| First Author | Singh BK | Year | 2023 |
| Journal | Cell Immunol | Volume | 393-394 |
| Pages | 104780 | PubMed ID | 37918056 |
| Mgi Jnum | J:342885 | Mgi Id | MGI:7561247 |
| Doi | 10.1016/j.cellimm.2023.104780 | Citation | Singh BK, et al. (2023) Diacylglycerol kinase zeta deficiency attenuates papain-induced type 2 airway inflammation. Cell Immunol 393-394:104780 |
| abstractText | Allergic airway diseases are caused by inappropriate immune responses directed against inhaled environmental antigens. We previously reported that the inhibition of diacylglycerol (DAG) kinasezeta (DGKzeta),an enzyme that terminates DAG-mediated signaling,protects against T cell-mediated allergic airway inflammation by blocking Th2 cell differentiation.In this study, we tested whether DGKzeta deficiency also affects allergic airway disease mediated by type 2 innate lymphoid cells (ILC2)s. DGKzeta-deficient mice displayed diminished ILC2 function and reduced papain-induced airway inflammation compared to wildtype mice. Unexpectedly, however, mice with hematopoietic cell-specific deletion ofDGKzeta displayed intact airway inflammation upon papain challenge. Rather, bone marrow chimera studies revealed thatDGKzeta deficiency in the non-hematopoietic compartment was responsible for the reduction in papain-induced airway inflammation. These data suggest that DGK might represent a novel therapeutic target not only for T cell-dependent but also ILC2-dependent allergic airway inflammation by affecting non-hematopoietic cells. |
