Inflammation and Tissue Injury II. Local Release of Lysosomal Enzymes During Mixed Bacterial Infection in the Skin of Rabbits.

Freedman, Harvey L.; Taichman, Norton S.; Keystone, Jay S.

doi:10.3181/00379727-125-32315

Cited by 10 publications

(1 citation statement)

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“…Consistent with this hypothesis is the observation that macrophages isolated from NOD mice and lpr lupus-prone mice secrete large amounts of IL-12 (Liu and Beller 2002) and that exogenous IL-12 treatment reverses clodronate-induced inhibition of diabetes in the NOD mouse (Jun et al, 1999). Macrophages may also play a role in the pathogenesis of autoimmune disease by mediating tissue damage through the release of lytic enzymes (Freedman et al, 1967). Therefore, macrophages could be involved in initiating the autoimmune response and/or mediating the pathogenic tissue damage associated with drug-induced autoimmunity.…”

Section: Introductionmentioning

confidence: 55%

Investigation of the Involvement of Macrophages and T Cells in D-Penicillamine-Induced Autoimmunity in the Brown Norway Rat

Masson

Teranishi²,

Shenton

et al. 2004

Journal of Immunotoxicology

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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.

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Section: Introductionmentioning

confidence: 55%