Neutrophils leave the bloodstream and migrate to infection sites by following intermediary chemokine signals (such as IL-8) that are generated by damaged host cells. End-target signals like fMLP or LPS, either released by the pathogen itself or by the body in response to the bacteria, also attract neutrophils. Since the blood cells prefer to pursue end-targets when both signals are present, the authors speculated, correctly, that different pathways controlled the two responses.
The pathways can be distinguished by their kinase-dependence. Migration to intermediary chemoattractants depended on PI3K, which phosphorylated Akt. End-targets induced migration...
The Rockefeller University Press
2002
The Rockefeller University Press
2002
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