Interferon-β therapy against EAE is effective only when development of the disease depends on the NLRP3 inflammasome. [electronic resource]
Producer: 20120917Description: ra38 p. digitalISSN:- 1937-9145
- Animals
- Apoptosis Regulatory Proteins
- CARD Signaling Adaptor Proteins
- CD4-Positive T-Lymphocytes -- transplantation
- Carrier Proteins -- genetics
- Caspase 1 -- physiology
- Cytoskeletal Proteins -- deficiency
- Disease Models, Animal
- Encephalomyelitis, Autoimmune, Experimental -- drug therapy
- Enzyme Activation
- Gene Expression Regulation -- drug effects
- Inflammasomes -- physiology
- Interferon beta-1b
- Interferon-beta -- therapeutic use
- Interleukin-1beta -- biosynthesis
- Macrophages -- physiology
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Mice, Transgenic
- NLR Family, Pyrin Domain-Containing 3 Protein
- Neuropeptides -- antagonists & inhibitors
- Proto-Oncogene Proteins c-vav -- antagonists & inhibitors
- Reactive Oxygen Species -- metabolism
- Receptor, Interferon alpha-beta -- deficiency
- Recombinant Proteins -- therapeutic use
- Suppressor of Cytokine Signaling 1 Protein
- Suppressor of Cytokine Signaling Proteins -- antagonists & inhibitors
- rac GTP-Binding Proteins -- antagonists & inhibitors
- rac1 GTP-Binding Protein
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Publication Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
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