Bystander activation and autoimmunity
| Autor: | M. Eric Gershwin, Christopher Chang, Diana M. Monsalve, Yovana Pacheco, Juan-Manuel Anaya, Yeny Acosta-Ampudia |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Autoimmune thyroiditis Gap junction Autoimmune diseases T-Lymphocytes Mediator Individuality Autoimmunity Review Disease Autoimmune hepatitis medicine.disease_cause Bystander activation Immune tolerance Bystander effect Bacterium 0302 clinical medicine Autoimmune disease T-cell activation Immunology and Allergy Priority journal Hashimoto disease Host Vaccination Immunological tolerance Memory t lymphocyte Molecular mimicry Graves disease Cytokines Infection Human Insulin dependent diabetes mellitus Latent period Virus infection Immunology Auto-reactive t cells Biology Cell communication T lymphocyte activation Legionella pneumophila Autoimmune Diseases Xenobiotics Multiple sclerosis 03 medical and health sciences Systemic lupus erythematosus Immune Tolerance medicine Animals Humans Epigenetics Rheumatoid arthritis Bystander Effect Nonhuman medicine.disease 030104 developmental biology Gene-Environment Interaction Bacterial infection Parasitosis 030215 immunology |
| Zdroj: | Repositorio EdocUR-U. Rosario Universidad del Rosario instacron:Universidad del Rosario |
| ISSN: | 0896-8411 |
| DOI: | 10.1016/j.jaut.2019.06.012 |
| Popis: | The interaction over time of genetic, epigenetic and environmental factors (i.e., autoimmune ecology) increases or decreases the liability an individual would have to develop an autoimmune disease (AD) depending on the misbalance between risk and protective effects. Pathogens have been the most common antecedent events studied, but multiple other environmental factors including xenobiotic chemicals, drugs, vaccines, and nutritional factors have been implicated into the development of ADs. Three main mechanisms have been offered to explain the development of autoimmunity: molecular mimicry, epitope spreading, and bystander activation. The latter is characterized by auto-reactive B and T cells that undergo activation in an antigen-independent manner, influencing the development and course of autoimmunity. Activation occurs due to a combination of an inflammatory milieu, co-signaling ligands, and interactions with neighboring cells. In this review, we will discuss the studies performed seeking to define the role of bystander activation in systemic and organ-specific ADs. In all cases, we are cognizant of individual differences between hosts and the variable latency time for clinical expression of disease, all of which have made our understanding of the etiology of loss of immune tolerance difficult and enigmatic. © 2019 Elsevier Ltd |
| Databáze: | OpenAIRE |
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