Abstract
The hypothesis that type I, insulin-dependent diabetes mellitus (IDDM) results, at least in part, from the autoimmune destruction of pancreatic beta-cells has been discussed in several reviews,1–3 as well as in other chapters in this volume. Relatively early in the analysis of autoimmunity and diabetes, a small number of papers presented evidence of a direct anti-beta—cell (or pancreatic islet-cell) cellular immune response in individuals with diabetes. It has become clear over the last decade, however, that the results of such studies in humans are limited, at least to the extent that they may be considered beta-cell—specific, by the so-called major histocompatibility complex (MHC)-restriction of the cell-mediated arm of the immune system. The specific effector cell, typically a thymus-derived cell, the T-cell, and the target cell must share identity at one of the class I (cytotoxic/suppressor cells, CD8+) or class II (helper/inducer cells CD4+). This issue of MHC-restriction in the immune system has been reviewed recently.4–5 Although MHC-restriction is not now considered to be an absolute requirement for cell-mediated cytolysis, further research in the description and analysis of the role of the cell-mediated immune response in human diabetes has virtually stopped because of the lack of a biologically relevant, MHC-restricted beta-cell for use as a target. Fortunately studies of the cell-mediated immune response against pancreatic beta-cells are possible in experimental models of diabetes using both in vitro and in vivo techniques.
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References
Powers AC, Eisenbarth GS. Autoimmunity to islet cells in diabetes mellitus. Ann Rev Med1985; 36: 533 – 544.
Janeway C. The immune destruction of the pancreatic beta cells. Immunol Today1985; 6: 229 – 232.
Handwerger B. The immunology of diabetes mellitus, in Volpe R (ed): Autoimmunity and Endocrine Disease. New York: Marcel Dekker, 1985, pp 287 – 344.
McDevitt HO. The HLA system and its relation to disease. Hosp Prac1985; 15: 57 – 72.
Marrack P, Kappler J. The T cell and its receptor. Sci Am1986; 254: 36 – 45.
Nerup J, Andersen O, Bendiken G, et al. Antipancreatic cellular hypersensitivity in diabetes mellitus. Diabetes1971; 20: 424 – 427.
Huang S-W, MacLaren NK. Insulin-dependent diabetes: A disease of autoaggression. Science1976; 192: 64 – 66.
Segain J, Valentin A, Bardet S, et al. T4 lymphocytes from type I diabetics specifically bind in vitro to xenogeneic beta cell antigens via the T cell receptor. Diabetes 1988;37(Suppl 1):56A, Abstr 223.
Suzuki M, Charles A, Ong K, et al. In vitro islet cell cytotoxicity assays for evaluation of potential cellular and antibody-mediated immunological mechanisms in diabetes mellitus. Diabetes 1980;30(Suppl 1):65A, Abstr 224.
Scott J, Daniels JC, Poffenbarger PL. In vitro cell-mediated cytolysis of intact islets of Langerhans in studies of IDDM. Diabetologia 1981;21:78, Absr. 12.
Charles MA, Suzuki M, Waldeck N, et al. Immune islet killing mechanisms associated with insulin-dependent diabetes: In vitro expression of cellular and antibody-mediated islet cell cytotoxicity in humans. J Immunol1983; 130: 1189 – 1194.
Gupta S, Charles MA, Waldeck N, et al. Multiparameter immunologic studies In patients with newly diagnosed type I insulin-dependent diabetes mellitus. Diabetes Res1986; 3: 225 – 229.
Like AA, Rossini AA. Streptozotocin-induced pancreatic insulitis: A new model of diabetes mellitus. Science1976; 193: 415 – 417.
Kolb H. Mouse models of insulin-dependent diabetes low-dose streptozotocin-induced diabetes and non-obese diabetic (NOD) mice. Diabetes Metab Rev1987; 3: 751 – 778.
Rossini AA, Appel MC, Williams RM, et al. Genetic influence on streptozotocin-induced insulitis and hyperglycemia. Diabetes1977; 26: 916 – 920.
Kolb H, Kiesel U. Localization of genes controlling an experimental model of human IDDM within and without the major histocompatibility complex. Immunobiology1981; 160: 58 – 62.
Wolf J, Lilly F, Shin S-I. The influence of genetic background on the susceptibility of inbred mice to streptozotocin-induced diabetes. Diabetes1984; 33: 567 – 571.
