Dendritic cell expression of the Notch ligand jagged2 is not essential for Th2 response induction in vivo

Item Type:	Article
Title:	Dendritic cell expression of the Notch ligand jagged2 is not essential for Th2 response induction in vivo
Creators Name:	Worsley, A.G.F. and LeibundGut-Landmann, S. and Slack, E. and Phng, L.K. and Gerhardt, H. and Reis e Sousa, C. and MacDonald, A.S.
Abstract:	We have addressed the hypothesis that Notch ligands play a decisive role in determining the ability of antigen-presenting cells to influence T cell polarization. Dendritic cells displayed distinct expression profiles of Delta and Jagged ligands for Notch when exposed to biologically relevant pathogen preparations associated with Th1 or Th2 responses. Expression of delta4 was increased, and jagged2 decreased, after dendritic cell exposure to the Th1-promoting bacterium Propionibacterium acnes. In contrast, soluble egg antigen (SEA) from the parasitic helminth Schistosoma mansoni, a potent Th2 inducer, failed to significantly alter dendritic cell expression of any of the Notch ligands measured. Irrespective of this, jagged2-deficient dendritic cells were severely impaired in their ability to instruct Th2 polarization of naive T cells in vitro. However, the ability of SEA-pulsed jagged2-deficient dendritic cells to induce a Th2 response in vivo was unimpaired relative to jagged2-sufficient dendritic cells. Further, jagged2-deficient dendritic cells activated by P. acnes exhibited no evidence of enhanced (or impaired) Th1 induction in vivo. These data suggest that, although involved in Th2 direction in vitro, jagged2 is not fundamentally required for Th2 induction by SEA-activated dendritic cells in vivo.
Keywords:	Cell Differentiation, Dendritic Cells, Infectious Diseases, Notch Signalling, T Helper Cells, Animals, Mice
Source:	European Journal of Immunology
ISSN:	0014-2980
Publisher:	Wiley
Volume:	38
Number:	4
Page Range:	1043-1049
Date:	April 2008
Official Publication:	https://doi.org/10.1002/eji.200737335
PubMed:	View item in PubMed

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