China
Africa
Explore chapters and articles related to this topic
Parasite Versus Host: Pathology and Disease
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
The phenomenon of immunopathology raises the question as to why it exists in the first place. Why has natural selection not eliminated these harmful responses? The answer is actually straightforward. It’s a dangerous world out there. Potential hosts simply must have a powerful array of defensive, immunological weapons on hand to protect them from a never-ending onslaught of both micro- and macroparasites. From the parasites’ perspective, hosts are resources to be exploited. Without an immune system, potential hosts could never survive. In addition, it is worth repeating that evolution via natural selection never ends in perfectly adapted organisms. Evolution results in a compromise. The various characteristics that we observe in any organism reflect the evolutionary trade-off that has been struck. Both immunopathology and successful immune defense represent the adaptive middle ground between competing demands that any living thing must deal with. This topic will be revisited in Chapter 6, where we explore the fascinating and recently emerging field of immunoecology, and in Chapter 7, where we address the topic of parasite evolution specifically.
Suffering with two dissimilar diseases
Published in Dinesh Kumar Jain, Homeopathy, 2022
“Immunity also plays a protective role in polio and a number of other viral infections. Immunity to many viral infections is life long” (Greenwood et al., 1997, p. 149). “It is also known that infections with influenza, rubella, measles and other viruses predisposes to bacterial and other infection” (Greenwood et al., 1997, p. 151). “Susceptibility to infection is generally greater in being young and old because of a weaker immune response. However, the immunopathology tends to be less severe” (Greenwood et al., 1997, p. 152). “Natural infection with a virus is an extremely effective means of giving life long immunity from the disease. In most cases where there is one virus type, it means that second attacks are extremely rare” (Greenwood et al., 1997, p. 153). “Because of the intimate relationship of viruses to the metabolism of their host cells, immunity may be raised or lowered by nutritional changes, endocrine disturbances, heat, cold, shock, radiation and other factors that stimulate or inhibit the activity of intracellular enzymes” (Pinkerton, 1971, p. 378).
Dermal Hypersensitivity: Immunologic Principles and Current Methods of Assessment
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
Dermal hypersensitivity reactions are inflammatory reactions of the skin that either defend the host against pathologic agents or damage host tissue and cause disease. The protective effects of hypersensitivity are a desirable part of host “immunity”, while the detrimental effects arise from immune-mediated lesions defined as “immunopathologic” disease.17 The terms “allergy” and “hypersensitivity” commonly denote deleterious immune reactions, which involve the pathophysiologic interaction of antigens (substances that induce an immune response) with specific antibodies (gamma globulin proteins) or with sensitized T lymphocytes.18 The immunopathologic consequences of these interactions are quite diverse, and will be discussed later. The term “allergy” generally designates immediate or humoral antibody reactions, while “hypersensitivity” usually signifies delayed cellular immune reactivity.17,19 The preferred term for delayed dermal hypersensitivity to contact allergens is “allergic contact dermatitis”, clinically known as dermatitis venenata.13
Biologics for dengue prevention: up-to-date
Published in Expert Opinion on Biological Therapy, 2023
Adam T Waickman, Krista Newell, Timothy P Endy, Stephen J Thomas
Despite great advances in the dengue field, a number of important questions remain and introduce risk into developing anti-dengue vaccines and drugs. Why some people avoid dengue disease with infection and others succumb largely remain a mystery? Secondary infections are known to carry a significantly increased risk of severe disease but a complete understanding of the immunopathologic and immune-protective mechanisms eludes the field. The impact of non-dengue flaviviruses on subsequent dengue infection is unclear. The duration of a protective immune response following natural infection or vaccination is unknown, but it is becoming increasingly clear that ‘lifelong immunity’ may not be the case. Along these lines there needs to be expanded study of how natural and vaccine-induced immunity may impact DENV evolution and how this may impact the dengue countermeasure development space over time (for example, to need to re-formulate vaccines to make circulating DENV strains). The importance of immunity to dengue’s non-structural proteins can be inferred from the Dengvaxia experience (i.e. you need it) but requires additional proof from field trials. Exploring the potential of antivirals as prophylaxis against DENV infection or disease also deserves attention. Addressing these questions and others requires controlling the virus and host factors, which could impact the outcome of infection. One way to close these knowledge gaps is through the execution of controlled human infection model (CHIMs) studies.
Autoimmune encephalitis: novel therapeutic targets at the preclinical level
Published in Expert Opinion on Therapeutic Targets, 2021
Josefine Sell, Holger Haselmann, Stefan Hallermann, Michael Hust, Christian Geis
None of the routinely applied immunotherapies directly interferes with aAB-induced pathomechanism or efficiently depletes aAB-producing cells in the CNS compartment, thus explaining the often prolonged recovery from disease symptoms [8]. Therefore, more specific and effective therapeutic approaches are needed. In principle, two different strategies are promising to establish such novel therapeutics. First, target-directed, symptomatic treatment that can be applied in addition to immunotherapy might overcome the temporal delay of treatment response and will improve disease symptoms more effectively. In the peripheral nervous system, this approach has been established in Myasthenia gravis (MG) several decades ago and the combination of immunotherapy with choline esterase inhibitors is still the gold standard in the therapy of MG with aABs to the acetylcholine receptor [54]. Second, there is need for immunotherapy specifically interfering with immunopathology of disease, e.g. with aAB production and with binding of aABs to the antigen (Figure 1). However, in AE the development of such novel and exciting therapeutic approaches is still in its infancies. In this review, we summarize the current progress in developing and establishing specific treatment strategies in the spectrum of AE.
Approaches for deciphering the molecular basis of disease and its translational benefits
Published in International Reviews of Immunology, 2019
Inflammation is an initial alert response to infection, injuries, and endogenous changes in cellular and molecular homeostasis. A moderate level of inflammation is essential for the clearance of microbial infection, wound healing, and/or tissue repair. In contrast, chronic or heightened inflammation leads to a wide range of immunopathology, such as pain and fever, or even metabolic, autoimmune diseases, or cancer. The first review article of this issue by Chen et al. discusses the links among adipose cells, lipid metabolism, proinflammatory cytokines, and metabolic diseases, including cancer, and how lipid metabolism induces oncogenesis through the production of inflammatory cytokines [1]. This article is useful to researchers and clinicians investigating the boundaries of metabolism and development of multifactorial metabolic diseases and looking for sustainable novel therapeutic targets (Figure 1).