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Between hope and fear : a history of vaccines and human immunity
\"An intelligent and compelling examination of the science of immunity, the public policy implications of vaccine denial, and the real-world outcomes of failing to vaccinate. If you have a child in school, you may have heard stories of long-dormant diseases suddenly reappearing--cases of measles, mumps, rubella, and whooping cough cropping up everywhere from elementary schools to Ivy League universities. How does a small group of people's failure to vaccinate have the potential to affect future generations? Are we at a turning point in medical history, where deadly diseases, once dormant, flourish anew? Will our children face summers of abandoned swimming pools due to polio outbreaks just like our great-grandparents did? Pioneering medical researcher Michael Kinch tells the remarkable story of vaccine-preventable infectious diseases in [this book], which explains how the science of immunity actually works and places immunology within the context of its social and political implications. While detailing the history of vaccine invention, from the steppes of Mongolia to the serendipitous connection between cowpox and smallpox, Kinch reveals the ominous reality that our victories against vaccine-preventable diseases are not permanent--and could easily be undone. ... Between Hope and Fear illuminates the fascinating intersection of science, technology, and disease that has helped eradicate many of the deadliest plagues known to man.\"-- Jacket.
Book
Is atherosclerosis an autoimmune disease?
Immunologic research into pathogenic mechanisms operating in autoimmune-mediated atherosclerosis initially focused on adaptive immunity. Current interest is directed to more basic inflammatory mechanisms. Chronic inflammation (innate immunity-associated) may trigger initial events that can lead to atherosclerotic cardiovascular disease. This chronic inflammation may start early in life and be perpetuated by classic atherosclerosis risk factors. Lipid peroxidation of low-density lipoprotein seems to be a key event in the initiation and progression of atherosclerosis. Oxidized low-density lipoprotein triggers inflammatory and immunogenic events that promote endothelial dysfunction and the synthesis and secretion of pro-inflammatory cytokines, leading to an autoimmune response capable of accelerating the intracellular accumulation of lipids within atherosclerotic plaques. Oxidized low-density lipoprotein binds β2-glycoprotein I to form circulating complexes found in both autoimmune and non-autoimmune atherosclerosis. It is likely that β2-glycoprotein I and/or these complexes contribute to early atherogenesis by stimulating pro-inflammatory innate immunity through endogenous sensors and inflammasome/interleukin-1 pathways. We discuss the chronic inflammatory (innate) and autoimmune (adaptive) responses operating in atherosclerosis to discern the role of autoimmunity in atherosclerotic cardiovascular disease.
Journal Article
Toll-Like Receptor Signaling and Its Role in Cell-Mediated Immunity
Innate immunity is the first defense system against invading pathogens. Toll-like receptors (TLRs) are well-defined pattern recognition receptors responsible for pathogen recognition and induction of innate immune responses. Since their discovery, TLRs have revolutionized the field of immunology by filling the gap between the initial recognition of pathogens by innate immune cells and the activation of the adaptive immune response. TLRs critically link innate immunity to adaptive immunity by regulating the activation of antigen-presenting cells and key cytokines. Furthermore, recent studies also have shown that TLR signaling can directly regulate the T cell activation, growth, differentiation, development, and function under diverse physiological conditions. This review provides an overview of TLR signaling pathways and their regulators and discusses how TLR signaling, directly and indirectly, regulates cell-mediated immunity. In addition, we also discuss how TLR signaling is critically important in the host’s defense against infectious diseases, autoimmune diseases, and cancer.
Journal Article
Modulation of Inflammatory Responses by Wnt/β-Catenin Signaling in Dendritic Cells: A Novel Immunotherapy Target for Autoimmunity and Cancer
The Wnt/β-catenin pathway is an evolutionarily conserved signaling pathway critical for several biological processes. An aberrant Wnt/β-catenin signaling is linked to several human diseases. Emerging studies have highlighted the regulatory role of the Wnt/β-catenin signaling pathway in normal physiological processes of parenchymal and hematopoietic cells. Recent studies have shown that the activation of Wnt/β-catenin pathway in dendritic cells (DCs) play a critical role in mucosal tolerance and suppression of chronic autoimmune pathologies. Alternatively, tumors activate Wnt/β-catenin pathway in DCs to induce immune tolerance and thereby evade antitumor immunity through suppression of effector T cell responses and promotion of regulatory T cell responses. Here, we review our work and current understanding of how Wnt/β-catenin signaling in DCs shapes the immune response in cancer and autoimmunity and discuss how Wnt/β-catenin pathway can be targeted for successful therapeutic interventions in various human diseases.
