Mechanisms of action of therapeutic amyloidogenic hexapeptides in amelioration of inflammatory brain disease.
J Exp Med
; 211(9): 1847-56, 2014 Aug 25.
Article
em En
| MEDLINE
| ID: mdl-25073790
ABSTRACT
Amyloid fibrils composed of peptides as short as six amino acids are effective therapeutics for experimental autoimmune encephalomyelitis (EAE). Immunosuppression arises from at least two pathways (1) expression of type 1 IFN by pDCs, which were induced by neutrophil extracellular traps arising from the endocytosis of the fibrils; and (2) the reduced expression of IFN-γ, TNF, and IL-6. The two independent pathways stimulated by the fibrils can act in concert to be immunosuppressive in Th1 indications, or in opposition, resulting in inflammation when Th17 T lymphocytes are predominant. The generation of type 1 IFN can be minimized by using polar, nonionizable, amyloidogenic peptides, which are effective in both Th1 and Th17 polarized EAE.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fragmentos de Peptídeos
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Encefalomielite Autoimune Experimental
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Amiloide
Limite:
Adult
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Animals
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Female
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Humans
Idioma:
En
Revista:
J Exp Med
Ano de publicação:
2014
Tipo de documento:
Article