6. Conclusions
Our understanding of antibody-mediated renal damage has not changed drastically in recent years. However, within this framework a lot of new data emerged to change our way of looking at “old” diseases. For example, APSGN, which in the past has been regarded as a typical CIC-mediated disease, may also show ICs formed in situ. In Goodpasture’s syndrome, once considered to be the classical model of autoantibody-mediated disease, it is now realized that nephritogenic T cells play an important role. Complement, formerly thought to be a pathogenic factor in nephritis, is now believed to be crucial for the protection of immune-mediated renal injury. At the same time, components of the fibrinolytic system play a role as autoantibody targets in renal damage, and a disregulation of this pathway may be a mechanism in different renal diseases.
Furthermore, new hypotheses are emerging to explain how the immune system interacts with the external world. One of them suggests that a great deal more is involved than the mere discrimination between self and nonself: the immune system is able to handle all elements, even endogenous ones, that pose a potential danger to the host (Matzinger, 1994). Thus, tissues themselves play a central role: when healthy, they may induce tolerance and when distressed, they may stimulate immunity.
In this view, autoimmunity can be regarded as a defect in the “cross-talk” between the immune system and the body tissues, a perspective that opens up fascinating new avenues for research on the mechanisms that regulate the expression of renal antigens in health and disease.
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References
Amoura, Z., Chabre, H., Koutouzov, S., Lotton, C., Cabrespines, A., Bach, J.F., and Jacob, L. (1994). Nucleosome-restricted antibodies are detected before anti-dsDNA and/or antihistone antibodies in serum of MRL-Mp lpr/lpr and +/+ mice, and are present in kidney eluates of lupus mice with proteinuria. Arthritis Rheum., 37, 1684–1688.
Berden, J.H., Licht, R., van Bruggen, M.C., and Tax, W.J. (1999). Role of nucleosomes for induction and glomerular binding of autoantibodies in lupus nephritis. Curr. Opin. Nephrol. Hypertens., 8, 299–306.
Birmingham, D.J., Chen, W., Liang, G., Schmitt, H.C., Gavit, K., and Nagaraja, H.N. (2003). A CR1 polymorphism associated with constitutive erythrocyte CR1 levels affects binding to C4b but not C3b. Immunology, 108, 531–538.
Borza, D.B. and Hudson, B.G. (2003). Molecular characterization of the target antigens of antiglomerular basement membrane antibody disease. Springer Semin. Immunopathol., 24, 345–361.
Botto, M. and Walport, M.J. (2002). C1q, autoimmunity and apoptosis. Immunobiology, 205, 395–406.
Burova, L., Thern, A., Pigarevsky, P., Gladilina, M., Seliverstova, V., Gavrilova, E., Nagornev, V., Schalen, C., and Totolian, A. (2003). Role of group A streptococcal IgG binding proteins in triggering experimental glomerulonephritis in the rabbit. Acta Pathol. Microbiol. Immunol. Scand., 111, 955–962.
Caponi, L., Chimenti, D., Pratesi, F., and Migliorini, P. (2002). Anti-ribosomal antibodies from lupus patients bind DNA. Clin. Exp. Immunol., 130, 541–547.
Chan, O.T., Hannum, L.G., Haberman, A.M., Madaio, M.P., and Shlomchik, M.J. (1999). A novel mouse with B cells but lacking serum antibody reveals an antibody-independent role for B cells in murine lupus. J. Exp. Med., 189, 1639–1648.
Clynes, R., Dumitru, C., and Ravetch, J.V. (1998). Uncoupling of immune complex formation and kidney damage in autoimmune glomerulonephritis. Science, 279, 1052–1054.
Craig, M.L., Bankovich, A.J., McElhenny, J.L., and Taylor, R.P. (2000). Clearance of anti-double-stranded DNA antibodies: The natural immune complex clearance mechanism. Arthritis Rheum., 43, 2265–2275.
Cu, G.A., Mezzano, S., Bannan, J.D., and Zabriskie, J.B. (1998). Immunohistochemical and serological evidence for the role of streptococcal proteinase in acute post-streptococcal glomerulonephritis. Kidney Int., 54, 819–826.
