AI Article Synopsis
- SIRPα is an immune inhibitory receptor that myeloid cells use to prevent phagocytosis and activation of immune cells, and its potential as a treatment for autoimmune inflammation is being explored.
- Elevated SIRPA levels have been linked to severe cases of inflammatory diseases like rheumatoid arthritis and ulcerative colitis.
- An anti-SIRPα agonistic antibody has shown promise in reducing inflammation by decreasing neutrophil and monocyte infiltration in preclinical models of these conditions.
Article Abstract
Signal regulatory protein (SIRPα) is an immune inhibitory receptor expressed by myeloid cells to inhibit immune cell phagocytosis, migration, and activation. Despite the progress of SIRPα and CD47 antagonist antibodies to promote anti-cancer immunity, it is not yet known whether SIRPα receptor agonism could restrain excessive autoimmune tissue inflammation. Here, we report that neutrophil- and monocyte-associated genes including SIRPA are increased in inflamed tissue biopsies from patients with rheumatoid arthritis and inflammatory bowel diseases, and elevated SIRPA is associated with treatment-refractory ulcerative colitis. We next identify an agonistic anti-SIRPα antibody that exhibits potent anti-inflammatory effects in reducing neutrophil and monocyte chemotaxis and tissue infiltration. In preclinical models of arthritis and colitis, anti-SIRPα agonistic antibody ameliorates autoimmune joint inflammation and inflammatory colitis by reducing neutrophils and monocytes in tissues. Our work provides a proof of concept for SIRPα receptor agonism for suppressing excessive innate immune activation and chronic inflammatory disease treatment.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10439247 | PMC |
| http://dx.doi.org/10.1016/j.xcrm.2023.101130 | DOI Listing |
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