Agonistic anti-DCIR antibody inhibits ITAM-mediated inflammatory signaling and promotes immune resolution

Chen L
May 23, 2024
JCI Insight
https://pubmed.ncbi.nlm.nih.gov/38781017

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/38781017

Research summary

This study explores the therapeutic potential of an agonistic antibody targeting dendritic cell immunoreceptor (DCIR) in modulating immune responses. The research investigates how engaging DCIR with a specific antibody can inhibit ITAM-mediated inflammatory signaling pathways, thereby promoting the resolution of inflammation.

Key outcome of the study

Treatment with the agonistic anti-DCIR antibody effectively inhibited ITAM-mediated signaling, leading to reduced pro-inflammatory cytokine production and enhanced immune resolution. These findings suggest that targeting DCIR could be a viable strategy for treating inflammatory and autoimmune diseases.

Mouse model

The study utilized a genetically engineered mouse model developed in collaboration with genOway. This model features a humanized version of the DCIR gene (CLEC4A), replacing the murine counterpart, allowing for the assessment of human-specific antibody interactions and their immunomodulatory effects in vivo.

TARGET:
Clec4a
DCIR, LLIR, DDB27

Keywords

Inflammatory diseases, Autoimmunity, Immunotherapy, Monoclonal antibody treatment, Immune regulation

Technical specifications

Humanized gene replacement, Transgenic mouse model, Immune receptor targeting, In vivo antibody efficacy, Human-mouse chimeric model

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