The various lines of mice currently being used by HSDRC investigators are listed below. Many of these unique lines of transgenic models are available to interested investigators at both academic and non-academic institutions. Inquiries about use of these mice are welcome and can be directed to Arlene Sharpe or Benjamin Rich.

Interleukin-1-Related Molecules

1. K14/IL-1 Alpha Line 2; K14 promoter/enhancer targeting overexpression of the 17 kD form of mouse IL-1 alpha to basal keratinocytes. Overproductionof IL-1alpha, a protoype primary cytokine, by keratinocytes leads to induction of numerous secondary cytokines, induction of endothelial cell adhesion molecules, and inflammatory skin disease.
Reference: Groves, R.W., H. Mizutani, J.D. Kieffer, and T.S. Kupper.1995. Inflammatory skin disease in transgenic mice that express high levels of interleukin-1 alpha in basal epidermis. Proc. Natl. Acad. Sci. USA, 92:11874-11878.

2. K14/IL-1R type I Line 1R10; K14 promoter/enhancer targeting overexpressionof the mouse type I IL-1 receptor to basal keratinocytes. Overexpression of the signal transducing IL-1 receptor by keratinocytes leads to heightened susceptibility to cutaneous inflammation in response to IL-1 or IL-1-inducing stimuli.

Reference: Groves R.W., T. Rauschmayr, K. Nakamura, S. Sarkar, I.R.Williams, and T.S. Kupper. 1996. Modulation of induced inflammation in transgenic mice that overexpress type-1 IL-1 receptor in epidermis. Evidence for cutaneous IL-1 mediated autocrine feedback pathways in vivo. J. Clin. Invest. 98:336-344.

3. K14/IL-1R type II; K14 promoter/enhancer targeting overexpression of the mouse type II IL-1 receptor to basal keratinocytes.

Reference: Rauschmayr, T., R.W. Groves, and T.S. Kupper. 1997. Keratinocyte expression of the type 2 interleukin 1 receptor mediates local and specific inhibition of interleukin 1-mediated inflammation. Proc. Natl. Acad. Sci.USA 94:5814, 1997.

4. K14/IL-1Ra; K14 promoter/enhancer targeting overexpression ofmouse interleukin-1 receptor antagonist to basal keratinocytes.

Reference: Groves, R.W., I.R. Williams, S. Sarkar, K. Nakamura, andT.S. Kupper. 1994. Analysis of epidermal IL-1 family members in vivo usingtransgenic mouse models. J. Invest. Dermatol. 102:556 (abstract).

5. K14/IL-1 alpha pro

Non-IL-1 Cytokines

6. K14/IL-12 p40; K14 promoter/enhancer targeting overexpression of the p40 chain of mouse IL-12 to basal keratinocytes.

7. K14/IL-7; K14 promoter/enhancer targeting overexpression of mouse IL-7 to basal keratinocytes. Keratinocyte overexpression of the T cell growthfactor IL-7 leads to increased mobilization of a population of activatedgamma/delta T cells to the skin. The increased T cell content of the skin in turn leads to a drastic hyperresponsiveness (with as much as 100-foldincrease in sensitivity) to a variety of irritant stimuli applied to skin.
Reference: Williams, I.R., E.A. Rawson, L. Manning, T. Karaoli, B.E.Rich, and T.S. Kupper. 1997. IL-7 overexpression in transgenic mouse keratinocytescauses a lymphoproliferative skin disease dominated by intermediate TCRcells. Evidence for a hierarchy in IL-7 responsiveness among cutaneous T cells. J. Immunol. 159:3044-3056.

8. Ig/IL-7; Immunoglobulin promoter and enhancer directing the expression of IL-7 to lymphocytes. These mice devlop a progressive cutaneous lymphoproliferaive disorder that progresses to malignancy and stochastic lymphomas.
Reference: Rich, B.E, J. Campos-Torres, R.I. Tepper, R.M. Moreadith and P. Leder (1993) Cutaneouus Lymphoroliferation and Lymphomas in Interleukin 7 Transgenic Mice. J. Exp. Med. 177:305-316

9. IL-7 KO (Balb/c)

10. IL-7 KO (FVB/N)

11. IL4-EGFP Knock-in