Interleukin-7, a Non-Redundant Potent Cytokine whose Over-Expression Massively Perturbs B-Lymphopoiesis

Abstract

Interleukin-7, originally described as a factor controlling the survival of B-cell progenitors, has been shown by gene knock-out technology to be a non-redundant cytokine. Of all single cytokine knock-out mice, those in which the IL-7 gene has been ablated show a profound defect in lymphocyte development. Likewise, mice in which signals emanating from the corresponding receptor, whether it be by ablation of the unique α or common 7 chain of the receptor, or by interference with downstream signalling elements generated by this receptor complex, also show profound defects in lymphocyte differentiation. Transgenic mice over-expressing the IL-7 gene also show profound changes in lymphocyte development which, in some instances can result in the development of lymphoid tumours. Here, we review some of these aspects of IL-7 biology with particular reference to an IL-7 over-expressing transgenic mouse line in which the IL-7 transgene is controlled by the mouse MHC class II promoter.

Key Words:

• Interleukin-7
• Interleukin-7 receptor
• Gene knock-out
• Review
• Transgenic mice