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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
The innate immune response provides an immediate and relatively non-specific response to challenge. In contrast, the adaptive immune system, involving T cells and antibodies secreted by B cells, requires an initial priming stage followed by cell proliferation when it encounters a target for the first time. Adaptive immunity is highly specific for individual antigens and, following an initial encounter, can persist to provide a memory response.
The immune and lymphatic systems, infection and sepsis
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Michelle Treacy, Caroline Smales, Helen Dutton
The way in which the body responds to infection varies and is related to several factors, such as our own genetic disposition, previous exposure to antigens and the pathogenicity or virulence of the organism. Inflammatory responses also vary: some individuals may exhibit an excessive immunological response which can cause many problems and, in some cases, may actually lead to death, such as in anaphylaxis or hypersensitivity to allergens. Inflammation is another innate immune response and is described below.
Infections in Cirrhosis in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
John M. Horne, Laurel C. Preheim
Cirrhosis-associated immune dysfunction (CAID) is a complex phenomenon involving alterations of both innate and acquired immunity, leading to both immunodeficiency and systemic inflammation (reviewed in [9]). Innate immunity is affected by impaired liver synthesis or expression of pattern recognition receptors (PRRs), Toll-like receptors (TLRs), and C-reactive protein (CRP), factors integral to the recognition and elimination of bacterial pathogens. Hepatic Kupffer cells (macrophages) act as scavenger cells to filter blood and, when activated, release cytokines and other inflammatory mediators of innate host defense. Hepatocytes synthesize complement, another important component of innate immune response to infection. Examples of CAID identified by human and experimental animal studies include impairment of chemotaxis, phagocytosis, and intracellular killing by polymorphonuclear leukocytes (PMNL) and monocytes [10–12]; reduction in serum bactericidal activity and opsonic activity [13,14]; depression of serum complement [15–17]; dysregulation of cytokine synthesis and metabolism [18]; and reduced protective efficacy of type-specific antibody [19] and granulocyte colony-stimulating factor [20].
A standardized extract of Echinacea purpurea containing higher chicoric acid content enhances immune function in murine macrophages and cyclophosphamide-induced immunosuppression mice
Published in Pharmaceutical Biology, 2023
Heggar Venkataramana Sudeep, Kuluvar Gouthamchandra, Illuri Ramanaiah, Amritha Raj, Puttaswamy Naveen, Kodimule Shyamprasad
The term immunity defines the body’s natural defense system against a massive array of diseases and disorders. Surprisingly complicated and advanced among vertebrates, the complex immune system is capable to produce a boundless variety of cells and molecules to block enormous variety of infections and undesirable elements (Patil et al. 2012; Dutt 2013; Sharma et al. 2017). The strategy of avoiding them all may be extraordinarily tricky or difficult and many of the pathogens have mechanisms that allow them to evade the full effects of host defenses. The innate immune responses are generally rapid and independent of immunological memory unlike the adaptive immunity. Innate immune responses include the cellular mechanisms, for example phagocytosis and cytotoxicity, or secretions (cytokines, complimentary factors, antimicrobial peptides, etc.) (Degn and Thiel 2013; Hilchie et al. 2013; Sokol and Luster 2015). Our knowledge of immune functioning is constantly evolving over the years. There exists a paradigm from emerging evidence that the innate and adaptive immunity have mutually interacted and overlapped at times (Gasteiger et al. 2017). With recent advances in the understanding of how cells communicate with each other to signal effector functions, it has become possible to conceive of strategies to manipulate these signaling pathways to influence host responses (Tzianabos 2000). Compounds that can interact with the immune system to upregulate or downregulate specific aspects of the host response can be classified as immunomodulators or biologic response modifiers.
Association of Killer Cell Immunoglobulin-Like Receptors and Their HLA-Ligands with Type 1 Diabetes Among South Indian Population
Published in Immunological Investigations, 2023
Nagarajan Gunavathy, Arthur Asirvatham, Ayyappan Chitra, Mariakuttikan Jayalakshmi
Type 1 diabetes (T1D) is an organ-specific, multifactorial autoimmune disease characterized by the complete destruction of pancreatic β-cells leading to absolute insulin dependency. Genetic and environmental factors play crucial roles in the predisposition to T1D (Bluestone et al. 2010). The incidence of T1D is mostly observed in children and young adults, although it occurs at any age (Lammi et al. 2008). The Diabetes Atlas 2021 released by the International Diabetes Federation illustrates that India has the World’s highest number of children and young adults with T1D (Brussels 2021). The underlying mechanisms that lead to the development of T1D still remain unexplained. Natural Killer (NK) cells play a vital role in modulating the innate immune response with their ability to produce cytokines and chemokines (Trinchieri 1989). Killer cell immunoglobulin-like receptors (KIRs) present on the NK cell surface, are the key receptors having a major role in regulating the function of NK cells (Lanier 1998). KIRs are also expressed on the subsets of T lymphocytes, especially on CD8+ cells (Parham 2005).
Negative Regulation of RIG-I by Tim-3 Promotes H1N1 Infection
Published in Immunological Investigations, 2023
Qingzhu Shi, Ge Li, Shuaijie Dou, Lili Tang, Chunmei Hou, Zhiding Wang, Yang Gao, Zhenfang Gao, Ying Hao, Rongliang Mo, Beifen Shen, Renxi Wang, Yuxiang Li, Gencheng Han
Innate immune responses have attracted much attention recently in the treatment of immune disorders, including infectious diseases. The RLR RIG-I is a cytoplasmic RNA sensor that detects viral RNA and triggers the signal to induce type I IFN and proinflammatory cytokine production during viral infection. As an important trigger of antiviral innate immunity, RIG-I should be tightly regulated to avoid autoimmune damage mediated by an excessive immune response. The mechanisms by which RIG-I is regulated under different physio-pathological conditions is of great interest to be determined. In this study, we found a new mechanism by which Tim-3 induces viral immune evasion: by suppressing RIG-I transcription and promoting its ubiquitination and degradation, Tim-3 inhibits type I IFN production and antiviral activity. Our findings confirm that Tim-3 may also contribute to infection tolerance by regulating the activity of innate immunity.