NDLI: Dectin-2 regulates the effector phase of house dust mite-elicited pulmonary inflammation independently from its role in sensitization.

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Dectin-2 regulates the effector phase of house dust mite-elicited pulmonary inflammation independently from its role in sensitization.

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Dectin-2 regulates the effector phase of house dust mite-elicited pulmonary inflammation independently from its role in sensitization.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Saijo, Shinobu Li, Li Barrett, Nora A. Lee, Min Jung Iwakura, Yoichiro Wallace, Aaron M. Fernandez, James M. Austen, K. Frank Parsons, Matthew W. Katz, Howard R. Kanaoka, Yoshihide
Description	Author Affiliation: Parsons MW ( Department of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA 02115)
Abstract	The myeloid C-type lectin receptor Dectin-2 directs the generation of Th2 and Th17 immune responses to the house dust mite Dermatophagoides farinae through the generation of cysteinyl leukotrienes and proinflammatory cytokines, respectively, but a role for Dectin-2 in effector phase responses has not been described. In this study, we demonstrate that administration of the Dectin-2 mAb solely at the time of D. farinae challenge abrogated eosinophilic and neutrophilic inflammation in the bronchoalveolar lavage fluid and Th1, Th2, and Th17 inflammation in the lung of previously sensitized mice. Furthermore, Dectin-2 null mice (Clec4n(-/-)) sensitized with the adoptive transfer of D. farinae-pulsed wild-type (WT) bone marrow-derived dendritic cells (DCs) also had less D. farinae-elicited pulmonary inflammation, supporting an effector function for Dectin-2. The protection from pulmonary inflammation seen with the Dectin-2 mAb or in Clec4n(-/-) mice was associated with little or no reduction in lung-draining lymph node cells or their cytokine production and with no reduction in serum IgE. WT and Clec4n(-/-) mice recipients, sensitized with D. farinae-pulsed WT bone marrow-derived DCs, had comparable levels of D. farinae-elicited IL-6, IL-23, TNF- , and cysteinyl leukotrienes in the lung. By contrast, D. farinae-elicited CCL4 and CCL8 production from pulmonary CD11c(+)CD11b(+)Ly6C(+) and CD11c(+)CD11b(+)Ly6C(-)CD64(+) monocyte-derived DCs was reduced in Clec4n(-/-) recipients. Addition of CCL8 at the time of D. farinae challenge abrogated the protection from eosinophilic, neutrophilic, and Th2 pulmonary inflammation seen in Clec4n(-/-) recipients. Taken together, these results reveal that Dectin-2 regulates monocyte-derived DC function in the pulmonary microenvironment at D. farinae challenge to promote the local inflammatory response.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1301809
Journal	The Journal of Immunology
Issue Number	4
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Dendritic Cells Immunology Dermatophagoides Farinae Lectins, C-type Pneumonia Adoptive Transfer Animals Antibodies, Monoclonal Antigens, Cd11b Metabolism Antigens, Cd11c Antigens, Dermatophagoides Antigens, Ly Bronchoalveolar Lavage Fluid Cytology Chemokine Ccl4 Biosynthesis Chemokine Ccl8 Cysteine Transplantation Eosinophils Immunoglobulin E Blood Interleukin-23 Interleukin-6 Deficiency Genetics Leukotrienes Lung Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Neutrophils Receptors, Igg Th1 Cells Th17 Cells Th2 Cells Tumor Necrosis Factor-alpha Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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