Cutting edge: NLRP12 controls dendritic and myeloid cell migration to affect contact hypersensitivity

Janelle C. Arthur, John D. Lich, Zhengmao Ye, Irving C. Allen, Denis Gris, Justin E. Wilson, Monika Schneider, Kelly E. Roney, Brian P. O'Connor, Chris B. Moore, Amy Morrison, Fayyaz S. Sutterwala, John Bertin, Beverly H. Koller, Zhi Liu, Jenny P.Y. Ting

Research output: Contribution to journalArticlepeer-review

110 Scopus citations

Abstract

Nucleotide-binding domain leucine-rich repeat (NLR) proteins are regulators of inflammation and immunity. Although first described 8 y ago, a physiologic role for NLRP12 has remained elusive until now. We find that murine Nlrp12, an NLR linked to atopic dermatitis and hereditary periodic fever in humans, is prominently expressed in dendritic cells (DCs) and neutrophils. Nlrp12-deficient mice exhibit attenuated inflammatory responses in two models of contact hypersensitivity that exhibit features of allergic dermatitis. This cannot be attributed to defective Ag processing/presentation, inflammasome activation, or measurable changes in other inflammatory cytokines. Rather, Nlrp12-/- DCs display a significantly reduced capacity to migrate to draining lymph nodes. Both DCs and neutrophils fail to respond to chemokines in vitro. These findings indicate that NLRP12 is important in maintaining neutrophils and peripheral DCs in a migration-competent state.

Original languageEnglish (US)
Pages (from-to)4515-4519
Number of pages5
JournalJournal of Immunology
Volume185
Issue number8
DOIs
StatePublished - Oct 15 2010
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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