The age of an individual is an important, independent risk factor for many of the most common diseases afflicting modern societies. Interleukin-7 (IL-7) plays a central, critical role in the homeostasis of the immune system. Recent studies support a critical role for IL-7 in the maintenance of a vigorous healthspan. We describe the role of IL-7 and its receptor in immunosenescence, the aging of the immune system. An understanding of the role that IL-7 plays in aging may permit parsimonious preventative or therapeutic solutions for diverse conditions. Perhaps IL-7 might be used to “tune” the immune system to optimize human healthspan and longevity.
Stroke is one of the predominant causes of long-term disability and death, and is characterized by the cessation of blood flow to part of the brain, preventing it from accessing oxygen and nutrients needed for ATP production and proper function. Ischemic stroke, the most prevalent type of stroke, involves an obstruction such as a blood clot in a blood vessel. Current treatments seek to remove the obstruction and restore blood flow, but are time-limited and do not reverse tissue damage once it has occurred. The endogenous response to ischemic stroke involves an increase in neurogenesis but falls short in producing functional recovery. Gene therapy that enhances neurogenesis has provided encouraging results in animal models. Preclinical studies in this area have utilized neurotrophic factors that can promote migration of cells from the subventricular zone (SVZ). The transcription factor NeuroD1 converts reactive glial cells, which increase during ischemia, into neurons that integrate into the existing circuits of the brain. The clinical value of gene therapy depends upon the development of safe and efficient administration methods. In this review, we draw from scientific literature to evaluate the relevant genes and vectors for treating ischemic stroke through neurogenesis, and discuss strategies to overcome current limitations of gene therapy in human patients.
Necroptosis, a type of pathological and inflammatory cell death, resembles necrosis, the termination of function of a bodily tissue, but adopts a unique molecular pathway that is not like apoptosis, resulting in vastly different immunological consequences. Until recently, necroptosis was believed to mainly function as a protective mechanism that counteracts the viral barrier of apoptosis. However, mouse model studies have indicated that deficiency in elements of the apoptosis machinery such as caspase-8 or FADD can result in embryonic lethality driven by necroptosis. Previous studies using conditional depletion of cellular inhibitors of apoptosis (cIAPs) revealed that the necroptosis pathway is triggered under certain stressor conditions. These data support a new approach of targeting molecules within the cell death pathways to identify the origin of autoimmune diseases. Hence, distinguishing between these two types of cell death may prove crucial during pathologic evaluations. This review provides a detailed insight into the emerging discussion on the various forms of cell death and the essential roles which certain molecules play in the development and progression of autoimmune diseases. Armed with this knowledge, greater efforts can be targeted towards devising more effective treatments for interception of pathological diseases, prior to their uncontrollable progression.
Type 1 Diabetes (T1D) is one of the most common chronic autoimmune diseases characterized by islet autoimmunity. This is followed by immune destruction of the β-cells as T cells attack and destroy insulin-secreting pancreatic β cells, leading to insulin deficiency. Currently, life-long insulin therapy is the primary treatment option for the condition with research being centered around islet transplantation to restore glycemic stability. However, this procedure is limited by risks and supply shortages, highlighting the need for a safer, more effective therapy for the approximately 9 million people across the world with Type 1 Diabetes. This literature review serves to assess stem cells and their potential as a vast β-cell supply towards the treatment of Type 1 diabetes. Stem cells may differentiate to become a self-renewing β-cell line that may reverse Type 1 Diabetes; however, further studies expanding on encapsulation techniques, methods whereby living cells are entrapped in semi-permeable membranes for the purpose of disease treatment, are required. With this new horizon of possibilities, targeted efforts towards stem cell manipulation in expressing β-cell phenotype can pave the way for a highly efficacious treatment for Type 1 Diabetes.
Gene therapy is a growing field in research and development that may offer a long-lasting solution to several complex diseases, including chronic obstructive pulmonary disease (COPD). COPD is characterized by chronic inflammation in the lungs and the airways, leading to respiratory problems. COPD includes chronic bronchitis and emphysema. Optimizing treatments for gene therapy in COPD is of paramount importance given COPD's prominence as the fourth leading cause of disease-related death in the United States. We reviewed delivery methods in the current research, including liposomes, nanoparticles, electroporation, adeno-viruses, and adenoassociated viruses (AAV). The broad customizability in the diagnostic and treatment methods is evident in the recent studies. In this paper we explore each method and/or biomarker and evaluate several gene therapy avenues for COPD.
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