Document Detail


Notch ligand delta-like 4 regulates development and pathogenesis of allergic airway responses by modulating IL-2 production and Th2 immunity.
MedLine Citation:
PMID:  20944009     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Activation of the canonical Notch pathways has been implicated in Th cell differentiation, but the role of specific Notch ligands in Th2-mediated allergic airway responses has not been completely elucidated. In this study, we show that delta-like ligand 4 (Dll4) was upregulated on dendritic cells in response to cockroach allergen. Blocking Dll4 in vivo during either the primary or secondary response enhanced allergen-induced pathogenic consequences including airway hyperresponsiveness and mucus production via increased Th2 cytokines. In vitro assays demonstrated that Dll4 regulates IL-2 in T cells from established Th2 responses as well as during primary stimulation. Notably, Dll4 blockade during the primary, but not the secondary, response increased IL-2 levels in lung and lymph node of allergic mice. The in vivo neutralization of Dll4 was associated with increased expansion and decreased apoptosis during the primary allergen sensitization. Moreover, Dll4-mediated Notch activation of T cells during primary stimulation in vitro increased apoptosis during the contraction/resting phase of the response, which could be rescued by exogenous IL-2. Consistent with the role for Dll4-mediated IL-2 regulation in overall T cell function, the frequency of IL-4-producing cells was also significantly altered by Dll4 both in vivo and in vitro. These data demonstrate a regulatory role of Dll4 both in initial Th2 differentiation and in Th2 cytokine production in established allergic responses.
Authors:
Sihyug Jang; Matthew Schaller; Aaron A Berlin; Nicholas W Lukacs
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-10-13
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-04     Completed Date:  2010-12-02     Revised Date:  2011-11-21    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5835-44     Citation Subset:  AIM; IM    
Affiliation:
Department of Pathology, University of Michigan, Ann Arbor, MI 48109, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Differentiation / immunology
Cell Separation
Dendritic Cells / immunology,  metabolism
Flow Cytometry
Interleukin-2 / biosynthesis*,  immunology
Intracellular Signaling Peptides and Proteins / immunology*,  metabolism
Lymphocyte Activation / immunology
Membrane Proteins / immunology*,  metabolism
Mice
Mice, Inbred BALB C
Respiratory Hypersensitivity / immunology*,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Th2 Cells / cytology,  immunology*,  metabolism
Grant Support
ID/Acronym/Agency:
AI036302/AI/NIAID NIH HHS; AI073876/AI/NIAID NIH HHS; R01 AI036302-14/AI/NIAID NIH HHS; R01 AI073876-04/AI/NIAID NIH HHS; R01 AI073876-05/AI/NIAID NIH HHS; T32 HL007517/HL/NHLBI NIH HHS; T32 HL007517-26A2/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/DLL4 protein, mouse; 0/Interleukin-2; 0/Intracellular Signaling Peptides and Proteins; 0/Membrane Proteins

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