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Microbial Biotechnology
Published in Nwadiuto (Diuto) Esiobu, James Chukwuma Ogbonna, Charles Oluwaseun Adetunji, Olawole O. Obembe, Ifeoma Maureen Ezeonu, Abdulrazak B. Ibrahim, Benjamin Ewa Ubi, Microbiomes and Emerging Applications, 2022
Olawole O. Obembe, Nwadiuto (Diuto) Esiobu, O. S. Aworunse, Nneka R. Agbakoba
Autoimmune disorders are those diseases whereby an individual’s immune system attacks self‐tissues. In an autoimmune disease, the immune system does not recognize self-cells, which it sees as foreign, and so releases autoantibodies that attack the healthy cells. Apart from aberrant autoantibodies production, genetic, immunologic, and environmental factors also play contributory roles in autoimmune diseases. A significant function of the gut microbiota is the maintenance of homeostasis of the human immune system, and so, any dysbiosis in the gut can adversely affect the host. Dysbiosis of the gut microbiome, which can come in the form of excessive growth of potentially pathogenic organisms, loss of beneficial organisms, or the entire loss of microbial diversity, can induce autoimmune disease in people (De Gruttola et al., 2016). Several autoimmune diseases are known, and some of them include type 1 diabetes mellitus (T1DM), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and inflammatory bowel disease.
Autologous Stem Cell Transplantation in Animal Models of Autoimmune Diseases
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
In view of these data, that are reviewed elsewhere,9 the differences between the spontaneous and the inducible AD may well be less fundamental than is generally assumed. In both disease categories, there is a genetic disposition that allows activation of anti-self immunity; in the case of the spontaneous diseases, activation is by relatively weak ubiquitous antigens; in the case of the inducible AD by strong specific antigens. Both mechanisms leave ample room for a role of infectious agents acting as the initiating stimulus, either by providing antigens that resemble tissue targets (so-called mimicry), or by acting as regulators of the immune reactivity, similar to adjuvants, hormones and dietary factors. All these determinants, genetic as well as environmental, have also been implicated in the pathogenesis of human AD. The ethiology of human AD is undisputedly multifactorial. In almost all autoimmune conditions there is a familial tendency. Many AD are induced by drugs: more than 70 different drugs have been reported to induce SLE. Furthermore, many xenobiotics e.g food supplements, heavy metals and environmental toxins, have been linked to the development of SLE-like illnesses. Although in many patients with AD the causative agent remains unknown, the low concordance in identical twins seems to argue in favor of the inducible disease models as being the more appropriate tools for translational research.
Auto-antibodies as Biomarkers for Disease Diagnosis
Published in Raj Bawa, János Szebeni, Thomas J. Webster, Gerald F. Audette, Immune Aspects of Biopharmaceuticals and Nanomedicines, 2019
Angelika Lueking, Heike Göhler, Peter Schulz-Knappe
Auto-antibodies are a class of biomarkers suitable for risk assessment, screening, prognosis, disease stratification, and therapy monitoring. Auto-antibodies, i.e., antibodies directed against certain human proteins, are induced by immune system activity in response to a disease process. Auto-antibody production reflects the immune response to a continuous remodeling of cells or tissues caused by protein turnover and chronic disease processes. In this context, the immune system fails to properly distinguish between self and nonself, and attacks its own cells and tissues. However, in so-called autoimmune diseases, the auto-antibodies present in blood are indicative for the clinical symptoms and the state of the disease. Prominent examples of autoimmune diseases are rheumatoid arthritis (RA), multiple sclerosis (MS), coeliac disease, diabetes mellitus type 1, systemic lupus erythematosus (SLE), Sjogren’s syndrome, inflammatory bowel disease, and Hashimoto’s thyroiditis.
Exposure of Akwesasne Mohawk women to polychlorinated biphenyls and hexachlorobenzene is associated with increased serum levels of thyroid peroxidase autoantibodies
Published in Journal of Toxicology and Environmental Health, Part A, 2023
Florence Lee, Mia V. Gallo, Lawrence M. Schell, Julia Jennings, David A. Lawrence, Akwesasne Task Force On the Environment
Autoimmune diseases might affect multiple systems within the body and represent a range of disorders in which the immune system might harm healthy organs and cells. Autoimmune thyroid disease (AITD) occurs when there is aberrant immune activity, leading to dysregulation of the thyroid gland (Antonelli et al. 2015; Kyritsi and Kanaka-Gantenbein 2020; Lee et al. 2015; Weetman 2021). While the cause of AITD is unknown, it is postulated that the onset of AITD is associated with genetic susceptibility and environmental exposures that could become catalysts in disease development (Lee and Lawrence 2018; Tomer and Huber 2009). While twin studies showed that a portion of AITD is related to genetic predisposition (Hansen et al. 2006; Ringold et al. 2002), environmental exposure may help explain up to 30% of AITD incidence (Benvenga et al. 2020; Brent 2010; Colucci et al. 2015; Ferrari et al. 2017).
Epigenotoxicity: a danger to the future life
Published in Journal of Environmental Science and Health, Part A, 2023
Farzaneh Kefayati, Atoosa Karimi Babaahmadi, Taraneh Mousavi, Mahshid Hodjat, Mohammad Abdollahi
Genetic diversity, environmental effects, and epigenetic factors may bring about autoimmune diseases. Enzymes involved in the histone modification process can impair DNA repair processes. Some HDAC inhibitors (HDACi) increase the possibility of transcription of specific genes such as those involved in autoimmune diseases. These enzymes are more active in T cells and cause post-translational changes. Such changes eventually lead to the immune tolerance modulation and autoimmune diseases. lncRNAs control the expression of genes involved in the differentiation of immune cell types. Also, dysregulation of miRNAs was linked with the incidence of many autoimmune diseases by altering epigenetic mechanisms like DNA methylation, RNA-dependent mechanisms, and post-translational histone modifications.[90] Many chemical agents in the environment, such as various types of hydrocarbons, heavy metals, and agricultural chemicals that have already been addressed, are immunotoxic and cause structural, functional, or combined changes in various immune system components and alter the immune response.[176]
Analysis of autoantibody profiles in two asbestiform fiber exposure cohorts
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Jean C. Pfau, Christopher Barbour, Brad Black, Kinta M. Serve, Marvin J. Fritzler
Autoimmune diseases are reported to be the consequence of an environmental trigger factor in the context of genetic predisposition (Bernatsky et al. 2017b; Cooper et al. 2010; Lee and Lawrence 2018). In this setting, both the genetic and trigger components could have variability that leads to varying degrees of severity (Lee and Lawrence 2018). Autoantibodies can occur during pre-clinical phases of disease development, with ultimate disease development being dependent on other variables (Choi et al. 2016). With forms of asbestos, silica and nanofibers which all have complex surface properties, such variables might include cooperative cell interactions such as scavenger receptors which modulate responses in the early cellular responses including inflammasome activation, anti-oxidant regulation, and oxidative damage (Murthy et al. 2015; Nakayama 2018; Pfau et al. 2012; Thompson et al. 2014). Further research is needed to determine specific variables relating to differential B cell responses.