This multi-omic longitudinal analysis of the healthy human peripheral immune system constructs the Human Immune Health Atlas and assembles data on immune cell composition and state changes w...

Background Amidst the ongoing COVID-19 pandemic, understanding factors that influence vaccine efficacy is crucial, particularly in older adults. Regular physical exercise and/or structured physical ac...

Sepsis constitutes a profoundly heterogeneous and dynamic clinical syndrome, precipitated by a maladaptive host response to infection in which the immune sys...

Sarcopenia and atherosclerosis are prevalent age-related conditions increasingly recognized as interconnected through shared immune-mediated pathways. This review elucidates how “inflammaging” driven ...

The specific contribution of smoking to oxidative stress (OS) and systemic inflammation in lung cancer (LC) patients, as well as the potential synergi…

Mitochondrial and lysosomal signaling orchestrates Treg cell metabolic states and functional fitness.

Inflammation represents one of the most fundamental and evolutionarily conserved biological responses for host defense against pathogens and tissue injury (1...

Researchers at VIB and Ghent University have uncovered a key mechanism that protects the skin from harmful inflammation. The findings, published in Immunity, could open new avenues for treating chroni...

One fundamental feature of neurodegenerative diseases is a breakdown in communication. Even before brain cells die, the delicate machinery that keeps neurons in touch—by clearing away protein waste at...

Cellular senescence is a fundamental biological process characterized by stable cell cycle arrest, genomic instability, and the acquisition of a proinflammatory secretory phenotype. While senescence is traditionally associated with aging, growing evidence reveals that chronic infections such as viral, bacterial, and protozoan parasites can serve as powerful inducers of senescence, contributing to premature aging and long-term tissue damage. This review explores the diverse mechanisms by which persistent pathogens trigger or sustain senescence in host cells. We highlight how these chronic infections manipulate host DNA repair, mitochondrial dynamics, telomere maintenance, oxidative stress, and immune function to promote senescence and immunosenescence. Emerging findings also reveal how pathogens hijack the host cellular machinery to induce senescence across various tissue types. In many cases, senescence not only enables pathogen persistence but also drives pathological outcomes such as fibrosis, neurodegeneration, cardiomyopathy, and immune exhaustion. Collectively, this emerging evidence highlights a unifying strategy among diverse pathogens: the exploitation of cellular senescence to support chronic infection and promote disease. Understanding how infectious agents drive senescence offers new insights into age-related pathologies and highlights potential therapeutic targets, such as senolytic and senomorphic agents, to mitigate the long-term impacts of chronic infections.

Known as immunosenescence, the major dysregulation of the immune system with age is associated with poor vaccination efficacy, and increased susceptibility to infections, age-related pathologies, and neoplasms, with incidences exacerbated with age. Cellular senescence is a crucial process that puts cells in an irreversible cell-cycle arrest which prevents damaged or stressed cells from uncontrolled propagation and eventually potential malignancy. Paradoxically, senescence also contributes to the occurrence of cancer and increases the risk of metastasis through different secretory mediators. Altogether, the recent use of senotherapy to eliminate senescent cells has been shown to delay tumorigenesis, attenuate age-related deterioration of organs, and promote healthy aging. Interestingly, immune cells have been shown to specifically interact with, and kill senescent cells, thus opening new opportunities for the development of specific therapeutic strategies similar to immunotherapy in cancer. Through its detrimental impact on the immune system, immunosenescence is also leading to the accumulation of senescent cells with age thus further contributing to the occurrence and worsening of multiple age-related pathologies such as cancer. Understanding the molecular and cellular events occurring during the aging process, and triggering immunosenescence as well as the mechanisms by which senescent cells escape immune surveillance would help to improve immune responses to senescent cells and their clearance. In this review, we highlight how senescent cells interact with immune cells, and how immunosenescence-associated phenotypical and functional deregulation hinder the ability of immune cells to clear senescent cells. We further characterize strategies aimed at promoting the clearance of senescent cells by the immune system.

Aging is a complex biological phenomenon, which involved in a large number of diseases such as cancer, neurodegeneration, and cardiovascular diseases. Unders...

Objective: This retrospective study aimed to evaluate the effects of a 12-week combined supplementation of vitamin D3, vitamin K2, vitamin B6, vitamin B12, and magnesium on immune function, body compo...

AbstractBackground and Aims. Cardiovascular ageing is a progressive loss of physiological reserve, modified by environmental and genetic risk factors, that

Immune pathways and cell types that protect against neurodegenerative processes with aging remain poorly understood. Sulka et al. demonstrate that the innate immune adaptor, STING, provides essential ...

AbstractBackground and Aims. Interventions in preventive cardiology traditionally focus on four standard modifiable cardiovascular risk factors (SMuRFs): h

Objective: Gout is a condition strongly associated with dietary patterns and elevated risk of cardiovascular disease (CVD) in affected individuals. Given the...

CAPPSID relies on an engineered S. typhimurium to act as a synthetic ‘capsid’ to transcribe and deliver viral RNA inside cancer cells, launching a virus that can directly lyse surrounding cells.

Our research provides new insights into how respiratory syncytial virus (RSV) infection affects the host's gut microbiota, lipid metabolism, and the immune-inflammatory network. The findings demonstra...

Introduction Type 2 diabetes mellitus (T2DM) is associated with cognitive impairment, with dysregulation of the interleukin-6 (IL-6) signaling pathway—particularly its soluble receptors—implicated in ...

In-depth characterization of the hyperacute phase (<3 h) following ischemic stroke reveals severe neuroinflammation before the arrival of brain-infiltrating peripheral immune cells, driven by micro...

Studies in rodents and humans suggest that low levels of the metal contribute to cognitive decline.