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

doi:10.4049/jimmunol.1002227

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 journal › Article › peer-review

124 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 language	English (US)
Pages (from-to)	4515-4519
Number of pages	5
Journal	Journal of Immunology
Volume	185
Issue number	8
DOIs	https://doi.org/10.4049/jimmunol.1002227
State	Published - Oct 15 2010
Externally published	Yes

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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Arthur, J. C., Lich, J. D., Ye, Z., Allen, I. C., Gris, D., Wilson, J. E., Schneider, M., Roney, K. E., O'Connor, B. P., Moore, C. B., Morrison, A., Sutterwala, F. S., Bertin, J., Koller, B. H., Liu, Z., & Ting, J. P. Y. (2010). Cutting edge: NLRP12 controls dendritic and myeloid cell migration to affect contact hypersensitivity. Journal of Immunology, 185(8), 4515-4519. https://doi.org/10.4049/jimmunol.1002227

Arthur, JC, Lich, JD, Ye, Z, Allen, IC, Gris, D, Wilson, JE, Schneider, M, Roney, KE, O'Connor, BP, Moore, CB, Morrison, A, Sutterwala, FS, Bertin, J, Koller, BH, Liu, Z & Ting, JPY 2010, 'Cutting edge: NLRP12 controls dendritic and myeloid cell migration to affect contact hypersensitivity', Journal of Immunology, vol. 185, no. 8, pp. 4515-4519. https://doi.org/10.4049/jimmunol.1002227

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title = "Cutting edge: NLRP12 controls dendritic and myeloid cell migration to affect contact hypersensitivity",

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.",

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AU - Morrison, Amy

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

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