References

ƒReferences relevant to the present research projects„

Sakaguchi, S., Takahashi, T., Yamazaki, S., Kuniyasu, Y., Itoh, M., Sakaguchi, N., and Shimizu, J.: Immunologic self-tolerance maintained by T cell-mediated control of self-reactive T cells: implications for autoimmunity and tumor immunity. Microbes and Immunity. In press.

Sakaguchi, S.: Nontransgenic model of autoimmune disease. Current Opinion in Immunology. In press.

Kuniyasu, Y., Takahashi, T., Itoh, M., Shimizu, J., Toda, G., and Sakaguchi, S.: Naturally anergic and suppressive CD25+ CD4+ T cells as a functionally and phenotypically distinct immunoregulatory T-cell subpopulation. Int. Immunol. 12: 1145-1155, 2000.

Sakaguchi, S.: Regulatory T cells: key controllers of immunologic self-tolerance. Cell. 101: 455-458, 2000.

Takahashi, T., Tagami, T., Yamazaki, S., Uede, T., Shimizu, J., Sakaguchi, N., Mak, T. W., and Sakaguchi, S.: Dominant immunologic self-tolerance maintained by CD25+ CD4+ regulatory T cells constitutively expressing CTLA-4. J. Exp. Med. 192: 303-309, 2000.

Sakaguchi, S., and Sakaguchi, N.: Role of genetic factors in organ-specific autoimmune diseases induced by manipulating the thymus/T cells, and not self-antigens. Rev. Immunogenetics. 2: 147-153, 2000.

Sakaguchi, S., Takahashi, T., and Shimizu, J.: Breaking immunologic tolerance to tumor cells as a novel immunotherapy for cancer. In Cell Therapy. Y. Ikeda, J. Hata, S. Koyasu, Y. Kawakami, Y. Hattori (Eds). Springer-Verlag, Tokyo, P3-13, 2000.

Shimizu, J., Yamazaki, S., and Sakaguchi, S.: Induction of tumor immunity by removing CD25+ CD4+ T cells: a common basis between tumor immunity and autoimmunity. J. Immunol. 163: 5211-5218, 1999.

Onizuka, S., Tawara, I., Shimizu, J., Sakaguchi, S., Fujita, T., and Nakayama, E.: Tumor rejection by invitro administration of anti-CD25 (Interleukin-2 receptor) monoclonal antibody. Cancer Research. 59: 3128-3133, 1999.

Itoh., M., Takahashi, T., Sakaguchi, N., Kuniyasu, Y., Shimizu, J., Ohtsuka, F., and Sakaguchi, S.: Thymus and autoimmunity: Production of CD25+ CD4+ naturally anergic and suppressive T cells as a key function of the thymus in maintaining immunologic self-tolerance. J. Immunol. 162: 5317-5326, 1999.

Morse, S. S., Sakaguchi, N., and Sakaguchi, S.: Virus and autoimmunity: Induction of autoimmune disease in mice by mouse T-lymphotropic virus (MTLV) destroying CD4+ T cells. J. Immunol. 162: 5309-5316, 1999.

Takahashi, T., Kuniyasu, Y., Toda, M., Sakaguchi, N., Itoh, M., Iwata, M., and Sakaguchi, S.: Immunologic self-tolerance maintained by CD25+ CD4+ T cells: Induction of autoimmune disease by breaking their anergic/suppressive state. Int. Immunol. 10: 1969-1980, 1998.

Asano, M., Toda, M., Sakaguchi, N., and Sakaguchi, S.: Autoimmune disease as a consequence of developmental abnormality of a T-cell subpopulation. J. Exp. Med. 184: 387-396, 1996.

Sakaguchi, S., Toda, M., Asano, M., Itoh, M., Morse, S. S., and Sakaguchi, N.: T cell-mediated maintenance of self-tolerance and its breakdown as a possible cause of various autoimmune diseases. J. Autoimmunity. 9: 211-220, 1996. 

Sakaguchi, S., Sakaguchi, N., Asano, M., and Toda, M.: Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor a-chains (CD25): breakdown of a single mechanism of immunologic self-tolerance causes various autoimmune diseases in mice. J. Immunol. 155:1151-1164, 1995.

Sakaguchi, S., Ermak, T. H., Toda, M., Berg, L. J., Fazekas de St. Groth, B., Ho, W., Peterson, P. A., and Davis, M. M.: Induction of autoimmune disease in mice by germ line alteration of the T-cell receptor gene expression. J. Immunol. 152: 1471-1484, 1994.

