Two murine monoclonal antibodies specific for IFN-γ, ADI-1, and ADI-23 (both IgG1 kappa), were generated in BALB/c mice. The ADI-1 exhibited a higher avidity for canine rIFN-γ than for nIFN-γ and human rIFN-γ. In contrast, the ADI-23 showed equal avidity for the three IFN-γ preparations. The anti-canine IFN-γ mAb did not bind to mouse and rat rIFN-γ. The ADI-1, and ADI-23 mAb were also tested for binding to human rTFN-α and, contrary to our expectations, it was found that ADI-23 showed significant binding to human rTFN-α and rIFN-γ, in contrast to ADI-1. Both anti-canine IFN-γ mAb stained 48-h PHA-induced dog lymphoblasts. A two-site mAb ELISA was developed, which was linear in the range of 7-500 ng of canine rIFN-γ, which indicated that the two mAb detected non-overlapping epitopes on the canine rIFN-γ molecule. We studied the effect of ADI-1 on the prolongation of canine renal allografts. Recipients of kidney allografts, that were treated with ADI-1 by continuous arterial infusion, were prolonged to 22 and 25 days, compared to 9 and 13 days for animals given the IgG1 isotype control.
|Original language||English (US)|
|Number of pages||7|
|State||Published - Mar 1994|
ASJC Scopus subject areas
- Immunology and Allergy