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Albumin (ALB) has numerous vital physiological outcomes for healthy aging. A decrease in serum albumin, i.e., hypoalbuminemia, is one of the risk factors associated with aging, which affects physiological functioning. Hypoalbuminemia is the outcome of either decreased ALB synthesis or increased degradation. However, the potential mechanism controlling ALB's mRNA level expression in aged individuals is yet to be explored. We noted decreased serum ALB concentrations in aged individuals participating in our study, as compared to the young ones. We found that IL-10, a paradoxical inflammaging marker, reduced ALB concentration in HepG2 cells. Inhibiting the JAK/STAT3 signalling increased albumin mRNA suggesting its IL-10-driven regulation via JAK/STAT3 pathway. Albumin promotor analysis revealed the presence of a CEBP-β binding site. We showed that CEBP-β binds to the albumin promoter in an IL-10-dependent manner. Further, IL-10 increased the expressions of all CEBP-β isoforms, including the inhibitory isoform (LIP). The CEBP-β inhibition either by a functional inhibitor (i.e., quercetin) or shRNA silencing increased albumin mRNA in HepG2 cells. Our finding showed that IL-10 likely regulates albumin expression in a JAK/STAT3 and CEBP-β dependent manner in aging. A better understanding of the underlying condition can improve albumin protein levels and the well-being of the aged population., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

The progressive decline of the anatomical architecture and loss of functional integrity of an individual is aging. Accumulation of degenerative cellular and molecular changes in the aging cells increases the fragility at the cellular and molecular levels. It pushes towards age-associated diseases like Alzheimer's disease, hypertension, cancer, cardiovascular diseases, etc. The impaired T cell function in aging is a leading contributor to increased susceptibility to pathogens, minimized vaccine response, and skewed inflammation. Recent studies about the role of T cells in the remodelling of the immune system have provided ways to examine and explore aging puzzles and their correlation with T cell functions. Here we review the metabolic aspect of T cell function and its possible restoration. IL-7 and mTOR mediated pathways and their association with reactivation of effector T cell function could help understanding the dark side of the compromised adaptive immune system, particularly T cell response, in aging. Understanding these crucial fundamentals could help design and target new molecules to prevent loss of T cell functionality in aging., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.)

The CD6 molecule, a cell surface marker, is involved in immunological synapse formation between T cell and antigen-presenting cell and T lymphocyte activation for adequate immune response. Geriatric individuals fail to mount a satisfactory immunological response against pathogens thus, insights into the functionality of CD6 may provide information for competence building in elderly immune cells. However, limited information is available regarding the status of CD6 in geriatric individuals. In this study, various isoforms of CD6 were analysed in aged mononuclear cells (MNCs) and compared with young individuals. In geriatric individuals, protein and mRNA expressions of CD6 molecule/isoforms were found to be decreased compared to their young counterparts. Furthermore, geriatric MNCs failed to show any change in CD6 levels and its isoforms upon polyclonal activation compared to young MNCs, marked by reduced Ca ++ release and IL-2 expression. We suggest an overall decrease in CD6 levels in geriatric MNCs and T cells with suboptimal T cell activation in aged individuals.

Aging is a discrete phenomenon and hard to understand. A coordinated and gradual loss of structure and function causes impaired responsiveness at cellular and organ levels. It makes an aged individual prone to several chronic diseases and opportunistic infections. The failed interplay among different organ systems is what orchestrates aging. Simultaneously, the involvement of more molecular participants makes it more challenging to understand and examine. This mini-review comprehensively reviewed physiological changes in immune aging and their correlation with overall aging anomalies. [ABSTRACT FROM AUTHOR]