| First Author | Chognard G | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 2 | Pages | e89092 |
| PubMed ID | 24586521 | Mgi Jnum | J:213436 |
| Mgi Id | MGI:5584348 | Doi | 10.1371/journal.pone.0089092 |
| Citation | Chognard G, et al. (2014) the dichotomous pattern of IL-12r and IL-23R expression elucidates the role of IL-12 and IL-23 in inflammation. PLoS One 9(2):e89092 |
| abstractText | IL-12 and IL-23 cytokines respectively drive Th1 and Th17 type responses. Yet, little is known regarding the biology of these receptors. As the IL-12 and IL-23 receptors share a common subunit, it has been assumed that these receptors are co-expressed. Surprisingly, we find that the expression of each of these receptors is restricted to specific cell types, in both mouse and human. Indeed, although IL-12Rbeta2 is expressed by NK cells and a subset of gammadelta T cells, the expression of IL-23R is restricted to specific T cell subsets, a small number of B cells and innate lymphoid cells. By exploiting an IL-12- and IL-23-dependent mouse model of innate inflammation, we demonstrate an intricate interplay between IL-12Rbeta2 NK cells and IL-23R innate lymphoid cells with respectively dominant roles in the regulation of systemic versus local inflammatory responses. Together, these findings support an unforeseen lineage-specific dichotomy in the in vivo role of both the IL-12 and IL-23 pathways in pathological inflammatory states, which may allow more accurate dissection of the roles of these receptors in chronic inflammatory diseases in humans. |
