Molecular Mimicry and T Cell–mediated Autoimmune Disease
نویسندگان
چکیده
منابع مشابه
Molecular Mimicry and T Cell–mediated Autoimmune Disease
B oth T cell tolerance and productive T cell responses require the interaction of the TCR with specific MHC–peptide ligands, triggering a cascade of signals that ultimately can lead to either proliferation or cell death (1– 3). These two opposing processes, which can occur during both peripheral T cell activation and/or positive/negative selection of T cells in the thymus, seem to be tuned by t...
متن کاملMolecular mimicry in autoimmune disease.
The origins of autoimmune disease are multifactorial. Environmental factors and a genetic predisposition result in tissue injury caused by autoreactive T cells or antibodies. Usually a single organ or individual cell type is aVected in the absence of gross abnormalities of the immune system. Autoimmune diseases tend to have long, asymptomatic prodromal periods and the initiating events leading ...
متن کاملDisease mimicry--a pathogenetic concept for T cell-mediated autoimmune disorders triggered by molecular mimicry?
Molecular mimicry is considered as a mechanism by which infectious pathogens may break immunological tolerance and cause autoimmune disease. It implicates that peptides shared between pathogen and host may induce cross-reactive immune reactions. According to this hypothesis, the resulting autoimmune response actually represents a secondary immune response. It is mediated by cross-reactive T cel...
متن کاملMolecular mimicry between neurons and an intracerebral pathogen induces a CD8 T cell-mediated autoimmune disease.
To identify basic mechanisms of how infections may induce a neuron-specific autoimmune response, we generated mice expressing OVA as neuronal autoantigen under control of the neuron-specific enolase promoter (NSE-OVA mice). Intracerebral, but not systemic, infection with attenuated Listeria monocytogenes-secreting OVA induced an atactic-paretic neurological syndrome in NSE-OVA mice after bacter...
متن کاملMolecular mimicry in the autoimmune pathogenesis of rheumatic heart disease.
Molecular mimicry is a hallmark of the pathogenesis of rheumatic fever where the streptococcal group A carbohydrate epitope, N-acetyl glucosamine, and the a-helical coiled-coil streptococcal M protein structurally mimic cardiac myosin in the human disease, rheumatic carditis, and in animal models immunized with streptococcal M protein and cardiac myosin. Recent studies have unraveled the potent...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Experimental Medicine
سال: 1997
ISSN: 0022-1007,1540-9538
DOI: 10.1084/jem.185.9.1529