Interplay between the hematopoetic factor Flt3L and IFNalpha,beta

We further our understanding of different DC populations and their soluble products in adults but in particular in neonatal mice. We have concentrated on the evaluation of the interplay between the hematopoetic factor Flt3L and IFNalpha,beta and have data available from our studies. We found that the cooperation between IFNalpha,beta and Flt3L (FL) plays an important role in the defense against Herpes simplex virus type 1 (HSV-1) in neonates. Treatment of neonatal mice with recombinant IFNalpha has a short-term, FL-independent and a long-term, FL-dependent protective effect against HSV-1. In mice lacking FL, neonatal resistance against HSV-1 is very low and DC numbers in the spleen are reduced. The treatment of these mice with rIFNalpha at day 6 resulted in an increased resistance against infection with HSV-1 at day 7. In C57BL/6 mice, treatment with rIFNalpha at birth induced both FL and plasmacytoid DC (pDC) that resulted in enhanced resistance against HSV-1 at day 7. In contrast, in mice lacking FL, IFNalpha treatment at birth did not influence splenic cell composition and had no effect on viral protection. The transfer of pDC to mice lacking FL enhanced viral resistance. Therefore, the induction and function of pDC, normally controlled by IFNalpha,beta and FL, are decisive for viral resistance in neonatal mice.

• organism type
• Mus musculus,
• HSV1

• molecule type
• Fms-related tyrosine kinase 3 ligand,
• interferon alpha,
• interferon beta

• cell type
• plasmacytoid dendritic cell

• organ type
• human spleen

created over 16 years ago (2 March 2009)    last modified over 12 years ago (24 September 2012)   [ RDF ]   [ RelFinder ]