Molecular mimicry and autoimmunity
Molecular mimicry is one of the leading mechanisms by which infectious or chemical agents may induce autoimmunity. It occurs when similarities between foreign and self-peptides favor an activation of autoreactive T or B cells by a foreign-derived antigen in a susceptible individual. However, molecul...
- Autores:
- Tipo de recurso:
- Fecha de publicación:
- 2018
- Institución:
- Universidad del Rosario
- Repositorio:
- Repositorio EdocUR - U. Rosario
- Idioma:
- eng
- OAI Identifier:
- oai:repository.urosario.edu.co:10336/22261
- Acceso en línea:
- https://doi.org/10.1016/j.jaut.2018.10.012
https://repository.urosario.edu.co/handle/10336/22261
- Palabra clave:
- Vaccine
Autoantibody
Autoantigen
Bacterial antigen
Lymphocyte antigen receptor
Virus antigen
Autoimmune disease
Autoimmune hepatitis
Autoimmune liver disease
Autoimmune thyroiditis
Autoimmunity
Cross reaction
Guillain barre syndrome
Human
Insulin dependent diabetes mellitus
Molecular mimicry
Multiple sclerosis
Nonhuman
Primary biliary cirrhosis
Priority journal
Review
Rheumatoid arthritis
Sjoegren syndrome
Systemic lupus erythematosus
Systemic sclerosis
Animal
Autoimmune disease
B lymphocyte
Biosynthesis
Gene expression
Genetics
Immunology
Microbiology
Molecular mimicry
Mouse
T lymphocyte
Virology
Animals
Autoantibodies
Autoantigens
Autoimmune diseases
Autoimmunity
B-lymphocytes
Cross reactions
Gene expression
Humans
Mice
Molecular mimicry
T-lymphocytes
Autoimmune diseases
Autoimmunity
Cross reactions
Cross-reactivity
Molecular mimicry
viral
bacterial
antigen
t-cell
Antigens
Antigens
Receptors
- Rights
- License
- Abierto (Texto Completo)
Summary: | Molecular mimicry is one of the leading mechanisms by which infectious or chemical agents may induce autoimmunity. It occurs when similarities between foreign and self-peptides favor an activation of autoreactive T or B cells by a foreign-derived antigen in a susceptible individual. However, molecular mimicry is unlikely to be the only underlying mechanism for autoimmune responses; other factors such as breach in central tolerance, non-specific bystander activation, or persistent antigenic stimuli (amongst others) may also contribute to the development of autoimmune diseases. Host genetics, exposure to microbiota and environmental chemicals are additional links to our understanding of molecular mimicry. Our current knowledge of the detailed mechanisms of molecular mimicry is limited by the issues of prolonged periods of latency before the appearance of disease, the lack of enough statistical power in epidemiological studies, the limitations of the potential role of genetics in human studies, the relevance of inbred murine models to the diverse human population and especially the limited technology to systematically dissect the human T-cell repertoire and B-cell responses. Nevertheless, studies on the role of autoreactive T-cells that are generated secondary to molecular mimicry, the diversity of the T-cell receptor repertoires of auto-reactive T-cells, the role of exposure to cryptic antigens, the generation of autoimmune B-cell responses, the interaction of microbiota and chemical adjuvants with the host immune systems all provide clues in advancing our understanding of the molecular mechanisms involved in the evolving concept of molecular mimicry and also may potentially aid in the prevention and treatment of autoimmune diseases. © 2018 The Authors |
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