IL-23 produced by CNS-resident cells controls T cell encephalitogenicity during the effector phase of experimental autoimmune encephalomyelitis
Author:
Publisher
American Society for Clinical Investigation
Subject
General Medicine
Reference16 articles.
1. Experimental autoimmune encephalitis and inflammation in the absence of interleukin-12
2. IL-12p35-Deficient Mice Are Susceptible to Experimental Autoimmune Encephalomyelitis: Evidence for Redundancy in the IL-12 System in the Induction of Central Nervous System Autoimmune Demyelination
3. Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain
4. Novel p19 Protein Engages IL-12p40 to Form a Cytokine, IL-23, with Biological Activities Similar as Well as Distinct from IL-12
5. THE INTERLEUKIN-12/INTERLEUKIN-12-RECEPTOR SYSTEM: Role in Normal and Pathologic Immune Responses
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