Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525

Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
free
free
  English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |   
lüll Annexin-A1: a pivotal regulator of the innate and adaptive immune systems D'Acquisto F; Perretti M; Flower RJBr J Pharmacol 2008[Sep]; 155 (2): 152-69The glucocorticoids are the most potent anti-inflammatory drugs that we possess and are effective in a wide variety of diseases. Although their action is known to involve receptor mediated changes in gene transcription, the exact mechanisms whereby these bring about their pleiotropic action in inflammation are yet to be totally understood. Whilst many different genes are regulated by the glucocorticoids, we have identified one particular protein-annexin A1 (Anx-A1)-whose synthesis and release is strongly regulated by the glucocorticoids in many cell types. The biology of this protein, as revealed by studies using transgenic animals, peptide mimetics and neutralizing antibodies, speaks to its role as a key modulator of both of the innate and adaptive immune systems. The mechanism whereby this protein exerts its effects is likely to be through the FPR receptor family-a hitherto rather enigmatic family of G protein coupled receptors, which are increasingly implicated in the regulation of many inflammatory processes. Here we review some of the key findings that have led up to the elucidation of this key pathway in inflammatory resolution.|Animals[MESH]|Annexin A1/metabolism/*physiology[MESH]|Anti-Inflammatory Agents/*pharmacology[MESH]|Glucocorticoids/*pharmacology[MESH]|Humans[MESH]|Immune System/drug effects[MESH]|Immunity, Innate/*drug effects/immunology[MESH]|Inflammation/*immunology[MESH] |