Historical data suggested that a soluble protein, since identified as annexin-A1 (Anx-A1) was released from macrophages following glucocorticoid stimulation and could modulate eicosanoid production and other functions of these cells. Here, we review some recent findings using a line of Anx-A1 -/- mice to explore the impact of Anx-A1 gene deletion on macrophage biology. The absence of Anx-A1 selectively alters phagocytic capacity of rodent resident peritoneal macrophages apparently through changes in surface adhesion molecule expression. Anx-A1 is also apparently important in the tonic down-regulation of other macrophage functions such as COX-2 induction, PGE 2 release and the production of reactive oxygen species.
|Number of pages
|Prostaglandins Leukotrienes and Essential Fatty Acids
|2 SPEC. ISS.
|Published - Feb 2005
Bibliographical noteFunding Information:
RJF is a Principal Fellow of the Wellcome Trust, MP is a Senior Research Fellow of the Arthritis Research Campaign and SY holds a Ph.D. studentship from the Nuffield Foundation, UK. The authors wish to thank the Wellcome Trust (Grant no. 051887/97) and the Oliver Bird Fund (Project RHE/00057/G) for supporting this study.