Interactions of B6 Wild and B6 Gld Cells Engrafted within Athymic Nude Beige Recipients

References

• Cohen P. L., Eisenberg R. A. Lpr and gld: single gene models of systemic autoimmunity and lymphoproliferative disease. Ann. Rev. Immunol. 1991; 9: 243–269
   PubMed Web of Science ®Google Scholar
• Davidson W. F., Dumont F. J., Bedigian H. G., Fowlkes B. J., Morse H. C., III. Phenotypic, functional, and molecular genetic comparaisons of the abnormal lymphoid cells of C3H-lpr/lpr and C3H-gld/gld mice. J. Immunol. 1986; 136: 4075–4084
   PubMed Web of Science ®Google Scholar
• Allen R. D., Marshall J. D., Roths J. B., Sidman C. L. Differences denned by bone marrow transplantation suggest that Ipr and gld are mutations of genes encoding an interacting pair of molecules. J. Exp. Med. 1990; 172: 1367–1375
   PubMed Web of Science ®Google Scholar
• Froidevaux S., Rosenblatt N., Loor F. Adoptive transfer of the generalized lymphoproliferative disease (gld) syndrome in nude beige mice. Immunology 1992; 75: 693–699
   PubMedGoogle Scholar
• Froidevaux S., Rosenblatt N., Loor F. Adoptive transfer of the entire gld (generalized lymphoproliferative disease) syndrome in nude beige by a single gld thymocyte graft. Cell. Immunol. 1992; 143: 238–247
   PubMedGoogle Scholar
• Tiberghien F., Pflumio F., Kuntz L., Loor F. Lack of transfer of Ipr-type abnormalities (lymphoproliferation or lymphoid aplasia) in double congenic nude beige mice engrafted with Ipr haematopoietic cells. Immunology 1993; 79: 158–166
   PubMedGoogle Scholar
• Watanabc-Fukunaga R., Brannan C. I., Copeland N. G., Jenkins N. A., Nagata S. Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis. Nature 1992; 356: 314–317
   PubMedGoogle Scholar
• Takahashi T., Tanaka M., Brannan C. I., Jenkins N. A., Copeland N. G., Suda T., Nagata S. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell 1994; 76: 969–976
   PubMed Web of Science ®Google Scholar
• Yoshida H., Yoshida M., Merino R., Shibata T., Izui S. 5-Azacytidine inhibits the Ipr gene-induced lymphadenopathy and acceleration of lupus-like syndrome in MRL/MpJ-lpr/lpr mice. Eur. J. Immunol. 1990; 20: 1989–1993
   PubMedGoogle Scholar
• Mountz J. D., Smith H. R., Wilder R. L., Reeves J. P., Steinberg A. D. Cs-A therapy in MRL-lpr/lpr mice: amelioration of immunopathology despite autoantibody production. J. Immunol. 1987; 138: 157–163
   PubMed Web of Science ®Google Scholar
• Kim C., Siminovitch K. A., Ochi A. Reduction of lupus nephritis in MRL/lpr mice by a bacterial superantigen treatment. J. Exp. Med. 1991; 174: 1431–1437
   PubMed Web of Science ®Google Scholar
• Jabs D. A., Burek C. L., Hu Q., Kuppers R. C., Lee B., Prendergast R. A. Anti-CD4 monoclonal antibody therapy suppresses autoimmune disease in MRL/Mp-lpr/lpr mice. Cell. Immunol. 1992; 141: 496–507
   PubMedGoogle Scholar
• Asensi V., Kimeno K., Kawamura I., Sakumoto M., Nomoto K. Treatment of autoimmune MRL/lpr mice with anti-B220 monoclonal antibody reduces the level of anti-DNA antibodies and lymphadenopathies. Immunology 1989; 68: 204–208
   PubMedGoogle Scholar
• de Alboran I. M., Gonzalo J. A., Kroemcr G., Leonardo E., Marcos M. A., Martinez C. Attenuation of autoimmune disease and lymphocyte accumulation in MRL/lpr mice by treatment with anti-V beta 8 antibodies. Eur. J. Immunol. 1992; 22: 2153–2158
