Abstract
Autoimmune diseases result from the breakdown of “self” tolerance. Environmental factors appear to be responsible for triggering this errant immune response, directed against self-tissue determinants, only when a susceptible genetic background is present in an individual. Autoimmune diseases, normally characterized by their association with certain HLA alleles, also share other features: the presence of autoantibodies, autoreactive T lymphocytes, and an intermittent clinical course of exacerbations and remissions. In cases of organ-specific diseases, as well as in cases of multi-system autoimmune diseases, viruses are increasingly implicated as such environmental triggers. Current molecular biology techniques have permitted a fine dissection of the genetic background of susceptible individuals and have enabled a more complete characterization of the immunocompetent cells involved in this autoaggression. Molecular approaches will soon allow us to pinpoint the characteristics of the environmental stimuli, so that protective strategies could be formulated to spare susceptible individuals from their ill effects.
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Abbreviations
- AChR :
-
Acetylcholine receptor
- EAE :
-
Experimental allergic encephalomyelitis
- ERV :
-
Endogenous retrovirus
- GAD :
-
Glutamic acid decarboxylase
- HIV :
-
Human immunodeficiency virus
- hsp :
-
Heat-shock protein
- HTLV :
-
Human T cell leukemia virus
- ICA :
-
Islet-cell cytoplasmic autoantibodies
- IDDM :
-
Insulin-dependent diabetes mellitus
- JRA :
-
Juvenile rheumatoid arthritis
- MBP :
-
Myelin basic protein
- MHC :
-
Major histocompatibility complex
- MMTV :
-
Mouse mammary tumor virus
- NOD :
-
Nonobese diabetic
- RA :
-
Rheumatoid arthritis
- SLE :
-
Systemic lupus erythematosus
- TCR :
-
T cell receptor
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Luppi, P., Rossiello, M.R., Faas, S. et al. Genetic background and environment contribute synergistically to the onset of autoimmune diseases. J Mol Med 73, 381–393 (1995). https://doi.org/10.1007/BF00240137
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DOI: https://doi.org/10.1007/BF00240137