Journal Article
Periphery and brain, innate and adaptive immunity in Parkinson’s disease
Parkinson’s disease (PD) is a neurodegenerative disorder where alpha-synuclein plays a central role in the death and dysfunction of neurons, both, in central, as well as in the peripheral nervous system. Besides the neuronal events observed in patients, PD also includes a significant immune component. It is suggested that the PD-associated immune response will have consequences on neuronal health, thus opening immunomodulation as a potential therapeutic strategy in PD. The immune changes during the disease occur in the brain, involving microglia, but also in the periphery with changes in cells of the innate immune system, particularly monocytes, as well as those of adaptive immunity, such as T-cells. This realization arises from multiple patient studies, but also from data in animal models of the disease, providing strong evidence for innate and adaptive immune system crosstalk in the central nervous system and periphery in PD. Here we review the data showing that alpha-synuclein plays a crucial role in the activation of the innate and adaptive immune system. We will also describe the studies suggesting that inflammation in PD includes early changes in innate and adaptive immune cells that develop dynamically through time during disease, contributing to neuronal degeneration and symptomatology in patients. This novel finding has contributed to the definition of PD as a multisystem disease that should be approached in a more integratory manner rather than a brain-focused classical approach.
Journal Article
Role of inflammation, immunity, and oxidative stress in hypertension: New insights and potential therapeutic targets
Hypertension is regarded as the most prominent risk factor for cardiovascular diseases, which have become a primary cause of death, and recent research has demonstrated that chronic inflammation is involved in the pathogenesis of hypertension. Both innate and adaptive immunity are now known to promote the elevation of blood pressure by triggering vascular inflammation and microvascular remodeling. For example, as an important part of innate immune system, classically activated macrophages (M1), neutrophils, and dendritic cells contribute to hypertension by secreting inflammatory cy3tokines. In particular, interferon-gamma (IFN-γ) and interleukin-17 (IL-17) produced by activated T lymphocytes contribute to hypertension by inducing oxidative stress injury and endothelial dysfunction. However, the regulatory T cells and alternatively activated macrophages (M2) may have a protective role in hypertension. Although inflammation is related to hypertension, the exact mechanisms are complex and unclear. The present review aims to reveal the roles of inflammation, immunity, and oxidative stress in the initiation and evolution of hypertension. We envisage that the review will strengthen public understanding of the pathophysiological mechanisms of hypertension and may provide new insights and potential therapeutic strategies for hypertension.
Journal Article
The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer’s disease
Innate immunity is associated with Alzheimer’s disease
1
, but the influence of immune activation on the production of amyloid-β is unknown
2
,
3
. Here we identify interferon-induced transmembrane protein 3 (IFITM3) as a γ-secretase modulatory protein, and establish a mechanism by which inflammation affects the generation of amyloid-β. Inflammatory cytokines induce the expression of IFITM3 in neurons and astrocytes, which binds to γ-secretase and upregulates its activity, thereby increasing the production of amyloid-β. The expression of IFITM3 is increased with ageing and in mouse models that express familial Alzheimer’s disease genes. Furthermore, knockout of IFITM3 reduces γ-secretase activity and the formation of amyloid plaques in a transgenic mouse model (5xFAD) of early amyloid deposition. IFITM3 protein is upregulated in tissue samples from a subset of patients with late-onset Alzheimer’s disease that exhibit higher γ-secretase activity. The amount of IFITM3 in the γ-secretase complex has a strong and positive correlation with γ-secretase activity in samples from patients with late-onset Alzheimer’s disease. These findings reveal a mechanism in which γ-secretase is modulated by neuroinflammation via IFITM3 and the risk of Alzheimer’s disease is thereby increased.