Davies, K.A., Robson, M.G., Peters, A.M., Norsworthy, P., Nash, J.T., and Walport, M.J. (2002). Defective Fc-dependent processing of immune complexes in patients with systemic lupus erythematosus. Arthritis Rheum., 46, 1028–1038.
Dehan, P., Weber, M., Zhang, X., Reeders, S.T., Foidart, J.M., and Tryggvason, K. (1996). Sera from patients with anti-GBM nephritis including Goodpasture syndrome show heterogenous reactivity to recombinant NC1 domain of type IV collagen alpha chains. Nephrol. Dial. Transplant., 11, 2215–2222.
Deocharan, B., Qing, X., Lichauco, J., and Putterman, C. (2002). Alpha-actinin is a cross-reactive renal target for pathogenic anti-DNA antibodies. J. Immunol., 168, 3072–3078.
Ehrenstein, M.R., Katz, D.R., Griffiths, M.H., Papadaki, L., Winkler, T.H., Kalden, J.R., and Isenberg, D.A. (1995). Human IgG anti-DNA antibodies deposit in kidneys and induce proteinuria in SCID mice. Kidney Int., 48, 705–711.
Emlen, W. and Mannik, M. (1984). Effect of DNA size and strandedness on the in vivo clearance and organ localization of DNA. Clin. Exp. Immunol., 56, 185–192.
Fontan, P.A., Pancholi, V., Nociari, M.M., and Fischietti, V.A. (2000). Antibodies to streptococcal surface enolase react with human alpha-enolase: Implications in poststreptococcal sequelae. J. Infect. Dis., 182, 1712–1721.
Foster, M.H., Sabbaga, J., Line, S.R., Thompson, K.S., Barrett, K.J., and Madaio, M.P. (1993). Molecular analysis of spontaneous nephrotropic anti-laminin antibodies in an autoimmune MRL-lpr/lpr mouse. J. Immunol., 151, 814–824.
Friedman, J., van de Rijn, I., Ohkuni, H., Fischetti, V.A., and Zabriskie, J.B. (1984). Immunological studies of post-streptococcal sequelae. Evidence for presence of streptococcal antigens in circulating immune complexes. J. Clin. Invest., 74, 1027–1034.
Glurich, I., Winters, B., Albini, B., and Stinson, M. (1991). Identification of Streptococcus pyogenes proteins that bind to rabbit kidney in vitro and in vivo. Microb. Pathog., 10, 209–220.
Kalluri, R., Danoff, T.M., Okada, H., and Neilson, E.G. (1997). Susceptibility to anti-glomerular basement membrane disease and Goodpasture syndrome is linked to MHC class II genes and the emergence of T cell-mediated immunity in mice. J. Clin. Invest., 100, 2263–2275.
Karassa, F.B., Trikalinos, T.A., Ioannidis, J.P., and FcgammaRIIa-SLE Meta-Analysis Investigators (2002). Role of the Fc receptor IIa polymorphism in susceptibility to systemic lupus erythematosus and lupus nephritis: A meta-analysis. Arthritis Rheum., 46, 1563–1571.
Kitching, A.R., Holdsworth, S.R., Ploplis, V.A., Plow, E.F., Collen, D., Carmeliet, P., and Tipping, P.G. (1997). Plasminogen and plasminogen activators protect against renal injury in crescentic glomerulonephritis. J. Exp. Med., 185, 963–968.
Kos, C.H., Le, T.C., Sinha, S., Henderson, J.M., Kim, S.H., Sugimoto, H., Kalluri, R., Gerszten, R.E., and Pollak, M.R. (2003). Mice deficient in alpha-actinin-4 have severe glomerular disease. J. Clin. Invest., 111, 1683–1690.
Lin, C.Y. (1982). Serial studies of circulating immune complexes in poststeptococcal glomerulonephritis. Pediatrics, 70, 725–727.
Lopez-Alemany, R., Longstaff, C., Hawley, S., Mirshahi, M., Fabregas, P., Jardi, M., Merton, E., Miles, L.A., and Felez, J. (2003). Inhibition of cell surface mediated plasminogen activation by a monoclonal antibody against alpha-enolase. Am. J. Hematol., 72, 234–242.
Madaio, M.P., Carlson, J., Cataldo, J., Ucci, A., Migliorini, P., and Pankewycz, O. (1987). Murine monoclonal anti-DNA antibodies bind directly to glomerular antigens and form immune deposits. J. Immunol., 138, 2883–2889.
