As we age, our innate and adaptive immune system undergoes various changes, typically characterized by decreased lymphopoiesis and adaptive immunity, and increased inflammation and myeloid pathologies. Immunosenescence (the gradual deterioration of the immune system associated with ageing), makes individuals more susceptible to infections, less responsive to vaccines, and prone to the development of chronic inflammatory conditions and autoimmune diseases. Additionally, age-related alterations in the composition and function of the microbiota, the community of microorganisms living in and on the body, can further influence immune function and contribute to the overall ageing process.
This month, several papers related to antibodies and aging were published, including a comprehensive review by Quiros-Roldan et al., studying the impact of immune system aging on infectious diseases, including the progressive reduction of the body’s ability to trigger effective antibody responses. Here they describe the increased public interest in immune system aging due to prolonged life expectancy, contrasted to health expectancy. They also provide an analysis of the immune players involved, in addition to immune cells/mediators within endogenous and exogenous factors and co-morbidities.
Another paper this month provides insight into why age is a major risk factor for severe COVID-19. By evaluating the impact of aging and anti-IFN autoantibodies on host immune response in the blood, upper airway, and nasal microbiome, the researchers found that older age correlated with impaired viral clearance, dysregulated immune signaling, and persistent and potentially pathologic activation of pro-inflammatory genes and proteins.
Ending on a bright note, Ross et al.’s study in Nature demonstrates the antibody-mediated depletion of my-haematopoietic stem cells (HSCs) in aged mice restores characteristic features of a more youthful immune system. Their findings show it might be possible to reverse the ageing phenotype by eliminating my-HSCs in aged mice and contributes to the understanding and intervention of diseases exacerbated or caused by dominance of the haematopoietic system by my-HSCs.
This week, computationally designed antibody therapeutics have been high on the news, leveraging advanced deep learning and AI-driven methodologies to accelerate the discovery and optimization of antibodies.
Anti-amyloid antibodies are designed to target and remove amyloid-beta plaques in the brain, a hallmark of Alzheimer’s disease. These plaques are toxic protein clusters believed to disrupt communication between neurons, leading to cell death and cognitive decline. By binding to amyloid-beta, these antibodies aim to neutralize or clear the plaques, potentially slowing disease progression.
This past week, the Biomedical Advanced Research and Development Authority (BARDA) has provided funding for several antibody-related drug development programs. BARDA is a U.S. government agency within the Department of Health and Human Services (HHS) that funds and supports the development of medical countermeasures to protect against public health threats, such as pandemics, bioterrorism, and other emergencies.