Mahdieh Naghavi Alhosseini

Background and Aims: Malnutrition is common in acutely ill geriatric patients, worsening immune function and clinical outcomes. Immunonutrition, containing nutrients like omega-3 fatty acids, arginin and glutamine, may improve recovery in this population. This study aimed to evaluate the impact of immunonutrition on clinical outcomes, inflammatory markers, and immune responses in frail, hospitalized older adults. Methods: This is a retrospective observational study. In total, 36 subjects, during hospitalization, received either an immunonutrition formula or isoproteic and isocaloric enteral nutrition. The primary outcome was the length of hospital stay (LOS), with secondary outcomes focused on inflammatory cytokines and immune parameters within a week of hospitalization. Results: Patients were primarily oldest-old, with a mean age of 88.6 years ± 4.9 (range 79–96). The immunonutrition group had a significantly shorter LOS (11.37 ± 4.87 vs. 16.82 ± 10.83 days, p = 0.05) and showed increases in key cytokines (G-CSF, INF-α2, IL-12p70, IL-15, IL-2, and IL-3, p < 0.05) enhanced immune function. A decrease in T cells and an increased B/T cell ratio was also observed. No significant differences in infection rates or 90-day survival were found. Conclusions: Enteral immunonutrition improved clinical outcomes by reducing LOS and modulating immune responses in frail patients, suggesting potential benefits in recovery. Further studies are needed to confirm these findings.

B-acute lymphoblastic leukemia (B-ALL) is one of the most common pediatric cancers, wherein regulatory T cells (Treg) and exhausted CD8⁺ T cells may be important in its development and maintenance. In this bioinformatics study, we evaluated the expression of 20 Treg/CD8 exhaustion markers and their possible roles in patients with B-ALL. The mRNA expression values of peripheral blood mononuclear cell samples from 25 patients with B-ALL and 93 healthy subjects (HSs) were downloaded from publicly available datasets. Treg/CD8 exhaustion marker expression was normalized with that of the T cell signature and correlated with the expression of Ki-67, regulatory transcription factors (FoxP3, Helios), cytokines (IL-10, TGF-β), CD8⁺ markers (CD8α chain, CD8β chain), and CD8⁺ activation markers (Granzyme B, Granulysin). The mean expression level of 19 Treg/CD8 exhaustion markers was higher in the patients than in the HSs. In patients, the expression of five markers (CD39, CTLA-4, TNFR2, TIGIT, and TIM-3) correlated positively with Ki-67, FoxP3, and IL-10 expression. Moreover, the expression of some of them correlated positively with Helios or TGF-β. Our results suggested that Treg/CD8⁺ T cells expressing CD39, CTLA-4, TNFR2, TIGIT, and TIM-3 favor B-ALL progression, and targeted immunotherapy against these markers could be a promising approach for treating B-ALL.