- We’re highlighting a recent article using Fab-ZAP rat (Cat. #IT-55).
- Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic joint inflammation and damage, and current treatments don’t work equally well for everyone.
- Researchers identified a specific population of inflammatory immune cells in RA joints that express high levels of uPAR (PLAUR). These uPAR-high cells also produce inflammatory molecules such as IL-1β and CXCL8, making them attractive therapeutic targets.
- The team developed anti-uPAR antibody-drug conjugates (ADCs) to selectively eliminate these harmful cells. The authors then used Fab-ZAP rat (IT-55) to test the internalization capacity of anti-mouse uPAR antibodies. Saporin (PR-01) and Fab-IgG-SAP (IT-67) were used as control.
- ADCs carrying BCL-2 inhibitor payloads, selectively killed activated inflammatory monocytes and macrophages while sparing normal, resting immune cells. Treatment also reduced the release of the inflammatory cytokine CXCL8.
- Because mouse immune cells express less uPAR, the researchers used an MMAF payload to demonstrate proof of concept in a mouse model. The anti-uPAR–MMAF conjugate reduced inflammatory uPAR-high macrophages by about 39% compared to the control treatment.
- Overall, the study shows that targeted ADCs can selectively eliminate disease-causing immune cells, suggesting a promising new therapeutic strategy for RA and other autoimmune or inflammatory diseases.
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