| First Author | Linz BM | Year | 2017 |
| Journal | J Immunol | Volume | 198 |
| Issue | 6 | Pages | 2426-2433 |
| PubMed ID | 28159904 | Mgi Jnum | J:247736 |
| Mgi Id | MGI:5925685 | Doi | 10.4049/jimmunol.1601048 |
| Citation | Linz BM, et al. (2017) Innate Immune Cell Recovery Is Positively Regulated by NLRP12 during Emergency Hematopoiesis. J Immunol 198(6):2426-2433 |
| abstractText | With enhanced concerns of terrorist attacks, dual exposure to radiation and thermal combined injury (RCI) has become a real threat with devastating immunosuppression. NLRP12, a member of the NOD-like receptor family, is expressed in myeloid and bone marrow cells and was implicated as a checkpoint regulator of inflammatory cytokines, as well as an inflammasome activator. We show that NLRP12 has a profound impact on hematopoietic recovery during RCI by serving as a checkpoint of TNF signaling and preventing hematopoietic apoptosis. Using a mouse model of RCI, increased NLRP12 expression was detected in target tissues. Nlrp12-/- mice exhibited significantly greater mortality, an inability to fight bacterial infection, heightened levels of proinflammatory cytokines, overt granulocyte/monocyte progenitor cell apoptosis, and failure to reconstitute peripheral myeloid populations. Anti-TNF Ab administration improved peripheral immune recovery. These data suggest that NLRP12 is essential for survival after RCI by regulating myelopoiesis and immune reconstitution. |
