Summary and Conclusion

During the past decade, the most exciting and important finding in SLE-prone mice has been the discovery of Fas/Fas ligand systems in the pathogenesis of autoimmune phenomena. A human model for murine lpr/gld disease has also been reported (Sneller et al. 1992). Furthermore, as shown in Table 16.2, studies on immunoglobu-lin variable region genes, TCR genes, and MHC class II genes have given us much information concerning human and murine SLE. With respect to cytokines, IL-2 deficiency (Dauphinee et al. 1981) and the key role of IL-6 (Finck et al. 1994, Tang et al. 1991) have been found in SLE-prone mouse strains, and Th2 cytokine production has been demonstrated to play a more pathogenic role than Th1 cytokine production in human and murine SLE (Klinman and Steinberg 1995), except in MRL/lpr mice (Takahashi et al. 1996.). Transforming growth factor is also intriguing because transforming growth factor p-knockout mice show SLE-like autoantibodies and Sjogren's syndrome-like lymphoproliferation (Dang et al. 1995). Apart from these basic scientific investigations, there are also many promising and practical therapeutic approaches (Shoenfeld 1994). In particular, treatments with anti-CD4 antibody (Gilkeson et al. 1992) and murine CTLA4Ig, which bound B7 and blocked binding of CD28 to B7 (Finck et al. 1994), are outstanding. Recently, vaccine therapy has been attempted (Rook et al. 2000). However, it remains obscure whether such new approaches are effective for the skin lesions of SLE-prone mice, although some immunosuppressive agents, such as FK506, cyclosporine, and Chinese herbal medicines, have been evaluated to determine their selective effects on the skin lesions of MRL/lpr mice (Furukawa et al. 1995, Ito et al. 2002, Kanauchi et al. 1994a, b).

Needless to say, mouse models are not identical, but are similar, to human diseases. However, they are important in the search for the underlying pathogenesis of autoimmune diseases on the basis of careful evaluation of the similarities and differences between human diseases and these models. If such studies are steadily performed, then inbred or experimental models will become more promising tools for the investigation of CLE.

Acknowledgements. The author is grateful to T. Shirai of Juntendo University, M. Takigawa of Hamamatsu University, S. Imamura and Y. Hamashima of Kyoto University, Japan, and D. A. Norris of the University of Colorado, USA, for their scientific support. This work was also supported by grants from the Japanese Ministry of Education, Science, Culture, and Sports and from the Japanese Ministry of Health and Welfare. This review article is a minor modified version of our previous report (Furukawa 1997).

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