Acquired immunological tolerance in aged mice. II. The cellular basis of the loss of tolerance sensitivity.
Aged C57Bl/6 mice (12 and 24 month) become resistant to tolerance induction with deaggregated human IgG (DHGG). The cellular basis for this tolerance resistance was investigated using adoptive transfer systems and challenged with endotoxin and antigen in the form of heat aggregated HGG. DHGG induced antigen specific suppressor cells in the spleens of aged mice although not in young mice and aged normal splenocytes were more sensitive to suppression. Low dose cyclophosphamide treatment to ablate suppressor cells did not curtail tolerance induction in aged animals. These observations coupled with the transient nature of B cell tolerance in aged mice suggest that the tolerance defect of senescence lies in the B cell compartment.
Habicht
G S
GS
D000375:Aging; D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D005260:Female; D006183:H-2 Antigens / Q000032:analysis; D006358:Hot Temperature; D006801:Humans; D007108:Immune Tolerance / Q000187:drug effects; D007111:Immunity, Cellular; D007074:Immunoglobulin G / Q000276:immunology; D008297:Male; D008433:Mathematics; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D012737:Sex Factors; D013045:Species Specificity; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D006183:H-2 Antigens; D007074:Immunoglobulin G; D003520:Cyclophosphamide