ResearchIn-Press PreviewImmunology
Open Access | 10.1172/jci.insight.176064
1Cambridge Research Center, AbbVie, Cambridge, United States of America
2Abbvie Bioresearch Center, Worcester, United States of America
3AbbVie Bioresearch Center, Worcester, United States of America
4Cambridge Research Center, Abbvie, Cambridge, United States of America
5Transformational and Translational Immunology Discovery, AbbVie Bay Area, South San Francisco, United States of America
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1Cambridge Research Center, AbbVie, Cambridge, United States of America
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3AbbVie Bioresearch Center, Worcester, United States of America
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5Transformational and Translational Immunology Discovery, AbbVie Bay Area, South San Francisco, United States of America
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5Transformational and Translational Immunology Discovery, AbbVie Bay Area, South San Francisco, United States of America
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Published May 23, 2024 - More info
Dendritic cell inhibitory receptor (DCIR) is a C-type lectin receptor selectively expressed on myeloid cells, including monocytes, macrophage, dendritic cells, and neutrophils. Its role in immune regulation has been implicated in murine models and human genome-wide association studies (GWAS), suggesting defective DCIR function associates with increased susceptibility to autoimmune diseases such as rheumatoid arthritis, lupus and Sjogren’s syndrome. However, little is known about the mechanisms underlying DCIR activation to dampen inflammation. Here, we developed anti-DCIR agonistic antibodies that promote phosphorylation on DCIR’s immune receptor tyrosine-based inhibitory motifs (ITIM) and recruitment of SH2 containing protein tyrosine phosphatase-2 (SHP2) for reducing inflammation. We also explored the inflammation resolution by depleting DCIR+ cells with antibodies. Utilizing a human DCIR knock-in mouse model, we validated the anti-inflammatory properties of the agonistic anti-DCIR antibody in experimental peritonitis and colitis. These findings provide critical evidence for targeting DCIR to develop transformative therapies for inflammatory diseases.