Sakaguchi, N., Miyai, K., and Sakaguchi, S.: Ionizing radiation and autoimmunity: Induction of autoimmune disease in mice by high dose fractionated total lymphoid irradiation and its prevention by inoculating normal T cells. J. Immunol. 152: 2586-2595, 1994. 

H. Ishida, Muchamuel, T., Sakaguchi, S., Andrade, S., Menon, S., and Howard, M.: Continuous administration of anti-IL10- antibodies delays onset of autoimmunity in NZB/W mice. J. Exp. Med. 179: 305-310, 1994. 

Sakaguchi, S., and Sakaguchi, N.: Thymus, T cells, and autoimmunity: Various causes but a common mechanism of autoimmune disease. In Autoimmunity: Physiology and Disease, A. Coutinho and M. Kazatchikine, editor. Wiley-Liss, Inc., p203-227, 1993.

Sakaguchi, N., and Sakaguchi, S.: Causes and mechanism of autoimmune disease: Cyclosporin A as a probe for the investigation. J. Invest. Derm. 98: 70s-76s, 1992. 

Sakaguchi, S., and Sakaguchi, N.: Thymus and autoimmunity: Capacity of the normal thymus to produce pathogenic self-reactive T cells and conditions required for their induction of autoimmune disease. J. Exp. Med. 172: 537-545, 1990. 

Sakaguchi, S., and Sakaguchi, N.: Organ-specific autoimmune disease induced in mice by elimination of T-cell subsets. V. Neonatal administration of cyclosporin A causes autoimmune disease. J. Immunol. 142: 471-480, 1989.

Sakaguchi, S., and Sakaguchi, N.: Thymus and autoimmunity: Transplantation of the thymus from cyclosporin A-treated mice causes organ-specific autoimmune disease in athymic nude mice. J. Exp. .Med.. 167:1479-1485, 1988.

Fukuma, K., Sakaguchi, S., Chen, W-.L., Morishita, R., Masuda, T., and Uchino, H.: Immunological and clinical studies on murine experimental autoimmune gastritis induced by neonatal thymectomy. Gastroenterology. 94:274-283, 1988. 

Sakaguchi, S., and Rose, N. R.: Pathogenesis of autoimmune disease in endocrine organs, In Diagnosis and pathology of endocrine diseases, G. Mendelsohn G, editor, J. B. Lippincott Co. p619-640, 1988. 

Sakaguchi, S.: Organ-specific autoimmune disease induced in mice by elimination of T-cell subsets. In New Horizons in Animal Models for Autoimmune Disease, Wigzell H, Kyogoku M, editors, Academic Press, p121-132, 1987.

Sakaguchi, S., Fukuma, K., Kuribayashi, K., and Masuda, T.: Organ-specific autoimmune disease induced in mice by elimination of T-cell subset. I. Evidence for active participation of T cells in natural self-tolerance; deficit of a T-cell subset as a possible cause of autoimmune disease. J. Exp. Med. 161:72-87, 1985.

Kuribayashi, K., Keyaki, A., Sakaguchi, S., and Masuda, T.: Effector mechanism of syngeneic anti-tumor responses in mice. I. Establishment and characterization of an exogenous IL-2-independent cytotoxic T-lymphocyte line specific for radiation-induced leukemia RLo1. Immunology. 56:127-140, 1985.

Keyaki, A., Kuribayashi, K., Sakaguchi, S., Masuda, T., Yamashita, J., Handa, H., and Nakayama, E.: Effector mechanism of syngeneic anti-tumor responses in mice. II. Cytotoxic T lymphocytes mediate neutralization and rejection of radiation-induced leukemia RLoL in the nude mouse system. Immunology 56:141-151, 1985.

Sakaguchi, S., Takahashi, T., and Nishizuka, Y.: Study on cellular events in post-thymectomy autoimmune oophoritis in mice. I. Requirement of Lyt-1 cells in normal female mice for the prevention of oophoritis. J. Exp. Med. 156: 1577-1586, 1982.

Sakaguchi, S., Takahashi, T., and Y. Nishizuka, Y.: Study on cellular events in post-thymectomy autoimmune oophoritis in mice. II. Requirement of Lyt-1 effector T cells for oocyte damage after adoptive transfer. J. Exp. Med. 156:1565-1576, 1982.

Kyoizumi, S., Noro, N., Teshigawara, K., Sakaguchi, S., and Masuda, T.: A cloned cell line, Mk-1, possessing Ia antigens and accessory activity. J. Immunol. 125:2586-2594, 1982.