Abstract:
:The initiating events in drug-induced autoimmunity are poorly understood and difficult to study. We examined the role of macrophages and T-cells in the Brown Norway rat model of D-penicillamine-induced autoimmunity. When activated, macrophages can act as both antigen presenting cells, initiating immune responses, and as phagocytic cells mediating systemic tissue damage. We found that B7(+) macrophages are the major antigen-presenting cell type infiltrating the spleen and caecum early in the response to Dpenicillamine. As well, the increase in splenic B7(+) macrophages correlates with the incidence of autoimmune disease. Treatments that increase the incidence of disease accentuate the increase in splenic B7(+) macrophages, and treatments that prevent disease also prevent the increase in B7(+) macrophages. In vivo depletion of macrophages appeared to decrease, but not totally prevent, autoimmune disease. The role of T-cells in D-penicillamine-induced autoimmunity was also examined using the T-cell inhibitor tacrolimus. Short-term treatment with tacrolimus not only prevented disease onset but also reversed ongoing disease and prevented disease relapse upon re-challenge with D-penicillamine. The results of this study indicate that both macrophages and T-cells could be important immune cell types involved in D-penicillamine-induced autoimmunity. Furthermore, the effects of tacrolimus in this model suggest that short-term tacrolimus treatment may be an effective way to prevent or treat IDRs in high-risk patients.
journal_name
J Immunotoxicoljournal_title
Journal of immunotoxicologyauthors
Masson MJ,Teranishi M,Shenton JM,Uetrecht JPdoi
10.1080/15476910490496258subject
Has Abstractpub_date
2004-04-01 00:00:00pages
79-93issue
2eissn
1547-691Xissn
1547-6901pii
714035393journal_volume
1pub_type
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