Prevention of Type I Diabetes in NOD Mice by Adjuvant Immunotherapy
Autor: | Hui-Yu Qin, Bhagirath Singh, Michel Sadelain, Jana Lauzon |
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Rok vydání: | 1990 |
Předmět: |
medicine.medical_specialty
Cellular immunity T-Lymphocytes Endocrinology Diabetes and Metabolism medicine.medical_treatment Freund's Adjuvant Mice Inbred Strains Nod medicine.disease_cause Autoimmunity Mice Bone Marrow Internal medicine Diabetes mellitus Internal Medicine Animals Medicine NOD mice B-Lymphocytes business.industry Immunotherapy medicine.disease Immunity Innate Disease Models Animal Diabetes Mellitus Type 1 Endocrinology medicine.anatomical_structure Freund's adjuvant Hyperglycemia Immunology Bone marrow Lymphocyte Culture Test Mixed business Spleen |
Zdroj: | Diabetes. 39:583-589 |
ISSN: | 1939-327X 0012-1797 |
DOI: | 10.2337/diab.39.5.583 |
Popis: | The nonobese diabetic (NOD) mouse is an excellent model of insulin-dependent (type I) human diabetes mellitus. We report that a single injection of complete Freund's adjuvant (CFA) given at an early age (5 wk) prevented the appearance of diabetes and greatly increased the life span of NOD mice without additional therapy. No treated mouse developed hyperglycemia by the age of 12 mo (n = 13), whereas all untreated mice died of diabetes before 8 mo of age (n = 38). All CFA-treated mice were alive and healthy at 12 mo of age. Some CFA-treated NOD mice that were monitored for long-term survival are still alive with no sign of disease at 18 mo of age (n = 5). Administration of CFA resulted in decreased in vitro splenic lymphocyte proliferative responses to alloantigen and mitogen. Cell-mixing experiments indicated that antigen-nonspecific inhibitory cells were elicited in the spleen and increased in the bone marrow. These regulatory cells were Thy-1− ; and nonadherent to nylon wool, as has been described for natural suppressor (NS) cells. These data lend support to a relationship between the boosting of endogenous NS activity and the establishment of tolerance to self in the context of autoimmunity. Our results suggest that early nonspecific immunotherapy of genetically predisposed individuals could prevent the development of autoimmune diabetes. |
Databáze: | OpenAIRE |
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