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Biotech / Medical : XOMA. Bull or Bear? -- Ignore unavailable to you. Want to Upgrade?

To: aknahow who wrote (8583)	2/2/1999 12:34:00 AM
From: Bluegreen	Respond to of 17367

George, the old locomotion through your vessel walls. And you thought it was a brand new dance now! Now what does this have to do with the Hemo. trauma trial? We are still doing a Hemo. trauma trial, aren't we? One might think Pulmonary vasculature structure? And dang it all, where does all that collagen come from during our inflammatory escapades? Leukocyte transendothelial migration is an essential process in inflammation and the immune response. The mechanisms involved in leukocyte adhesion to the endothelium, forming the first step in leukocyte extravasation, have been fairly well documented. However, subsequent steps, which include de-adhesion, coupled with locomotion, remain largely unknown. As part of our efforts to study leukocyte transendothelial migration, we previously established a monoclonal antibody (mAb) that sequentially up-regulates and down-regulates beta2 integrin-dependent adhesion of human neutrophils, as well as transendothelial migration in vitro. The molecule recognized by this mAb is a glycosyl phosphatidyl inositol, (GPI)-anchored glycoprotein. This protein may prove to be a new member of the family of integrin-associated, GPI-anchored proteins, which includes urokinase-type plasminogen activator receptor (uPAR), lipopolysaccharide (LPS)/LPS binding protein (LBP) receptor (CD14), and Fcgamma receptor IIIB (CD16b); all of which are regulators of integrin function. The mechanisms involved in beta2 integrin regulation by this new GPI-anchored glycoprotein are discussed.