Infection with Schistosoma mansoni prevents insulin dependent diabetes mellitus in non‐obese diabetic mice

• Published in: Parasite immunology Vol. 21; no. 4; pp. 169 - 176
• Main Authors: COOKE, ANNE, TONKS, PAUL, JONES, FRANCIS M., O'SHEA, HELEN, HUTCHINGS, PATRICIA, FULFORD, ANTHONY J.C., DUNNE
• Format: Journal Article
• Language: English
• Published: Oxford, U.K. and Cambridge, USA Blackwell Science Ltd 01.04.1999
• Subjects: AIDS/HIV; Animals; Antigens, Helminth - immunology; Antigens, Helminth - therapeutic use; Autoantibodies; Diabetes Mellitus, Type 1 - immunology; Diabetes Mellitus, Type 1 - parasitology; Diabetes Mellitus, Type 1 - prevention & control; Eosinophilic Granuloma - immunology; eosinophils; Immunoglobulin Class Switching; Insulin - immunology; insulin dependent diabetes mellitus; Mice; Mice, Inbred NOD; non‐obese diabetic mice; Ovum - immunology; Schistosoma mansoni; Schistosomiasis mansoni - immunology; Th1 Cells - immunology; Th2 Cells - immunology
• ISSN: 0141-9838; 1365-3024
• DOI: 10.1046/j.1365-3024.1999.00213.x

The spontaneous development of insulin dependent diabetes mellitus in non‐obese diabetic (NOD) mice has been shown to be mediated by a Th1 response against beta cell antigens. It is known that in murine models of Schistosoma mansoni infection, egg production is associated with a switch from a Th1 to Th2 response. This subsequent dominance of a Th2 response in S.mansoni infected mice has been shown to influence the response to other infectious agents or antigens. We therefore determined whether infection with S.mansoni could influence the spontaneous incidence of insulin dependent diabetes mellitus (IDDM) in NOD mice. Infection with this helminth significantly reduced the spontaneous incidence of IDDM. IDDM was also prevented by injecting parasite eggs alone. Because until relatively recently humans might expect to succumb to a variety of infectious agents, the current freedom from infection might permit the expression of a genetic predisposition to autoimmune pathology and be responsible for the increased incidence of IDDM.