| First Author | Huang J | Year | 2021 |
| Journal | Immunity | Volume | 54 |
| Issue | 4 | Pages | 673-686.e4 |
| PubMed ID | 33852831 | Mgi Jnum | J:305813 |
| Mgi Id | MGI:6706541 | Doi | 10.1016/j.immuni.2021.03.018 |
| Citation | Huang J, et al. (2021) Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93. Immunity 54(4):673-686.e4 |
| abstractText | The interleukin (IL)-17 family, consisting of six members, promotes host defense but can in some context promote the development of autoimmune disease. Here, we examined the role of IL-17D, a poorly understood member in the IL-17 family. IL-17D was expressed primarily by colonic epithelial cells. Il17d(-/-) mice were more susceptible to acute colitis, bacterial infection and experimentally induced colon cancer than their wildtype counterparts. Il17d deficiency impaired IL-22 production by group 3 innate lymphoid cells (ILC3s) and reduced expression of IL-22-dependent antimicrobial peptides, RegIIIbeta and RegIIIgamma, in colon tissue at steady state and in colitis; this was associated with changes in microbial composition and dysbiosis. Protein purification studies revealed that IL-17D bound not canonical IL-17 receptors, but rather CD93, a glycoprotein expressed on mature ILC3s. Mice lacking Cd93 in ILC3s exhibited impaired IL-22 production and aggravated colonic inflammation in experimental colitis. Thus, an IL-17D-CD93 axis regulates ILC3 function to preserve intestinal homeostasis. |
