Replication of donor lymphocytes in recipients is not essential for the passive transfer of allergic encephalomyelitis.
Gliotoxin is a fungal metabolite belonging to the class of epipolythiodioxopiperazines which possesses both immunomodulating and anti-phagocytic activities. We have examined the effect of gliotoxin on passively induced allergic encephalomyelitis and report here that pulse treating activated experimental allergic encephalomyelitis (EAE) effector lymphocytes with gliotoxin inhibits, in a dose-dependent manner, their ability to transfer disease. Cells treated with 300 ng/ml are unable to replicate in vitro in response to concanavalin A stimulation, nor did they produce interleukin-2 (IL-2) following stimulation. Furthermore this concentration of gliotoxin also causes complete fragmentation of genomic DNA in treated cells, yet these cells are still capable of transferring clinical EAE. These data suggest that replication of donor lymphocytes in the recipient is not essential for the development of EAE.
Willenborg
D O
DO
Neurosciences Research Unit, Royal Canberra Hospital, Australia.
Eichner
R D
RD
Waring
P
P
Müllbacher
A
A
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002490:Central Nervous System / Q000473:pathology; D004249:DNA Damage; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000473:pathology; D005260:Female; D005912:Gliotoxin / Q000494:pharmacology; D007116:Immunization, Passive; D007376:Interleukin-2 / Q000096:biosynthesis; D017710:Lymphocyte Transfusion; D008214:Lymphocytes / Q000166:cytology / Q000276:immunology; D051381:Rats; D011917:Rats, Inbred Lew
D007376:Interleukin-2; D005912:Gliotoxin