Abstract
This review outlines the known cellular pathways and mechanisms involved in Drosophila age-dependent immunity to pathogenic microorganisms such as bacteria and fungi. We discuss the implication of host signaling pathways such as the Toll, Immune Deficiency (IMD), Janus kinase signal transducer and activator of transcription (JAK/STAT), and Insulin/Insulin Growth Factor/Target of Rapamycin (IIS/TOR) on immune function with aging. Additionally, we review the effects that factors such as sexual dimorphism, environmental stress, and cellular physiology exert on age-dependent immunity in Drosophila. We discuss potential tradeoffs between heightened immune function and longevity in the absence of infection, and we provide detailed tables outlining the various assays and pathogens used in the cited studies, as well as the age, sex, and strains of Drosophila used. We also discuss the overlapping effects these pathways and mechanisms have on one another. We highlight the great utility of Drosophila as a model organism and the importance of a greater focus on age-dependent antiviral immunity for future studies.
Highlights
The common fruit fly, Drosophila melanogaster, with its short lifespan, low cost of culture, and potent conserved innate immune defenses against a variety of microorganisms, serves as an excellent model for investigating the consequences of immunosenescence, a conserved process characterized by the progressive decline of the immune system’s function with age [1,2,3,4]
Given that dysfunction of the intestinal barrier is a hallmark of aging in Drosophila [53], and that a functional intestinal barrier during aging is critical to maintaining lifespan [54], it is understandable how Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling may be involved in age-dependent immunity in Drosophila
There are a variety of cellular pathways and mechanisms, as well as environmental and physiological factors, that affect the ability of aged organisms to respond to infection
Summary
The common fruit fly, Drosophila melanogaster, with its short lifespan, low cost of culture, and potent conserved innate immune defenses against a variety of microorganisms, serves as an excellent model for investigating the consequences of immunosenescence, a conserved process characterized by the progressive decline of the immune system’s function with age [1,2,3,4]. In response to fungal and bacterial infection, activation of Toll and IMD pathways leads to the transcription of downstream antimicrobial peptides (AMPs) genes (reviewed in [15]). Infection especially important in maintaining homeostasis in the gut, where dysbiosis exacerbates This pathway is activated in response to bacterial pathogens and is especially imporwith age [21,22,23,24,25]. IMD, and sub-group O JAK/STAT transcription factor in (dFOXO), a downstream target of pathways in Drosophila [27,28,29,30,31]. Factor Relish and subsequent transcription of genes, including Diptericin, Drosocin, Cecropin, Attapathway is activated via Unpaired (Upd) cytokine detection in response to viral and bacterial infection, aging, and stress. Activation of dInR subsequently affects the activity of the Target of Rapamycin (dTOR) factor, as well as the dFOXO transcription factor
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
