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Inflammasome-Dependent Induction of Adaptive NK Cell Memory.

Abstract：

: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.

journal_name

Immunity

journal_title

Immunity

authors

van den Boorn JG,Jakobs C,Hagen C,Renn M,Luiten RM,Melief CJ,Tüting T,Garbi N,Hartmann G,Hornung V

doi

10.1016/j.immuni.2016.05.008

subject

Has Abstract

pub_date

2016-06-21 00:00:00

pages

1406-21

issue

6

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(16)30162-5

journal_volume

44

pub_type

杂志文章

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