   PubMedGoogle Scholar
• Cerny A., Kimota M., Hugin A. W., Merino R., Izui S. Anti-IgM treatment of C57BL/6-lpr/lpr mice: depletion of B cells reduces Ipr gene-induced lymphoproliferation and mononuclear cell vasculitis. Clin. Exp. Immunol. 1989; 77: 124–129
   PubMedGoogle Scholar
• Giese T., Davidson W. F. Chronic treatment of C3H-lpr/lpr and C3H-gld/gld mice with anti-CD8 monoclonal antibody prevents the accumulation of double negative T cells but not autoantibody production. J. Immunol. 1994; 152: 2000–2010
   PubMed Web of Science ®Google Scholar
• Steinberg A. D., Roths J. B., Murphy E. D., Steinberg R. T., Raveche E. S. Effects of thymectomy or androgen administration upon the autoimmune disease of MRL/Mp-lpr/lpr mice. J. Immunol. 1980; 125: 871–873
   PubMed Web of Science ®Google Scholar
• Ettinger R., Wang J. K. M., Bossu P., Papas K., Sidman C. L., Abbas A. K., Marshak-Rothstein A. Functional distinctions between MRL-lpr and MRL-gld lymphocytes. Normal cells reverse the gld but not lpr immunoregulatory defect. J. Immunol. 1994; 152: 1557–1568
   PubMed Web of Science ®Google Scholar
• Sobel E. S., Kakkanaiah V. N., Cohen P. L., Eisenberg R. A. Correction of gld autoimmunity by co-infusion of normal bone marrow suggests that gld is a mutation of the Fas ligand gene. Int. Immunol. 1993; 5: 1275–1278
   PubMed Web of Science ®Google Scholar
• Bennett M., Kumas V., Mikhacl A., Murphy W. J., Rembecki R. M., Sentman C. L., David C. S. Rejection of bone marrow cells by irradiated mice: NK and T cells recognize different antigens. Transplant. Proc. 1987; 19: 5–11
   PubMedGoogle Scholar
• Pflumio F., Fonteneau P., Gavcriaux C., Cammisuli S., Loor F. The C57BL/6 nude/beige mouse: a model of combined T cell and NK effector cell immunodeficiency. Cell. Immunol. 1989; 120: 218–229
   PubMedGoogle Scholar
• Klein-Schneegans A. S., Kuntz L., Fonteneau P., Loor F. An indirect asymmetrical sandwich ELISA using antiallotypc antibodies for the specific and quantitative measurement of mouse lgG2a of Igh-lb allotypc. J. Immunol. Methods 1989; 125: 207–213
   PubMed Web of Science ®Google Scholar
• Klein-Schneegans A. S., Gaveriaux C., Fonteneau P., Loor F. Indirect double sandwich ELISA for the specific and quantitative measurement of mouse IgM, IgA and IgG subclasses. J. Immunol. Methods 1989; 119: 117–125
   PubMed Web of Science ®Google Scholar
• Kuntz L., Velin D., Pflumio F., Loor F. Adoptive transfer of viable moth-eaten humoral autoimmunity in cyclophosphamide-immunodepressed beige recipient mice. Immunology 1990; 70: 520–526
   PubMed Web of Science ®Google Scholar
• Mosbach-Ozmen L., Gaveriaux C., Montecino-Rodriguez E., Loor F. The C57BL/6 nu/nu, Ipr/lpr. III Autoimmunity status. Thymus 1986; 8: 59–75
   PubMedGoogle Scholar
• Russel J. H., Wang R. Autoimmune gld mutation uncouples suicide and cytokine/proliferation pathways in activated, mature T cells. Eur. J. Immunol. 1993; 23: 2379–2382
   PubMedGoogle Scholar
• Giese T., Davidson W. F. Evidence for early onset, polyclonal activation of T cell subsets in mice homozygous for lpr. J. Immunol. 1992; 149: 3097–3106