Madaio, M.P., Fabbi, M., Tiso, M., Daga, A., and Puccetti, A. (1996). Spontaneously produced anti-DNA/DNase I autoantibodies modulate nuclear apoptosis in living cells. Eur. J. Immunol., 26, 3035–3041.
Madaio, M.P. and Shlomchik, M.J. (1996). Emerging concepts regarding B cells and autoantibodies in murine lupus nephritis. B cells have multiple roles; all autoantibodies are not equal. J. Am. Soc. Nephrol., 7, 387–396.
Madaio, M.P. and Yanase, K. (1998). Cellular penetration and nuclear localization of anti-DNA antibodies: Mechanisms, consequences, implications and applications. J. Autoimmun., 11, 535–538.
Mannik, M., Merrill, C.E., Stamps, L.D., and Wener, M.H. (2003). Multiple autoantibodies form the glomerular immune deposits in patients with systemic lupus erythematosus. J. Rheumatol., 30, 1495–1504.
Marin, C., Mosquera, J., and Rodirguez-Iturbe, B. (1997). Histological evidence of neuraminidase involvement in acute nephritis: Desialized leukocytes infiltrate the kidney in acute post-streptococcal glomerulonephritis. Clin. Nephrol., 47, 217–221.
Mason, L.J., Ravirajan, C.T., Rahman, A., Putterman, C., and Isenberg, D.A. (2004). Is alpha-actinin a target for pathogenic anti-DNA antibodies in lupus nephritis? Arthritis Rheum., 50, 866–870.
Matzinger, P. (1994). Tolerance, danger, and the extended family. Annu. Rev. Immunol., 12, 991–1045.
McIntosh, R.M., Garcia, R., Rubio, L., Rabideau, D., Allen, J.E., Carr, R.I., and Rodriguez-Iturbe, B. (1978). Evidence of an autologous immune complex pathogenic mechanism in acute poststreptococcal glomerulonephritis. Kidney Int., 14, 501–510.
Michel, M., Piette, J.C., Roullet, E., Duron, F., Frances, C., Nahum, L., Pelletier, N., Crassard, I., Nunez, S., Michel, C., Bach, J., and Tournier-Lasserve, E. (2000). The R131 low-affinity allele of the Fc gamma RIIA receptor is associated with systemic lupus erythematosus but not with other autoimmune diseases in French Caucasians. Am. J. Med., 108, 580–583.
Migliorini, P., Pratesi, F., Bongiorni, F., Moscato, S., Scavuzzo, M., and Bombardieri, S. (2002). The targets of nephritogenic antibodies in systemic autoimmune disorders. Autoimmun. Rev., 1, 168–173.
Miles, L.A., Dahlberg, C.M., Plescia, J., Felez, J., Kato, K., and Plow, E.J., (1991). Role of cell-surface lysines in plasminogen binding to cells: Identification of alpha-enolase as a candidate plasminogen receptor. Biochemistry, 30, 1682–1691.
Moodie, F.D.L., Leaker, B., Cambridge, G., Totty, N.F., and Segal, A.W. (1993). Alpha-enolase: A novel cytosolic autoantigen in ANCA positive vasculitis. Kidney Int., 43, 675–681.
Moscato, S., Pratesi, F., Sabbatini, A., Chimenti, D., Scavuzzo, M., Passatino, R., Bombardieri, S., Giallongo, A., and Migliorini, P. (2000) Surface expression of a glycolytic enzyme, alpha-enolase, recognized by autoantibodies in connective tissue disorders. Eur. J. Immunol., 30, 3575–3584.
Mostoslavsky, G., Fischel, R., Yachimovich, N., Yarkoni, Y., Rosenmann, E., Monestier, M., Baniyash, M., and Eilat, D. (2001). Lupus anti-DNA autoantibodies cross-react with a glomerular structural protein: A case for tissue injury by molecular mimicry. Eur. J. Immunol., 31, 1221–1227.
Nakamura, A., Yuasa, T., Ujike, A., Ono, M., Nukiwa, T., Ravetch, J.V., and Takai, T. (2000). Fcgamma receptor IIB-deficient mice develop Goodpasture’s syndrome upon immunization with type IV collagen: A novel murine model for autoimmune glomerular basement membrane disease. J. Exp. Med., 191, 899–906.