Leiter EH. Genetic control of the pathogenesis of diabetes in C3H mice. Influence of the major histocompatibility complex. Diabetes1984; 33: 1068 – 1072.
Le PH, Leiter EH, Leyendecker JR. Genetic control of susceptibility to streptozotocin diabetes in inbred mice. Effect of testosterone and H-2 haplotype. Endocrinology1985; 116: 2450 – 2455.
Rossini AA, Williams RM, Appel MC, et al. Sex differences in the multiple, low dose streptozotocin model of diabetes. Endocrinology1978; 103: 1518 – 1520.
Paik S-G, Fleischer N, Shin S-I. Insulin dependent diabetes mellitus induced by sub- diabetogenic doses of streptozocin: Obligatory role of cell-mediated autoimmune processes. Proc Natl Acad Sci USA1980; 77: 6129 – 6133.
MacLaren NK, Neufeld M, McLaughlin JV, et al. Androgen sensitization of streptozotocin-induced diabetes in mice. Diabetes1980; 29: 710 – 716.
Kuttler B, Schneider E. Diabetes mellitus in mice induced by multiple subdiabetogenic doses of streptozotocin: Age and sex dependence. Acta Biol Med Ger1982; 41: 1199 – 1201.
Rossini AA, Like AA, Chick WL, et al. Studies of streptozotocin-induced insulitis and diabetes. Proc Natl Acad Sci USA1977; 74: 2485 – 2489.
Rossini AA, Williams RM, Appel MC, et al. Complete protection from low-dose streptozotocin-induced diabetes in mice. Nature1978; 276: 182 – 184.
Buchard K, Rygaard J. T-lymphocytes transfer streptozotocin-induced diabetes mellitus in mice. Acta Pathol Microbiol Scand [C]1978; 86: 277 – 282.
Beattie G, Lannom R, Lipstick J, et al. Streptozotocin-induced insulitis model in athymic mice. Diabetes1980; 29: 146 – 150.
Rossini AA, Like AA, Appel MC, et al. Streptozotocin-induced insulitis model in athymic mice. Diabetes 1980;29(Suppl 2):51A, Abstr. 204.
Kiesel U, Freytag G, Kolb H, et al. Transfer of experimental autoimmune insulitis by spleen cells in mice. Diabetologia1980; 19: 516 – 520.
Kiesel U, Kolb H, Freytag G. Strain dependence of the transfer of autoimmune insulitis in mice. Clin Exp Immunol1981; 43: 430 – 433.
Nakamura M, Nagafuchi S, Yamaguchi K, et al. The role of thymic immunity and insulitis in the development of streptozotocin-induced diabetes in mice. Diabetes1984; 33: 894 – 900.
Koevary SB, Williams RM, Chick WL, et al. Passive transfer of diabetes in the BB rat. Science1983; 220: 727 – 729.
Kim YT, Steinberg C. Immunological studies on the induction of diabetes in experimental mice. Diabetes1984; 33: 771 – 777.
Schreiner G, Rossini A, Mordes J, et al. Essential fatty acid deficiency inhibits the development of diabetes. Diabetes 1988;37 (Suppl 1):80A, Abstr. 318.
Paik S-G, Blue ML, Fleischer N, et al. Diabetes susceptibility of BALC/cBom mice treated with streptozotocin: Inhibition by lethal irradiation and restoration by splenic lymphocytes. Diabetes1982; 31: 808 – 815.
Hahn HJ, Barnsdorf K, Nadrowitz R, et al. The effect of irradiation on the development of low dose streptozotocin diabetes in mice. Acta Biol Med Ger1982; 41: 1191 – 1197.
Nedergaard M, Egeberg J, Kromann H. Irradiation protects against pancreatic islet degeneration and hyperglycemia following streptozotocin treatment of mice. Diabetologia1983; 24: 382 – 386.
Blue ML, Shin S-I. Diabetes induced by sub-diabetogenic doses of streptozotocin in BALB/cBom mice: Noninvolvement of host B lymphocyte function. Diabetes1984; 33: 105 – 113.
Kiesel U, Grevlich B, Marx-Soho Moume C, et al. Induction of diabetes by low dose streptozotocin treatment in genetically resistant mice. Immunol Lett1981; 3: 227 – 230.
