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. Author manuscript; available in PMC: 2024 Dec 1.
Published in final edited form as: Curr Opin Cell Biol. 2023 Nov 11;85:102276. doi: 10.1016/j.ceb.2023.102276

Figure 2: Myeloid migration becomes clearer with zebrafish.

Figure 2:

In the last decade and a half, the neutrophil community has been engaged in unravelling the mechanism and pathological role of reverse migration. A. Calcium alarm signals in neutrophil clusters locally promote attractant synthesis and are dependent on ATP sensing and contact with necrotic tissue. Clustering neutrophils initiate and propagate calcium alarm signals via Cx43 channels Neutrophil swarms and Cx43 restrict wound colonization by opportunistic bacteria. B. CXCL8 and other chemoattractants regulate neutrophil migration to injuries via CXCR1. CXCR2 on the other hand is needed for forward migration. Additionally, several mediators coordinate neutrophil reverse migration such as PGE2. Some other molecules such as ROS-SFK signal in macrophages and cell-cell contact are also vital for proper neutrophil reverse migration. Cxcl12/CXCR4 signal has been identified as a druggable retention signal for neutrophils at tissue damage that can be blocked using AMD3100.