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Fenugreek in Management of Immunological, Infectious, and Malignant Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Rohini Pujari, Prasad Thakurdesai
Autoreactivity is a crucial mechanism that contributes to immunologic and non-immunologic disease pathogenesis (Rosenblum, Remedios, and Abbas 2015). Disordered innate immunity, including immune complex-mediated complement activation, adaptive immune responses against ‘self’-antigens, post-translationally modified proteins, dysregulated cytokine networks, osteoclast or chondrocyte activation, and imprinting of resident stromal cells are some of the factors responsible for most progressive autoimmune disorders (Firestein and McInnes 2017), which can lead to organ system dysfunction and premature death (Meyer, Decker, and Baughman 2010).
The Defended Body
Published in Roger Cooter, John Pickstone, Medicine in the Twentieth Century, 2020
But the defended body is not just one among many bodies waiting for analysis; it seems to offer an overarching view that articulates all the others — in “the age of immunology.”2 It links two major aspects of twentieth-century medicine: the successful fight against infectious diseases, and the scientific elaboration of a new function of the organism — immunity. Immunology, which stemmed from the germ theory of disease, has evolved to provide an encompassing view of the body which subordinates all physiological events to a common purpose: the defense and representation of the self.
Immunochemical Approaches to the Diagnosis of Alzheimer Disease
Published in Robert E. Becker, Ezio Giacobini, Alzheimer Disease, 2020
Every immunologic test requires a target molecule, which the antibody will detect. This target molecule, such as ß-hCG in the pregnancy test, is termed the antigen. Often the antigen is a fairly large molecule such as a protein and the antibody only binds to one part of protein. The site on a molecule recognized by the antibody is termed an epitope. A large molecule such as a protein has many potential epitopes.
The microbiome and rheumatic heart disease: current knowledge and future perspectives
Published in Acta Cardiologica, 2023
Gunavathy Nagarajan, Ramajayam Govindan, Maheshkumar Poomarimuthu, Rathinavel Andiappan, Sivakumar Elango, Stalinraja Maruthamuthu, Jayalakshmi Mariakuttikan, Sony Kadiam
Autoimmune disorders are characterised by the breakdown of immunologic tolerance that leads to the generation of autoantibody, autoreactive T cells, abnormal production of cytokines and increased inflammation. Various autoimmune disorders have been strongly associated with genetic and/or environmental predisposing factors. The microbiome plays a crucial role in maintaining the balance between host defense and immune tolerance. Dysbiosis have been linked with the dysregulation of multiple functions of the immune system [12] leading to autoimmune diseases through different mechanisms such as molecular mimicry, epitope spreading, pathogen persistence and bystander activation [50,51]. Further, the amplification of autoimmunity is influenced by the inflammatory milieu triggered by altered gut microbiota, altered expression of TLRs in APCs, the disproportion of Th1/Th17/Treg and the posttranslational modification of luminal proteins (PTMPs) facilitated by enzymes secreted from dysbiotic microbiota [49]. The defective PTMPs may produce neoepitopes that could become immunogenic and trigger autoimmunity. In addition, various studies demonstrated that microbial metabolites might regulate immune cells and cytokines by epigenetic modifications suggesting their potential role in autoimmunity [52].
Protein interaction, monocyte toxicity and immunogenic properties of cerium oxide crystals with 5% or 14% gadolinium, cobalt oxide and iron oxide nanoparticles – an interdisciplinary approach
Published in Nanotoxicology, 2021
Maria Assenhöj, Peter Eriksson, Pierre Dönnes, Stefan A. Ljunggren, Maritha Marcusson-Ståhl, Anna Du Rietz, Kajsa Uvdal, Helen Karlsson, Karin Cederbrant
Under normal conditions, immunologic tolerance toward autologous proteins is established to avoid autoimmunity. However, when an endogenous protein becomes part of a NP-protein complex structural changes may occur (Laera et al. 2011). These conformational alterations could potentially contribute to a higher risk for the protein being perceived as nonself. These endogenous proteins may also undergo ‘forced phagocytosis, by being phagocytosed as part of NP–protein complexes.’ If cytokine responses are induced simultaneously, a third factor for creating an antigen-specific response will be present. Taken together, these suggested mechanisms may very well contribute to affected tolerance by inducing immune responses to autologous structures derived from particle-borne proteins, resulting in autoimmunity.
Effect of inhaled anesthetic gases on immune status alterations in health care workers
Published in Journal of Immunotoxicology, 2021
Ashraf Mahmoud Emara, Khaled Ali Alrasheedi, Salha Dihim Alrashidi, Rehab Mohamed Elgharabawy
The major role of the immune system is in the identification/disposal of foreign antigens, production of immunologic memory, and bestowing tolerance to self-antigens. The lymphocyte populations of the immune system are comprised of thymus-derived (T-) lymphocytes, bone-marrow-derived (B-) lymphocytes, and natural-killer (NK) cells. CD4+ T-cells along with CD8+ T-cells constitute the majority of T-lymphocytes. CD4+ T-cells have several functions including activation of cells associated with innate immunity, B-cells, cytotoxic T-cells and non-immune cells (Luckheeram et al. 2012), in part, via secretion of a variety of cytokines. If the function of the immune system is made suboptimal, recovery from pathological states can be impaired and loss of immune regulation (Waters et al. 2018). Thus, effects of anesthesia on a host immune status can have an adverse clinical outcome.