Kolb H, Greulich B, Kiesel U, et al. Demonstration of suppressor lymphocytes which inhibit the manifestations of IDDM in mice. Diabetologia 1981;21:292, Abstr 282.
Flechner I, Muntefering H, Smadja Y, et al. Immunomodulation of streptozotocin-induced diabetes in mice by a lipopolysaccharide. Diabetes Res1984; 1: 231 – 232.
Kiesel U, Kolb H. Suppressive effect of antibodies to immune response gene products on the development of low dose streptozotocin-induced diabetes. Diabetes1983; 32: 869 – 871.
Sestier C, Odent-Pugo S, Bonneville M, et al. Cyclosporin enhances diabetes induced by low-dose streptozotocin-treatment in mice. Immunol Lett1985; 10: 57 – 60.
Andersson A, Hallberg A, Sandler S, et al. Direct toxicity of cyclosporin on beta cells in tissue culture. Diabetologia1984; 27: 66 – 69.
Sandler S, Andersson A. Modulation of streptozotocin-induced insulitis and hyperglycemia in the mouse. Acta Pathol Microbiol Immunol Scand [A]1985; 93: 93 – 98.
Gold G, Manning M, Heldt A, et al. Diabetes induced by multiple, subdiabetigenic doses of streptozotocin. Lack of protection by exogenous superoxide dismutase. Diabetes1981; 30: 634 – 638.
Sandler S. Protection by dimethyl urea against hyperglycemia but not insulitis in low dose streptozotocin-induced diabetes in the mouse. Diabetologia1984; 26: 386 – 388.
Andersson A. Islet transplantation normalizes hyperglycemia caused by streptozotocin-induced insulitis in the mouse. Lancet 1979;i:581–584.
Sandler S, Andersson A. Islet implantation into diabetic mice with pancreatic insulitis. Acta Pathol Micro Scand [A]1981; 89: 107 – 112.
Sandler S, Andersson A. Survival of intrasplenically implanted islets in mice with experimental insulitis and hyperglycemia. Diabetes1982; 31 (Suppl 4): 78 – 82.
McEvoy RC, Andersson J, Sandler S, Hellerstrom C. Multiple, low dose streptozotocin induced diabetes in the mouse: Evidence for stimulation of a cytotoxic cellular immune response against an insulin producing beta cell line. J Clin Invest1984; 74: 715 – 722.
McEvoy RC, Thomas NM, Hellerstrom C, et al. Multiple, low dose streptozotocin diabetes in the mouse: Further evidence for involvement of an anti-B cell cytotoxic cellular autoimmune response. Diabetologia1987; 30: 232 – 238.
Chappel CI, Chappel ER. The discovery and development of the BB rat colony. An animal model of spontaneous diabetes mellitus. Metabolism1983; 32 (Suppl. 1): 8 – 10.
Nakhooda AF, Like AA, Chappel CI, et al. The spontaneously diabetic Wistar rat. Metabolic and morphologic studies. Diabetes1977; 26: 100 – 112.
Mordes JP, Desemone J, Rossini AA. The BB rat. Diabetes Metab Rev1987; 7: 325 – 750.
Marliss EB. Recommended nomenclature for the spontaneously diabetic syndrome of the BB rat. Metabolism1983; 32 (Suppl l): 6 – 7.
Nakhooda AF, Wei CN, Like AA, et al. The spontaneously diabetic Wistar rat (the BB rat): The significance of transient glucosuria. Diabetes Metab1978; 4: 255 – 259.
Nakhooda AF, Poussier P, Marliss EB. Insulin and glucagon secretion in BB Wistar rats with impaired glucose tolerance. Diabetologia1983; 24: 58 – 62.
Like AA, Rossini AA. Spontaneous autoimmune diabetes in the BioBreeding/Wor-cester rat. Surv Synth Pathol Res1984; 3: 131 – 138.
Butler L, Guberski DL, Like AA. The effect of inbreeding on the BB/W diabetic rat. Metabolism1983; 32: 51 – 53.
Colle E, Guttman RD, Seemayer TA. Spontaneous diabetes mellitus in the rat. I. Association with the major histocompatibility complex. J Exp Med1981; 154: 1237 – 1242.