Nordstrand, A., Norgren, M., Ferretti, J.J., and Holm S.E. (1998). Streptokinase as a mediator of acute post-streptococcal glomerulonephritis in an experimental mouse model. Infect. Immun., 66, 315–321.
Nordstrand, A., Norgren, M., and Holm, S.E. (1999). Pathogenic mechanism of acute post-streptococcal glomerulonephritis. Scand. J. Infect. Dis., 31, 523–537.
Pankewycz, O.G., Migliorini, P., and Madaio, M.P. (1987). Polyreactive autoantibodies are nephritogenic in murine lupus nephritis. J. Immunol., 139, 3287–3294.
Park, S.Y., Ueda, S., Ohno, H., Hamano, Y., Tanaka, M., Shiratori, T., Yamazaki, T., Arase, H., Arase, N., Karasawa, A., Sato, S., Ledermann, B., Kondo, Y., Okumura, K., Ra, C., and Saito, T. (1998). Resistance of Fc receptor-deficient mice to fatal glomerulonephritis. J. Clin. Invest., 102, 1229–1238.
Peutz-Kootstra, C.J., Hansen, K., De Heer, E, Abrass, C.K., and Bruijn, J.A. (2000). Differential expression of laminin chains and anti-laminin autoantibodies in experimental lupus nephritis. J. Pathol., 192, 404–412.
Pratesi, F., Moscato, S., Sabbatini, A., Chimenti, D., Bombardieri, S. and Migliorini, P. (2000). Autoantibodies specific for alpha-enolase in systemic autoimmune disorders. J. Rheumatol., 27, 109–115.
Puccetti, A., Madaio, M.P., Bellese, G., and Migliorini, P. (1995). Anti-DNA antibodies bind to DNase I. J. Exp. Med., 181, 1797–1804.
Putterman, C. (2004). New approaches to the renal pathogenicity of anti-DNA antibodies in systemic lupus erythematosus. Autoimmun. Rev., 3, 7–11.
Ravetch, J.V. (2002). A full complement of receptors in immune complex diseases. J. Clin. Invest., 110, 1759–1761.
Raz, E., Ben-Bassat, H., Davidi, T., Shlomai, Z., and Eilat, D. (1993). Cross-reactions of anti-DNA autoantibodies with cell surface proteins. Eur. J. Immunol., 23, 383–390.
Raz, E., Brezis, M., Rosenmann, E., and Eilat, D. (1989). Anti-DNA antibodies bind directly to renal antigens and induce kidney dysfunction in the isolated perfused rat kidney. J. Immunol., 142, 3076–3082.
Reefman, E., Dijstelbloem, H.M., Limburg, P.C., Kallenberg, C.G., and Bijl, M. (2003). Fcgamma receptors in the initiation and progression of systemic lupus erythematosus. Immunol. Cell Biol., 81, 382–389.
Reichlin, M. (1996). Presence of ribosomal P protein on the surface of human umbilical vein endothelial cells. J. Rheumatol., 23, 1123–1125.
Reynolds, J., Cashman, S.J., Evans, D.J., and Pusey, C.D. (1991). Cyclosporin A in the prevention and treatment of experimental autoimmune glomerulonephritis in the brown Norway rat. Clin. Exp. Immunol., 85, 28–32.
Reynolds, J. and Pusey, C.D. (2001). Oral administration of glomerular basement membrane prevents the development of experimental autoimmune glomerulonephritis in the WKY rat. J. Am. Soc. Nephrol., 12, 61–70.
Rodriguez-Iturbe, B., Rabideau, D., Garcia, R., Rubio, L., and McIntosh, R.M. (1980). Characterization of the glomerular antibody in acute poststreptococcal glomerulonephritis. Ann. Intern. Med., 92, 478–481.
Rumore, P.M. and Steinman, C.R. (1990). Endogenous circulating DNA in systemic lupus erythematosus. Occurrence as multimeric complexes bound to histone. J. Clin. Invest., 86, 69–74.
Rutgers A., Meyers K.E., Canziani, G., Kalluri, R, Lin, J., and Madaio, M.P. (2000). High affinity of anti-GBM antibodies from Goodpasture and transplanted Alport patients to alpha3(IV)NC1 collagen. Kidney Int., 58, 115–122.
