Back to Search
Start Over
Unique and redundant functions of NKp46+ ILC3s in models of intestinal inflammation
- Source :
- The Journal of Experimental Medicine; October 2015, Vol. 212 Issue: 11 p1869-1882, 14p
- Publication Year :
- 2015
-
Abstract
- Group 3 ILCs (ILC3s) are innate sources of IL-22 and IL-17 and include lymphoid tissue-inducer (LTi)-like and NKp46+ subsets. Both depend on RORγt and aryl hydrocarbon receptor, but NKp46+ILC3s also require Notch and T-bet for their development and are transcriptionally distinct. The extent to which these subsets have unique functions, especially in the context of T cell– and B cell–sufficient mice, remains largely unclear. To investigate the specific function of NKp46+ILC3s among other ILC3 subsets and T cells, we generated mice selectively lacking NKp46+ILC3s or all ILC3s and crossed them to T cell–deficient mice, thus maintaining B cells in all mice. In mice lacking T cells, NKp46+ILC3s were sufficient to promote inflammatory monocyte accumulation in the anti-CD40 innate colitis model through marked production of GM-CSF. In T cell–competent mice, lack of NKp46+ILCs had no impact on control of intestinal C. rodentium infection, whereas lack of all ILC3s partially impaired bacterial control. Thus, NKp46+ILC3s have a unique capacity to promote inflammation through GM-CSF–induced accumulation of inflammatory monocytes, but are superseded by LTi-like ILC3s and T cells in controlling intestinal bacterial infection.
Details
- Language :
- English
- ISSN :
- 00221007 and 15409538
- Volume :
- 212
- Issue :
- 11
- Database :
- Supplemental Index
- Journal :
- The Journal of Experimental Medicine
- Publication Type :
- Periodical
- Accession number :
- ejs37031535
- Full Text :
- https://doi.org/10.1084/jem.20151403