Colle E, Guttman RD, Seemayer TA, et al. Spontaneous diabetes mellitus syndrome in the rat. IV. Immunogenetic interactions of MHC and non-MHC components of the syndrome. Metabolism 1983; 32 (Suppl. 1): 54 – 61.
Colle E, Guttman RD, Fuks A. Insulin dependent diabetes mellitus is associated with genes that map to the right of the class IRT1. A locus of the major histocompatibility complex of the rat. Diabetes1986; 35: 454 – 458.
Butler L, Guberski DL, Like AA. Genetic analysis of the BB/W diabetic rat. Can J Genet Cytol1983; 25: 7 – 15.
Jackson RA, Buse JB, Rifai P, et al. Two genes required for diabetes in BB rats. Evidence from cyclical intercrosses and backcrosses. J Exp Med1984; 159: 1629 – 1636.
Like AA, Guberski DL, Butler L. Diabetic BioBreeding/Wistar (BB/Wor) rats need not be lymphopenic. J Immunol1986; 136: 3254 – 3258.
Greiner DL, Handler ES, Nakano K, et al. Absence of the RT-6+ T cell subset in dia-betes prone BB/W rats. J Immunol1986; 136: 148 – 151.
Like AA, Forster RM, Woda BA, et al. T cell subsets in islets and lymph nodes of Bio-Breeding/Worcester (BB/W) rats. Diabetes 1983;32(Suppl 1):51A, Abstr 201.
Dean BM, Walker R, Bone AJ, et al. Prediabetes in the spontaneously diabetic BB/E rat: Lymphocyte sub-populations in the pancreatic infiltrate and expression of rat MHC class II molecules in endocrine cells. Diabetologia1985; 28: 464 – 466.
Weringer EJ, Like AA. Immune attack on pancreatic islet transplants in the spontaneously diabetes BioBreeding/Worcester (BB/W) rat is not MHC-restricted. J Immunol1985; 134: 2383 – 2386.
Prowse SJ, Bellgrau D, Lafferty KJ. Islet allografts are destroyed by disease occurrence in the spontaneously diabetic BB rat. Diabetes1986; 35: 110 – 114.
Naji A, Silvers WK, Barker CF. Cell-mediated immunity in type I (insulin-dependent) diabetes of man and the BB rat. Concepts Immunopathol1985; 2: 32 – 46.
Naji A, Bellgrau D, Anderson A, et al. Transplantation of islets and bone marrow cells to animals with immune insulitis. Diabetes1982; 31 (Suppl. 4): 84 – 91.
Woehrle M, Markmann JF, Silvers WK, et al. Transplantation of cultured pancreatic islets to BB rats. Surgery1986; 100: 334 – 341.
MacKay P, Boulton A, Rabinovitch A. Lymphoid cells of BB/W diabetic rats are cytotoxic to islet beta cells in vitro. Diabetes1985; 34: 706 – 709.
MacKay P, Jacobson J, Rabinovitch A. Spontaneous diabetes mellitus in the BioBreeding/Worcester rat. Evidence in vitrofor natural killer cell lysis of islet cells. J Clin Invest1986; 77: 916 – 924.
Prud’Homme GJ, Fuks A, Colle E, et al. Isolation of T lymphocyte lines with specificity for islet cell antigens from spontaneously diabetic (insulin-dependent) rats. Diabetes1984; 33: 801 – 803.
Prud’Homme GJ, Fuks A, Guttman RP, et al. T cell hybrids with specificity for islet cell antigens. J Immunol1986; 136: 1535 – 1536.
Laupacis A, Gardell C, Dupre J, et al. Cyclosporin prevents diabetes in BB Wistar rats. Lancet 1983;i:10–12.
Like AA, Dirodi V, Thomas S, et al. Prevention of diabetes mellitus in the BB/W rat with cyclosporin A. Am J Pathol1984; 117: 92 – 97.
Like AA, Weringer EJ, Holdash A, et al. Adoptive transfer of autoimmune diabetes mellitus in Bio-Breeding/Worcester (BB/W) inbred and hybrid rats. J Immunol1985; 134: 1583 – 1587.
Handler ES, Mordes JP, Geisberg M, et al. Effect of ultraviolet (UV) and X-irradiation on diabetes-prone and resistant BB/W rats. Diabetes 1985;34(Suppl 1):69A, Abstr 275.
