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

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 pathoge...

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Bibliographic Details
Published in:European journal of immunology 2008-04, Vol.38 (4), p.1043-1049
Main Authors: Worsley, Alan G.F, LeibundGut-Landmann, Salome, Slack, Emma, Phng, Li-Kun, Gerhardt, Holger, Sousa, Caetano Reis e, MacDonald, Andrew S
Format: Article
Language:English
Subjects:
Animals
Antigens - immunology
Cell differentiation
Cells, Cultured
Dendritic cells
Dendritic Cells - immunology
Dendritic Cells - metabolism
Egg Proteins - immunology
Infectious diseases
Jagged-2 Protein
Ligands
Membrane Proteins - deficiency
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Notch signalling
Receptors, Notch - metabolism
Solubility
Th1 Cells - immunology
Th2 Cells - immunology
T helper cells
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Summary: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.
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.200737335