Journal
JOURNAL OF IMMUNOLOGY
Volume 182, Issue 10, Pages 5904-5908Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0900732
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Funding
- National Institutes of Health
- National Multiple Sclerosis Society (NMSS) [RG-2571-D-9, RG-3882-A-1]
- NMSS Transition Award [TA 3014A1/1]
- European Molecular Biology Organization
- Deutsche Forschungsgememschaft
- Swiss National Science Foundation
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IL-23, an IL-12 family member, has been implicated in the development of Th17 cells and the progression of autoimmune diseases. However, due to the lack of availability of sensitive Ab reagents specific for the IL-23 receptor (IL-23R), it has been difficult to characterize the cell types that express the IL-23R and are responsive to IL-23 in vivo. To address the role of IL-23 in vivo, we have generated a novel knock-in mouse in which we have replaced the intracellular domain of the IL-23R with the GFP. We show that in addition to Th17 cells, a subset of myeloid cells express IL-23R and respond to IL-23 by producing IL-17 and IL-22. Our studies further demonstrate that IL-23R expression is crucial for generation of encephalitogenic Th17 cells, but its expression on the innate immune system is dispensible in the development of experimental autoimmune encephalomyelitis. The Journal of Immunology, 2009, 182: 5904-5908.
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