Greiner DL, Mordes JP, Handler ES, et al. Depletion of RT6.1+ T lymphocytes induces diabetes in resistant Bio-Breeding/Worcester (BB/W) rats. J Exp Med1987; 166: 461 – 475.
Koevary SB, Williams DE, Williams RM, et al. Passive transfer of diabetes from BB/W to Wistar-Furth rats. J Clin Invest1985; 75: 1904 – 1907.
Yale JF, Vigeant C, Ivanic D. Metabolism time course and immunological concomitants of passive transfer of type I (insulin dependent) diabetes in the BB rat. Diabetologia1986; 29: 608A.
Handler ES, Mordes JP, Seals J, et al. Diabetes in the Bio-Breeding/Worcester (BB/W) rat: Induction and acceleration by spleen cell conditioned media. J Clin Invest1985; 76: 1692 – 1694.
Mordes JP, Handler ES, Like AA, et al. Irradiated lymphocytes do not adoptively transfer diabetes or prevent spontaneous disease in the BB/W rat. Metabolism1986; 35: 552 – 554.
Like AA, Rossini AA. Guberski DL, et al. Spontaneous diabetes mellitus: Reversal and prevention in the BB/W rat with antiserum to rat lymphocytes. Science 1979; 206: 1421–1423.
Rossini A A, Slavin S, Woda BA, et al. Total lymphoid irradiation prevents diabetes mellitus in the BioBreeding/Worcester (BB/W) rat. Diabetes1984; 33: 543 – 547.
Oschilewski U, Kiesel U, Kolb H. Administration of silica prevents diabetes in BB rats. Diabetes1985; 34: 197 – 199.
Brayman KL, Armstrong J, Shaw LM, et al. Prevention of diabetes in BB rats by intermittent administration of cyclosporine. Surgery1985; 102: 235 – 241.
Brayman K, Markmann J, Barker C, et al. Prevention of diabetes in BB rats requires lymphocytes functionally restricted to MHC-compatible thymic determinants. Diabetes 1988;37(Suppl 1):55A, Abstr 218.
Naji A, Silvers WK, Bellgrau D, et al. Prevention of diabetes in rats by bone marrow transplant. Ann Surg1981; 194: 328 – 330.
Rossini AA, Mordes JP, Pelletier AM, et al. Transfusions of whole blood prevent spontaneous diabetes in the BB/W rat. Science1983; 219: 975 – 977.
Scott J, Engelhard VH, Curnow RT, et al. Prevention of diabetes in BB rats. I. Evidence suggesting a requirement for mature T cells in bone marrow inoculum of neonatally injected rats. Diabetes1986; 35: 1034 – 1040.
Mordes JP, Gallina DL, Handler ES, et al. Transfusions enriched for W3/25+ helper/inducer T lymphocytes prevent spontaneous diabetes in the BB/W rat. Diabetologia1987; 30: 22 – 26.
Jacobson JD, Markmann JF, Brayman K, et al. Prevention of recurrent autoimmune diabetes in BB rats by anti-asialo-GMl antibody. Diabetes1988; 37: 838 – 841.
Nakamura N, Greiner DL, Reynolds CW, et al. Cytotoxic effector cells of diabetes-prone and diabetes-resistant BB/Wor rats are different. Diabetes 1988;37(Suppl 1):55A, Abstr 220.
Tochino Y, Kanaya T, Makino S. Studies on spontaneously diabetic non-obese mice. J Japn Diabetes Soc1978; 21: 295.
Makino S, Kunimoto K, Maraoka Y, et al. Breeding of a non-obese, diabetic strain of mouse. Exp Animal1980; 29: 1 – 13.
Makino S, Hayashi Y, Muraoka Y, et al. Establishment of the non-obese diabetic mouse, in Sakamoto N (ed): Current Topics in Clinical and Experimental Aspects of Diabetes Mellitus. Amsterdam: Elsevier Science Publishers, 1985, pp 25 – 32.
Tarui S, Tochino Y, Nonaka K (eds). Insulitis and Type I Diabetes—Lessons from the NOD Mouse. New York: Academic Press, 1986.
Leiter EH, Prochazka M, Coleman DL. The non-obese diabetic (NOD) mouse. Am J Pathol1987; 128: 380 – 383.
Makino S, Kunimoto K, Muraoka Y, et al. Effect of castration on the appearance of diabetes in NOD mice. Exp Anim1980; 30: 137 – 140.
