TY - JOUR
T1 - Cutting Edge
T2 - IL-23 receptor GFP reporter mice reveal distinct populations of IL-17-producing cells
AU - Awasthi, Amit
AU - Riol-Blanco, Lorena
AU - Jäger, Anneli
AU - Korn, Thomas
AU - Pot, Caroline
AU - Galileos, George
AU - Bettelli, Estelle
AU - Kuchroo, Vijay K.
AU - Oukka, Mohamed
PY - 2009/5/15
Y1 - 2009/5/15
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=68649090645&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.0900732
DO - 10.4049/jimmunol.0900732
M3 - Article
C2 - 19414740
AN - SCOPUS:68649090645
SN - 0022-1767
VL - 182
SP - 5904
EP - 5908
JO - Journal of Immunology
JF - Journal of Immunology
IS - 10
ER -