First Author | Hansenne I | Year | 2006 |
Journal | J Immunol | Volume | 176 |
Issue | 8 | Pages | 4651-7 |
PubMed ID | 16585557 | Mgi Jnum | J:125076 |
Mgi Id | MGI:3723426 | Doi | 10.4049/jimmunol.176.8.4651 |
Citation | Hansenne I, et al. (2006) Dendritic cell differentiation and immune tolerance to insulin-related peptides in Igf2-deficient mice. J Immunol 176(8):4651-7 |
abstractText | 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. |