The IFITM3 innate immunity protein directly binds presenilin near the active site and upregulates γ-secretase activity and the production of amyloid-β, and IFITM3 is upregulated in patients with late-onset Alzheimer’s disease.
Journal Article
Roles of RNA silencing in viral and non-viral plant immunity and in the crosstalk between disease resistance systems
RNA silencing is a well-established antiviral immunity system in plants, in which small RNAs guide Argonaute proteins to targets in viral RNA or DNA, resulting in virus repression. Virus-encoded suppressors of silencing counteract this defence system. In this Review, we discuss recent findings about antiviral RNA silencing, including the movement of RNA through plasmodesmata and the differentiation between plant self and viral RNAs. We also discuss the emerging role of RNA silencing in plant immunity against non-viral pathogens. This immunity is mediated by transkingdom movement of RNA into and out of the infected plant cells in vesicles or as extracellular nucleoproteins and, like antiviral immunity, is influenced by the silencing suppressors encoded in the pathogens’ genomes. Another effect of RNA silencing on general immunity involves host-encoded small RNAs, including microRNAs, that regulate NOD-like receptors and defence signalling pathways in the innate immunity system of plants. These RNA silencing pathways form a network of processes with both positive and negative effects on the immune systems of plants.RNA silencing through small RNAs is a major antiviral immunity system in plants. Recent findings are uncovering the roles of RNA silencing in immunity against non-viral pathogens, which is mediated by trans-kingdom RNA movements in vesicles or as extracellular nucleoproteins. RNA silencing also enables the crosstalk between other plant immunity systems.
Journal Article
The interaction of innate immune and adaptive immune system
The innate immune system serves as the body's first line of defense, utilizing pattern recognition receptors like Toll‐like receptors to detect pathogens and initiate rapid response mechanisms. Following this initial response, adaptive immunity provides highly specific and sustained killing of pathogens via B cells, T cells, and antibodies. Traditionally, it has been assumed that innate immunity activates adaptive immunity; however, recent studies have revealed more complex interactions. This review provides a detailed dissection of the composition and function of the innate and adaptive immune systems, emphasizing their synergistic roles in physiological and pathological contexts, providing new insights into the link between these two forms of immunity. Precise regulation of both immune systems at the same time is more beneficial in the fight against immune‐related diseases, for example, the cGAS–STING pathway has been found to play an important role in infections and cancers. In addition, this paper summarizes the challenges and future directions in the field of immunity, including the latest single‐cell sequencing technologies, CAR‐T cell therapy, and immune checkpoint inhibitors. By summarizing these developments, this review aims to enhance our understanding of the complexity interactions between innate and adaptive immunity and provides new perspectives in understanding the immune system. This review begins with a complete description of the composition and function of innate and acquired immunity. On this basis we summarize how the two systems interact and influence disease progression. The paper concludes with a review of therapeutic options and future directions for immune system research.
Journal Article
How the immune system shapes atherosclerosis: roles of innate and adaptive immunity
Atherosclerosis is the root cause of many cardiovascular diseases. Extensive research in preclinical models and emerging evidence in humans have established the crucial roles of the innate and adaptive immune systems in driving atherosclerosis-associated chronic inflammation in arterial blood vessels. New techniques have highlighted the enormous heterogeneity of leukocyte subsets in the arterial wall that have pro-inflammatory or regulatory roles in atherogenesis. Understanding the homing and activation pathways of these immune cells, their disease-associated dynamics and their regulation by microbial and metabolic factors will be crucial for the development of clinical interventions for atherosclerosis, including potentially vaccination-based therapeutic strategies. Here, we review key molecular mechanisms of immune cell activation implicated in modulating atherogenesis and provide an update on the contributions of innate and adaptive immune cell subsets in atherosclerosis.Atherosclerosis involves a maladaptive inflammatory response. This Review summarizes the contributions of key innate and adaptive immune cell subsets and describes diverse mechanisms that regulate their activation. It also discusses the feasibility of developing immune-targeted interventions, such as tolerogenic vaccines.
Journal Article