Autoimmune diabetes in NOD mouse is L3T4 T-lymphocyte dependent.
Diabetes
; 36(4): 535-8, 1987 Apr.
Article
en En
| MEDLINE
| ID: mdl-3102301
ABSTRACT
Cultured BALB/c islets fail to function when transplanted into diabetic nonobese diabetic (NOD) mice; such grafted tissue is rapidly destroyed by disease recurrence. The cellular requirements for this graft damage are unclear. This study was designed to investigate the role of the L3T4+ T-lymphocyte subset in disease recurrence in the NOD mouse. L3T4+ T-lymphocytes were depleted by the in vivo administration of the L3T4-specific monoclonal antibody GK1.5. This treatment reduced the level of L3T4+ T-lymphocytes from an initial 43% of the peripheral blood lymphocytes to less than 4%. L3T4 levels remained at this low level for approximately 2 wk after withdrawal of GK1.5 treatment, after which the L3T4 levels slowly began to increase in the periphery. Grafting of cultured BALB/c islet tissue into GK1.5-treated diabetic NOD mice resulted in a rapid return to normoglycemia that persisted for 2-4 wk. The gradual return to the hyperglycemic condition roughly correlated with the reappearance of L3T4+ T-lymphocytes in the peripheral circulation. From these findings we conclude that the disease process in the NOD mouse is L3T4 T-lymphocyte dependent.
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Banco de datos:
MEDLINE
Asunto principal:
Enfermedades Autoinmunes
/
Linfocitos T
/
Diabetes Mellitus Experimental
/
Ratones Endogámicos
/
Antígenos de Superficie
Límite:
Animals
Idioma:
En
Año:
1987
Tipo del documento:
Article