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Insulin-Like Growth Factor-1 Controls Type 2 T Cell-Independent B Cell Response

Stephanie Baudler^*, Julia Baumgartl^*, Brigitte Hampel^*, Thorsten Buch^*, Ari Waisman^*, Clifford M. Snapper, Wilhelm Krone and Jens C. Brüning^1,*

^* Institute for Genetics, University of Cologne, and Klinik II und Poliklinik für Innere Medizin der Universität zu Koeln and Center of Molecular Medicine, Cologne, Germany; and Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814

The IGF-1 receptor (IGF-1R) is expressed on T and B lymphocytes, and the expression of the insulin- and IGF-1-signaling machinery undergoes defined changes throughout lineage differentiation, offering a putative role for IGF-1 in the regulation of immune responses. To study the role of the IGF-1R in lymphocyte differentiation and function in vivo, we have reconstituted immunodeficient RAG2-deficient mice with IGF-1R^–/– fetal liver cells. Despite the absence of IGF-1Rs, the development and ex vivo activation of B and T lymphocytes were unaltered in these chimeric mice. By contrast, the humoral immune response to the T cell-independent type 2 Ag 4-hydroxy-3-nitrophenyl acetyl-Ficoll was significantly reduced in mice reconstituted with IGF-1R-deficient fetal liver cells, whereas responses to the T cell-dependent Ag 4-hydroxy-3-nitrophenyl acetyl-chicken globulin were normal. Moreover, in an in vitro model of T cell-independent type 2 responses, IGF-1 promoted Ig production potently upon polyvalent membrane-IgD cross-linking. These data indicate that functional IGF-1R signaling is required for T cell-independent B cell responses in vivo, defining a novel regulatory mechanism for the immune response against bacterial polysaccharides.

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