Abstract
Cholera toxin and its close relative, Escherichia coli heat-labile enterotoxin, are potent immunogens and mucosal adjuvants. The recent findings that their B subunits can promote tolerance highlights the complexity of their interactions with the immune system. Here, Neil Williams and colleagues review the mechanisms by which these molecules modulate leukocyte populations and seek to explain the paradox.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adjuvants, Immunologic*
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Animals
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Arthritis / immunology
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Arthritis / therapy
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Autoantigens / administration & dosage
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Autoantigens / immunology
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Autoimmune Diseases / immunology
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Autoimmune Diseases / therapy
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Bacterial Toxins / chemistry
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Bacterial Toxins / immunology*
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Bacterial Toxins / metabolism
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Bacterial Toxins / therapeutic use
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Carbohydrate Sequence
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Cholera Toxin / chemistry
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Cholera Toxin / immunology*
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Cholera Toxin / metabolism
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Cholera Toxin / therapeutic use
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Collagen / immunology
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Diabetes Mellitus, Type 1 / immunology
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Diabetes Mellitus, Type 1 / therapy
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Encephalomyelitis, Autoimmune, Experimental / immunology
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Encephalomyelitis, Autoimmune, Experimental / therapy
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Enterotoxins / chemistry
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Enterotoxins / immunology*
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Enterotoxins / metabolism
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Enterotoxins / therapeutic use
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Escherichia coli Proteins*
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G(M1) Ganglioside / chemistry
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G(M1) Ganglioside / metabolism
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Gene Expression Regulation / drug effects
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Hydrogen Bonding
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Immune Tolerance / drug effects*
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Interferon-gamma / biosynthesis
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Interferon-gamma / genetics
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Mice
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Mice, Inbred NOD
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Models, Molecular
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Molecular Sequence Data
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Protein Binding
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Protein Conformation
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Rats
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Structure-Activity Relationship
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Th2 Cells / immunology
Substances
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Adjuvants, Immunologic
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Autoantigens
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Bacterial Toxins
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Enterotoxins
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Escherichia coli Proteins
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G(M1) Ganglioside
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Interferon-gamma
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Collagen
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Cholera Toxin
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heat-labile enterotoxin, E coli