Reference : Dendritic cell differentiation and immune tolerance to insulin-related peptides in Igf2-...
Scientific journals : Article
Human health sciences : Immunology & infectious disease
http://hdl.handle.net/2268/25872
Dendritic cell differentiation and immune tolerance to insulin-related peptides in Igf2-deficient mice
English
Hansenne, Isabelle [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Embryologie >]
Renard-Charlet, C. [> > > >]
Greimers, Roland mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Anatomie et cytologie pathologiques >]
Geenen, Vincent mailto [Université de Liège - ULg > > Centre d'immunologie >]
15-Apr-2006
Journal of Immunology (Baltimore, Md. : 1950)
Amer Assoc Immunologists
176
8
4651-4657
Yes (verified by ORBi)
International
0022-1767
Bethesda
[en] There is some evidence that insulin-like growth factor 2 (IGF-2) may intervene in the control of T cell differentiation. To further study the immunoregulatory function of this growth factor, we analyzed the immune system of Igf2(-/-) mice. Phenotypically, some immunological parameters such as lymphoid organ morphology and cellularity were unaltered in Igf2(-/-) mice, but an increase of CD8(+) cells and a decrease of B220(+) cells were observed in spleen. In vitro, the development of bone marrow-derived dendritic cells was affected by the absence of Igf2 expression. After maturation, a higher percentage of immature dendritic cells was observed in Igf2(-/-) population, together with a secondary decrease in allogenic T cell proliferation. Activation of T cells was also affected by the lack of expression of this growth factor. The profile of B cell response in mutant mice immunized with IGF-2 evidenced a T-dependent profile of anti-IGF-2 Abs that was absent in Igf2(+/+) mice. The influence of IGF-2 upon tolerance to insulin was also assessed in this model, and this showed that IGF-2 also intervenes in tolerance to insulin. The presence of a T-dependent response in Igf2-deficient mice should allow cloning of specific "forbidden" T CD4(+) lymphocytes directed against IGF-2, as well as further investigation of their possible pathogenic properties against insulin family.
http://hdl.handle.net/2268/25872

File(s) associated to this reference

Fulltext file(s):

FileCommentaryVersionSizeAccess
Open access
Hansenne et al. JI_06.pdfPublisher postprint206.94 kBView/Open

Bookmark and Share SFX Query

All documents in ORBi are protected by a user license.