐activated Tc/s lymphocytes (p < .05). Th, initial Th, initial Tc/s, total Treg, natural Treg, induced Treg, early activated T, and early activated Th lymphocyte levels showed no significant difference (p > .05). As the disease progressed, there was an uptick in midterm activated T lymphocytes (p < .05), while Breg, T, Tc/s, senescent Tc/s, and total senescent T levels dwindled (p < .05). Noteworthy patterns emerged across different groups for B1, T‐lymphocytes, Tc/s, B2, CD8+ Treg cells, and other subsets, highlighting variance in immune responses relative to disease severity. When juxtaposed, no significant difference was found in the expression levels of lymphocyte subsets between patients who died and those deemed critically ill (p > .05).Conclusion: Subsets of Treg and B‐cells could act as yardsticks for the trajectory of SARS‐CoV‐2 infection and might have potential in forecasting patient trajectories. A comprehensive evaluation of lymphocyte subsets, especially in real‐time, holds the key to discerning the clinical severity in those with COVID‐19. This becomes instrumental in monitoring treatment outcomes, tracking disease evolution, and formulating prognostications. Moreover, the results provide a deeper understanding of the cellular immune defense mechanisms against the novel coronavirus infection.

Treg cells play an important role in the induction of autoimmune tolerance, and their ability of antigen recognition and regulation is determined by the receptor (TCR). TCR diversity determines the autoimmune responses in RA and is closely associated with autoimmune diseases prognosis and prevention. Previous studies have found that there is immunosenescence in RA, that is, the decrease of the number of naïve CD4 ⁺ T cells and the reduction of TCR repertoire diversity. High disease activity is an independent risk factor for RA. We speculate that high disease activity is related to immunosenescence—the decline of adaptive immune function and a chronic inflammation, but its biological mechanism is still unclear and needs to be further elucidated. In this study, high-throughput Immuno-Seq sequencing and flow cytometry were used to compare normal subjects and RA patients, as well as RA patients whose disease activity changed to clinical remission after standard treatment. It was found that high disease activity not only led to a decrease in the number of naïve Treg cells, but also led to a decrease in the diversity of Treg cell receptor repertoire, weakening their ability to recognize self-antigens and induce immune tolerance, leading to the occurrence and development of RA. Besides, these characteristics of the TCR repertoire, particularly the disease activity related clones, can potentially serve as biomarkers and provide novel insights for disease status and therapeutical targets in autoimmune diseases.