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Original Article

Pim1 Reconstitutes Thymus Cellularity in Interleukin 7–And Common Chain–Mutant Mice and Permits Thymocyte Maturation in Rag- but Not Cd3-Deficient Mice

^a Basel Institute for Immunology, CH-4005 Basel, Switzerland
^b Division of Molecular Genetics and Centre of Biomedical Genetics, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands
^c Division of Immunology, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands
Basel Institute for Immunology, Grenzacherstr. 487, CH-4005 Basel, Switzerland.41-61-605-136441-61-605-1281

Jacobs{at}BII.CH

The majority of lymphomas induced in Rag-deficient mice by Moloney murine leukemia virus (MoMuLV) infection express the CD4 and/or CD8 markers, indicating that proviral insertions cause activation of genes affecting the development from CD4^–8^– pro-T cells into CD4⁺8⁺ pre-T cells. Similar to MoMuLV wild-type tumors, 50% of CD4⁺8⁺ Rag-deficient tumors carry a provirus near the Pim1 protooncogene. To study the function of PIM proteins in T cell development in a more controlled setting, a Pim1 transgene was crossed into mice deficient in either cytokine or T cell receptor (TCR) signal transduction pathways. Pim1 reconstitutes thymic cellularity in interleukin (IL)-7– and common chain–deficient mice. In Pim1-transgenic Rag-deficient mice but notably not in CD3-deficient mice, we observed slow expansion of the CD4⁺8⁺ thymic compartment to almost normal size. Based on these results, we propose that PIM1 functions as an efficient effector of the IL-7 pathway, thereby enabling Rag-deficient pro-T cells to bypass the pre-TCR–controlled checkpoint in T cell development.

Key Words: common chain • IL-7 • Rag • proviral tagging • lymphomagenesis • pre-T cell development

H. Jacobs and P. Krimpenfort contributed equally to this work.

© 1999 The Rockefeller University Press

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