Kataoka S, Satoh J, Fijiya H, et al. Immunologic aspects of the non-obese diabetic mouse. Diabetes1983; 32: 247 – 253.
Wicker LS, Miller BJ, Coker LZ, et al. Genetic control of diabetes and insulitis in the non-obese diabetic (NOD) mouse. J Exp Med1987; 165: 1639 – 1654.
Prochazka M, Leiter EH, Serreze DV, et al. Three recessive loci required for insulin- dependent diabetes in non-obese diabetic mice. Science1987; 237: 286 – 289.
Hattori M, Buse JB, Jackson RA, et al. The NOD mouse: Recessive diabetogenic gene in the major histocompatibility complex. Science1986; 231: 733 – 735.
Makino S, Harada M, Kishimoto Y, et al. Absence of insulitis and overt diabetes in athymic nude mice with NOD genetic background. Jikken Dobutsu1986; 33: 495 – 498.
Ikehara S, Ohtsuki H, Good RA, et al. Prevention of type I diabetes in non-obese diabetic mice by allogeneic bone marrow transplantation. Proc Natl Acad Set USA1985; 82: 7743 – 7747.
Yamada K, Nonake K, Hanafusa T, et al. Preventive and therapeutic effects of large-dose nicotanamide injections on diabetes associated with insulitis. An observation in diabetic (NOD) mice. Diabetes1982; 31: 749 – 753.
Herskowitz R, Jackson RA. Pilot trial of preventive therapy: Progression to overt hyperglycemia by 3/3 “prediabetes” despite oral nicotinamide. Diabetes 1988; 37(Suppl 1):59A, Abstr 233.
Mori Y, Suko M, Okudaira H, et al. Preventive effects of cyclosporin on diabetes in NOD mice. Diabetologia1986; 29: 244 – 247.
Wicker LS, Miller BJ, Mullen Y. Transfer of autoimmune diabetes mellitus with splenocytes from non-obese diabetic (NOD) mice. Diabetes1986; 35: 855 – 860.
Bendelac A, Carnaud C, Boitard C, et al. Syngeneic transfer of autoimmune diabetes from diabetic NOD mice to healthy neonates: Requirement and both L3T4+ and Lyt-2+ T cells. J Exp Med1987; 166: 823 – 832.
Miller BJ, Appel MC, O’Neil JJ, et al. Both the Lyt-2+ and L3T4+ T cell subsets are required for the transfer of diabetes in non-obese diabetic mice. J Immunol1988; 140: 52 – 58.
Serreze DV, Leiter EH, Worthen SM, et al. NOD marrow stem cells adoptively transfer diabetes to resistant (NOD × NON) F1 mice. Diabetes1988; 37: 252 – 255.
Maruyama T, Takei I, Taniyama M, et al. Immunological aspect of non-obese diabetic mice: Immune islet cell killing mechanism and cell-mediated immunity. Diabetologia1984; 27: 121 – 123.
Nagata M, Yokono K, Hayakawa M, et al. Destruction of pancreatic islets by cytotoxic T-lymphocytes in NOD mice. Diabetes 1988;37(Suppl 1):97A, Abstr 387.
Shizuru JA, Taylor-Edwards C, Banks BA, et al. Immunotherapy of the non-obese diabetic mouse: Treatment with an antibody to T-helper lymphocytes. Science1988; 240: 659 – 662.
Charlton B, Mandel TE. Progression from insulitis to beta cell destruction in NOD mouse requires L3T4+ T lymphocytes. Diabetes1988; 37: 1108 – 1112.
Oldstone MBA. Prevention of type I diabetes in non-obese diabetic mice by virus infection. Science1988; 239: 500 – 502.
Kelly VE, Gaulton GN, Hattori M, et al. Anti-interleukin 2 receptor antibody suppresses murine diabetic insulitis and lupus nephritis. J Immunol1988; 140: 59 – 61.
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McEvoy, R.C., Thomas, N.M. (1990). Cell-Mediated Anti-Islet—Cell Immune Response: Clinical Experience and Lessons from Animal Models. In: Ginsberg-Fellner, F., McEvoy, R.C. (eds) Autoimmunity and the Pathogenesis of Diabetes. Endocrinology and Metabolism, vol 4. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-3218-6_8
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