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Autoimmune Diseases and a Multidisciplinary Approach to Cancer
Published in Mehwish Iqbal, Complementary and Alternative Medicinal Approaches for Enhancing Immunity, 2023
Autoimmunity is caused by the uneasiness and abnormality of the human immune system, which gives rise to pathologic and extreme responses from adaptive and innate immunity against organ-precise self-antigens, consequently ensuing in dysfunction and destruction of tissues by means of inducing injury and inflammation in the systems that are affected (Davidson & Diamond, 2001).
Sjögren's Disease
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
In addition, we expect that biomarkers will enable better definition of patients with suspected or known SjD who lack characteristic autoantibodies, particularly anti-SSA/Ro and anti-SSB/La antibodies. Patients with so-called “seronegative” SjD are enriched with those who have small-fiber sensory neuropathy and greater pain. More precise diagnostic tools will enable determination as to whether these patients have underlying autoimmunity and would thus benefit from immunosuppressive therapies. This is often a diagnostic conundrum for clinicians.
Rheumatic Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
As the fundamental mechanisms of the immune response are becoming clearer, novel approaches to therapy are being developed for the treatment of RA and other systemic inflammatory diseases associated with autoimmunity. The major biological therapeutics in clinical use include protein molecules, such as monoclonal antibodies, and small molecule kinase inhibitors. Biological therapeutics have been developed that can: Interfere with cytokine function, signal transduction or productionInhibit the ‘second signal’ required for T-cell activationDeplete B cells
Beyond the amyloid hypothesis: how current research implicates autoimmunity in Alzheimer’s disease pathogenesis
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Miyo K. Chatanaka, Dorsa Sohaei, Eleftherios P. Diamandis, Ioannis Prassas
The immune system is a sophisticated organ that orchestrates the fight against foreign pathogens. The B cells of the humoral response of the adaptive immune system, showcase an almost infinite number of different receptors that can bind to pathogenic molecules, leading to their eventual destruction [1]. As explained in detail previously [2], B cells undergo a selection process in the thymus that filters out any cells that cannot distinguish “self” from “non-self” antigens. The T cells of the cell-mediated arm of adaptive immunity undergo a similar process in the thymus that establishes a central tolerance by eliminating naive T cells with T cell receptors (TCRs) that recognize “self” antigens [3,4]. In addition, any autoreactive T cells that escape thymic selection are further subjected to clonal anergy, deletion, and ignorance, and regulatory T cells (Tregs) assist in the tight regulation of these dangerous B and T cells [3]. Through various processes and physiological aging, however, this intricate system frequently deteriorates and the regenerative capacity of the organs that create immune cells progressively reduces their functional capabilities (see [5,6]). This allows for autoantibodies (antibodies directed against self-antigens) to initiate a chain reaction that leads to misdirected and harmful immune responses [7]. Therefore, autoimmunity is a biological process whereby the organism loses its immune tolerance and mounts attacks against self-antigens (autoantigens).
Prospects for CAR T cell immunotherapy in autoimmune diseases: clues from Lupus
Published in Expert Opinion on Biological Therapy, 2022
Marko Radic, Indira Neeli, Tony Marion
Approximately one in 14 people will, sometime during their lifetime, experience one of the known autoimmune disorders [1]. Autoimmunity arises in myriad ways and results in strikingly different pathologies. Dozens of clinical diagnoses for autoimmune disorders are possible and include familiar ones, such as rheumatoid arthritis, multiple sclerosis, type I diabetes, psoriasis, and immune vasculitis, as well as dozens of less frequent autoimmune diseases or syndromes [2]. The defining signs of many autoimmune diseases give clues to the targets of autoimmunity. Autoimmune reactivity thus defines many of the most characteristic features of autoimmune disorders. Destruction of islet cells in the pancreas leads to the insulin insufficiency of diabetes [3], the attack on myelin sheaths of neurons results in the neuropathology of multiple sclerosis [4], and the destruction of cartilage and bone contorts articular joints in rheumatoid arthritis [5]. Mechanisms of autoimmunity may involve the sudden appearance of autoantibodies, the activation of self-reactive cytotoxic T cells, the induction of self-sustaining, chronic inflammation, or a combination of contributing factors that overlap at different stages of pathogenesis in these disorders [6]. Manifestations of each autoimmune disease may be further modified by intrinsic factors or environmental contributions [2].
Evaluation of Expression of LRBA and CTLA-4 Proteins in Common Variable Immunodeficiency Patients
Published in Immunological Investigations, 2022
Fereshte Salami, Saba Fekrvand, Reza Yazdani, Sepideh Shahkarami, Gholamreza Azizi, Yasser Bagheri, Samaneh Delavari, Sahar Shariati, Seyed Alireza Mahdaviani, Mohammamd Nabavi, Afshin Shirkani, Hassan Abolhassani, Morteza Samadi, Asghar Aghamohammadi
In the present case-control study, all newly diagnosed patients (during 2018–2019) with CVID who were under clinical follow up based on the national consensus management for PID (Abolhassani et al. 2019b, 2018) at Children’s Medical Center (Pediatrics Center of Excellence) were enrolled. The diagnosis of CVID was made according to the newest criteria proposed by the European Society for Immunodeficiencies (ESID) (Seidel et al. 2019). At least one of the following should be manifested in the patient; increased susceptibility to infection, autoimmunity, granulomatous disease, unexplained polyclonal lymphoproliferation, or an affected family member with antibody deficiency, together with a marked decrease of IgG and IgA with or without low IgM, and poor antibody response to vaccines or low switched memory B cells in individuals more than four years old. Also, secondary causes of hypogammaglobulinemia should be excluded, and there should be no evidence of profound T-cell deficiency. CVID patients with infection, only phenotype were not recruited for further steps (Tak Manesh et al. 2017). The autoimmunity diagnosis was made by an immunologist and a subspecialist related to the affected organ based on the previously published clinical and laboratory diagnostic criteria (Azizi et al. 2017b). Age and sex-matched healthy individuals were included as the control group. This study was confirmed by the Ethics Committee of the Tehran University of Medical Sciences, and written informed consent was obtained from all the cases and/or children’s parent(s).