Ryan, J.J., Mason, P.J., Pusey, C.D., and Turner, N. (1998). Recombinant alpha-chains of type IV collagen demonstrate that the amino terminal of the Goodpasture autoantigen is crucial for antibody recognition. Clin. Exp. Immunol., 113, 17–27.
Sabbaga, J., Line, S.R., Potocnjak, P., and Madaio, M.P. (1989). A murine nephritogenic monoclonal anti-DNA autoantibody binds directly to mouse laminin, the major non-collagenous protein component of the glomerular basement membrane. Eur. J. Immunol., 19, 137–143.
Sabbatini, A., Dolcher, M.P., Marchini, B., Chimenti, D., Moscato, S., Pratesi, F., Bombardieri, S., and Migliorini, P. (1997). Alpha-enolase is a renal-specific antigen associated with kidney involvement in mixed cryoglobulinemia. Clin. Exp. Rheumatol., 15, 655–658.
Salmon, J.E., Millard, S., Schachter., L.A., Arnett, F.C., Ginzler, E.M., Gourley, M.F., Ramsey-Goldman, R., Peterson, M.G.E., and Kimberly, R.P. (1996). Fc-gamma-RIIA alleles are heritable risk factors for lupus nephritis in African Americans. J. Clin. Invest., 97, 1348–1354.
Sheerin, N.S., Springall, T., Carroll, M.C., Hartley, B., and Sacks, S.H. (1997). Protection against antiglomerular basement membrane (GBM)-mediated nephritis in C3-and C4-deficient mice. Clin. Exp. Immunol., 110, 403–409.
Shlomchik, M.J., Madaio, M.P., Ni, D., Trounstein, M., and Huszar, D. (1994). The role of B cells in lpr/lpr-induced autoimmunity. J. Exp. Med., 180, 1295–1306.
Siegert, C., Daha, M., Westedt, M.L., van der Voort, E., and Breedveld, F. (1991). IgG autoantibodies against C1q are correlated with nephritis, hypocomplementemia, and dsDNA antibodies in systemic lupus erythematosus. J. Rheumatol., 18, 230–234.
Sun, K.H., Liu, W.T., Tang, S.J., Tsai, C.Y., Hsieh, S.C., Wu, T.H., Han, S.H., and Yu, C.L. (1996). The expression of acidic ribosomal phosphoproteins on the surface membrane of different tissues in autoimmune and normal mice which are the target molecules for anti-double-stranded DNA antibodies. Immunology, 87, 362–371.
Sylvestre, D., Clynes, R., Ma, M., Warren, H., Carroll, M.C., and Ravetch, J.V. (1996). Immunoglobulin G-mediated inflammatory responses develop normally in complement-deficient mice. J. Exp. Med., 184, 2385–2392.
Takai, T. (2002). Roles of Fc receptors in autoimmunity. Nat. Rev. Immunol., 2, 580–592.
Tan Sardjono, C., Mottram, P.L., and Hogarth, P.M. (2003). The role of FcgammaRIIa as an inflammatory mediator in rheumatoid arthritis and systemic lupus erythematosus. Immunol. Cell Biol., 81, 374–381.
Tarzi, R.M., Davies, K.A., Claassens, J.W., Verbeek, J.S., Walport, M.J., and Cook, H.T. (2003). Both Fcgamma receptor I and Fcgamma receptor III mediate disease in accelerated nephrotoxic nephritis. Am. J. Pathol., 162, 1677–1683.
Tipping, P.G. and Holdsworth, S.R. (2003). T cells in glomerulonephritis. Springer Semin. Immunopathol., 24, 377–393.
Trouw, L.A., Duijs, J.M., van Kooten, C., and Daha, M.R. (2003a). Immune deposition of C1q and anti-C1q antibodies in the kidney is dependent on the presence of glomerular IgG. Mol. Immunol., 40, 595–602.
Trouw, L.A., Groeneveld, T.W., Seelen, M.A., Duijs, J.M., Bajema, I.M., Prins, F.A., Kishore, U., Salant, D.J., Verbeek, J.S., van Kooten, C., and Daha, M.R. (2004). Anti-C1q autoantibodies deposit in glomeruli but are only pathogenic in combination with glomerular C1q-containing immune complexes. J. Clin. Invest., 114, 679–688.
