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Abstract
The lipoxin A4 receptor (ALX) is an important target of LxA4 in synovial tissues of patients with inflammatory arthritis. Previously this receptor was known as the FPRL-1 on PMN and shown to interact with acute phase proteins and a variety of peptides. ALX signalling can either activate or deactivate PMN functions. In this study, we found that both LxA4 and a chemotactic lipid leishmania chemotactic factor released by the parasite leishmania increased infectivity of this pathogen in an ALX dependent fashion. This functional characterization of ALX could lead to development of novel, therapeutic targets for treatment inflammatory diseases.
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