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Dendritic Cell Differentiation and Immune Tolerance to Insulin-Related Peptides in Igf2-Deficient Mice¹

Isabelle Hansenne^2,*, Chantal Renard-Charlet^*, Roland Greimers and Vincent Geenen^*

^* Center of Immunology and Department of Anatomy and Cytopathology, University of Liege, Liege-Sart Tilman, Belgium

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.