Trouw, L.A., Seelen, M.A., Duijs, J.M., Benediktsson, H., Van Kooten, C., and Daha, M.R. (2003b). Glomerular deposition of C1q and anti-C1q antibodies in mice following injection of antimouse C1q antibodies. Clin. Exp. Immunol., 132, 32–39.
van Bruggen, M.C., Kramers, C., Walgreen, B., Elema, J.D., Kallenberg, C.G., van den Born, J., Smeenk, R.J., Assmann, K.J., Muller, S., Monestier, M., and Berden, J.H. (1997a). Nucleosomes and histones are present in glomerular deposits in human lupus nephritis. Nephrol. Dial. Transplant., 12, 57–66.
van Bruggen, M.C., Walgreen, B., Rijke, T.P., Tamboer, W., Kramers, K., Smeenk, R.J., Monestier, M., Fournie, G.J., and Berden, J.H. (1997b). Antigen specificity of anti-nuclear antibodies complexed to nucleosomes determines glomerular basement membrane binding in vivo. Eur. J. Immunol., 27, 1564–1569.
Wakui, H., Imai, H., Komatsuda, A., and Miura, A.B. (1999). Circulating antibodies against alphaenolase in patients with primary membranous nephropathy (MN). Clin. Exp. Immunol., 118, 445–450.
Waters, S.T., McDuffie, M., Bagavant, H., Deshmukh, U.S., Gaskin, F., Jiang, C., Tung, K.S., and Fu, S.M. (2004). Breaking tolerance to double stranded DNA, nucleosome, and other nuclear antigens is not required for the pathogenesis of lupus glomerulonephritis. J. Exp. Med., 199, 255–264.
Wu, J., Arends, J., Borillo, J., Zhou, C., Merszei, J., McMahon, J., and Lou, Y.H. (2004). A self T cell epitope induces autoantibody response: Mechanism for production of antibodies to diverse glomerular basement membrane antigens. J. Immunol., 172, 4567–4574.
Wu, J., Hicks, J., Borillo, J., Glass, W.F., 2nd, and Lou Y.H. (2002). CD4(+) T cells specific to a glomerular basement membrane antigen mediate glomerulonephritis. J. Clin. Invest., 109, 517–524.
Wu, J., Hicks, J., Ou, C., Singleton, D., Borillo, J., and Lou, Y.H. (2001). Glomerulonephritis induced by recombinant collagen IV alpha 3 chain noncollagen domain 1 is not associated with glomerular basement membrane antibody: A potential T cell-mediated mechanism. J. Immunol., 167, 2388–2395.
Yamamoto, T. and Wilson, C.B. (1987). Binding of anti-basement membrane antibody to alveolar basement membrane after intratracheal gasoline instillation in rabbits. Am. J. Pathol., 126, 497–505.
Yanase, K., Smith, R.M., Puccetti, A., Jarett, L., and Madaio, M.P. (1997). Receptor-mediated cellular entry of nuclear localizing anti-DNA antibodies via myosin 1. J. Clin. Invest., 100, 25–31.
Yoshizawa, N., Oshima, S., Takeuchi, A., Kondo, S., Oda, T., Shimizu, J., Nishiyama, J., Ishida, A., Nakabayashi, I., Tazawa, K., and Sakurai, Y. (1997). Experimental acute glomerulonephritis induced in the rabbit with a specific streptococcal antigen. Clin. Exp. Immunol., 107, 61–67.
Yoshizawa, N., Yamakami, K., Fujino, M., Oda, T., Tamura, K., Matsumoto, K., Sugisaki, T., and Boyle, M.D. (2004). Nephritis-associated plasmin receptor and acute poststreptococcal glomerulonephritis: Characterization of the antigen and associated immune response. J. Am. Soc. Nephrol., 15, 1785–1793.
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Migliorini, P., Anzilotti, C., Caponi, L., Pratesi, F. (2005). Autoantibodies and Nephritis: Different Roads May Lead to Rome. In: Zouali, M. (eds) Molecular Autoimmunity. Springer, Boston, MA. https://doi.org/10.1007/0-387-24534-0_13
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