Abstract
Recent studies have established an important role of Th17 in induction of autoimmune diseases. We have found that although IL-17 receptor A (IL-17RA)(-/-) mice were resistant to experimental autoimmune encephalomyelitis, a small number of them developed milder clinical signs of this autoimmune disease. In addition, blockade of TGF-beta in IL-17RA(-/-) mice resulted in much more severe clinical signs of experimental autoimmune encephalomyelitis and significantly increased parenchymal lymphocyte infiltration in the CNS. Furthermore, the number of autoreactive Th1 cells was greatly increased in the inflamed spinal cord of IL-17RA(-/-) mice. These data support a role of IL-17RA-independent mechanisms in causing autoimmunity and its regulation by TGF-beta.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Amino Acid Sequence
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Animals
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Central Nervous System / immunology
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Central Nervous System / metabolism
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Central Nervous System / pathology
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Down-Regulation / genetics
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Down-Regulation / immunology*
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Encephalomyelitis, Autoimmune, Experimental / immunology*
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Encephalomyelitis, Autoimmune, Experimental / metabolism*
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Encephalomyelitis, Autoimmune, Experimental / pathology
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Inflammation Mediators / antagonists & inhibitors
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Inflammation Mediators / physiology
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Interleukin-17 / deficiency
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Interleukin-17 / genetics
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Interleukin-17 / physiology*
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Molecular Sequence Data
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Receptors, Interleukin-17 / deficiency
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Receptors, Interleukin-17 / genetics
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Receptors, Interleukin-17 / physiology*
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Severity of Illness Index
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Signal Transduction / genetics
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Signal Transduction / immunology*
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Th1 Cells / immunology
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Th1 Cells / metabolism
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Th1 Cells / pathology
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Transforming Growth Factor beta / antagonists & inhibitors
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Transforming Growth Factor beta / physiology*
Substances
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Inflammation Mediators
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Interleukin-17
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Receptors, Interleukin-17
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Transforming Growth Factor beta