CCL3, also referred to as macrophage inflammatory protein 1-alpha (MIP-1α) or Scya3, is a chemokine that plays a pivotal role in immune regulation and inflammatory processes. It is a key mediator of chemotaxis, directing the migration of immune cells – particularly natural killer (NK) cells, T lymphocytes, and myeloid cells – to sites of inflammation or infection. In addition to its role in cellular trafficking, CCL3 is essential for modulating intercellular communication within the immune system and shaping the inflammatory microenvironment.

As such, the ability to monitor and understand CCL3 expression in vivo is fundamental for advancing research in immunology, infection biology, and the development of targeted therapies.

The CCL3-EASER (ErAse, SEnd, Receive) mouse is a genetically engineered knock-in model designed to provide unprecedented in vivo resolution of CCL3 expression and signaling dynamics. This innovative model integrates three key components into the endogenous Ccl3 locus:

• Ccl3-Venus: a fluorescent CCL3 fusion protein that is secreted and can be tracked upon uptake by recipient cells.
• tdTomato: a cytoplasmic fluorescent reporter that indicates Ccl3 transcriptional activity.
• DTR: the diphtheria toxin receptor that enables inducible and selective ablation of CCL3-expressing cells upon binding to the diphtheria toxin.

These elements are separated by P2A self-cleaving peptides, ensuring the independent expression of each protein while preserving regulation by the native Ccl3 promoter.