   PubMed Web of Science ®Google Scholar
• Mountz J. D., Gause W. C., Finkelman F. D., Steinberg A. D. Prevention of lymphadenopathy in MRL-lpr/lpr mice by blocking peripheral lymph node homing with Mel-14 in vivo. J. Immunol. 1988; 140: 2943–2949
   PubMed Web of Science ®Google Scholar
• Rouvier E., Luciani M. F., Golstein P. Fas involvement in Ca2+-independent T cell-mediated cytotoxicity. J. Exp. Med. 1993; 177: 195–200
   PubMed Web of Science ®Google Scholar
• Rosenblatt N., Hartmann K -U., Loor F. Development of grafted gld cells in athymic and euthymic recipients. Immunology 1995; 84, in the press (Ms # 94462)
   PubMedGoogle Scholar
• Drappa J., Brot N., Elkon K. B. The Fas protein is expressed at high levels on CD4+CD8+ thymocytes and activated mature lymphocytes in normal mice but not in the lupus-prone strain, MRL Ipr/lpr. Proc. Natl. Acad. Sci. USA 1993; 90: 10340–10344
   PubMed Web of Science ®Google Scholar
• Ju S. T., Cui H., Panka D. J., Ettinger R., Marshak-Rothstein A. Participation of target Fas protein in apoptosis pathway induced by CD4+ Th1 and CD9+ cytotoxic T cells. Proc. Natl. Acad. Sci. USA 1994; 91: 4185–4189
   PubMed Web of Science ®Google Scholar
• Hanabuchi S., Koyanagi M., Kawasaki A., Shinohara N., Matsuzawa A., Nishimura Y., Kobayashi Y., Yonehara S., Yagita H., Okumura K. Fas and its ligand in a general mechanism of T-cell-mediated cytotoxicity. Proc. Natl. Acad. Sci. USA 1994; 91: 4930–4934
   PubMed Web of Science ®Google Scholar
• Singer G. G., Abbas A. K. The Fas antigen is involved in peripheral but not thymic deletion of T lymphocytes in T cell receptor transgenic mice. Immunity 1994; 1: 365–371
   PubMed Web of Science ®Google Scholar
• Krammer P. H., Behrmann I., Daniel P., Dhein J., Debatin K. M. Regulation of apoptosis in the immune system. Cur. Op. Immunol. 1994; 6: 279–289
   PubMed Web of Science ®Google Scholar
• Vignaux F., Golstein P. Fas-based lymphocyte-mediated cytotoxicity against syngeneic activated lymphocytes: a regulatory pathway?. Eur. J. Immunol. 1994; 24: 923–927
   PubMed Web of Science ®Google Scholar
• Daniel P. T., Krammer P. H. Activation induces sensitivity toward APO-1 (CD95)-mediated apoptosis in human B cells. J. Immunol. 1994; 152: 5624–5632
   PubMed Web of Science ®Google Scholar
• Thomas M. L. The leukocyte common antigen family. Ann. Rev. Immunol. 1989; 7: 339–363
   PubMed Web of Science ®Google Scholar
• Whitlock C., Denis K., Robertson D., Witte O. In vitro analysis of murine B-cell development. Ann. Rev. Immunol. 1985; 3: 213–234
   PubMedGoogle Scholar
• Cheng J., Zhou T., Liu C., Shapiro J. P., Brauer M. J., Kiefer M. C., Barr P. J., Mountz J. D. Protection from Fasmediated apoptosis by a soluble form of the Fas molecule. Science 1994; 263: 1759–1762
   PubMed Web of Science ®Google Scholar
• Ogasawara J., Watanabe-Fukunaga R., Adachi M., Matsuzawa A., Kasugai T., Kitamura Y., Itoh N., Suda T., Nagata S. Lethal effect of the anti-Fas antibody in mice. Nature 1993; 364: 806–809
   PubMed Web of Science ®Google Scholar
• Suda T., Nagata S. Purification and characterization of the Fas-ligand that induced apoptosis. J. Exp. Med. 1994; 179: 873–879
   PubMed Web of Science ®Google Scholar