| First Author | van den Boorn JG | Year | 2016 |
| Journal | Immunity | Volume | 44 |
| Issue | 6 | Pages | 1406-21 |
| PubMed ID | 27287410 | Mgi Jnum | J:259362 |
| Mgi Id | MGI:6142284 | Doi | 10.1016/j.immuni.2016.05.008 |
| Citation | van den Boorn JG, et al. (2016) Inflammasome-Dependent Induction of Adaptive NK Cell Memory. Immunity 44(6):1406-21 |
| abstractText | Monobenzone is a pro-hapten that is exclusively metabolized by melanocytes, thereby haptenizing melanocyte-specific antigens, which results in cytotoxic autoimmunity specifically against pigmented cells. Studying monobenzone in a setting of contact hypersensitivity (CHS), we observed that monobenzone induced a long-lasting, melanocyte-specific immune response that was dependent on NK cells, yet fully intact in the absence of T- and B cells. Consistent with the concept of "memory NK cells," monobenzone-induced NK cells resided in the liver and transfer of these cells conferred melanocyte-specific immunity to naive animals. Monobenzone-exposed skin displayed macrophage infiltration and cutaneous lymph nodes showed an inflammasome-dependent influx of macrophages with a tissue-resident phenotype, coinciding with local NK cell activation. Indeed, macrophage depletion or the absence of the NLRP3 inflammasome, the adaptor protein ASC or interleukin-18 (IL-18) abolished monobenzone CHS, thereby establishing a non-redundant role for the NLRP3 inflammasome as a critical proinflammatory checkpoint in the induction of hapten-dependent memory NK cells. |
