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Biotech / Medical : Biotransplant(BTRN) -- Ignore unavailable to you. Want to Upgrade?

To: scaram(o)uche who wrote (558)	5/16/2000 4:51:00 PM
From: biowa	Read Replies (1) \| Respond to of 1475

Rick, Boy, is new SI slow on dial-up. Suffer with the rest of us. ATT@home has been promising that I'll be hooked up in "two weeks" since November; maybe they should make some of their employees come "2work" instead of being "@home." biowa

To: scaram(o)uche who wrote (558)	5/17/2000 10:43:00 AM
From: LLCF	Read Replies (1) \| Respond to of 1475

< Boy, is new SI slow on dial-up.> Not only that, but my treasure trove of bookmarks created in old SI are worthless... hundreds of manhours down the drain. DAK

To: scaram(o)uche who wrote (558)	6/5/2000 9:13:00 AM
From: scaram(o)uche	Respond to of 1475

don't know if I missed this or if it's just late getting into the database. More consistent with data from MEDI than with previous UCL observations, IMO...... Transplantation 2000 Apr 15;69(7):1420-8 The experimental (in vitro) and clinical (in vivo) immunosuppressive effects of a rat IgG2b anti-human CD2 mAb, LO-CD2a/BTI-322. Nizet Y, Chentoufi AA, de la Parra B, Lewalle P, Rouas R, Cornet A, Besse T, Mourad M, Malaise J, Squifflet JP, Bazin H, Latinne D Experimental Immunology Unit, School of Medicine, University of Louvain, Brussels, Belgium. [Medline record in process] BACKGROUND: CD2 is a cell surface glycoprotein expressed on most human T cells and natural killer (NK) cells, working as a cell adhesion and costimulatory molecule. The aim of this paper is to analyze the mechanism of action of a rat IgG2b anti-human CD2 monoclonal antibody (mAb) (LO-CD2a/BTI-322 mAb), which is a potent immunosuppressive agent and inducer of cell death. In vivo, this mAb is able to prevent or treat kidney allograft rejection. METHODS: The mechanisms by which the LO-CD2a/BTI-322 mAb is able to induce inhibition of cell activation and cell death were analyzed by mixed lymphocyte reactions and by flow cytometry. After in vivo treatment, levels of circulating mAb were measured by ELISA as well as anti-rat immunization and cytokine release. RESULTS: We show that the inhibition of cell activation induced by LO-CD2a/BTI-322 mAb after allogeneic or OKT3 stimulation is due to an Fcgamma receptor-dependent CD2 down-modulation and to T-cell depletion through an antibody-dependent cell-mediated cytotoxicity mechanism mediated by NK cells or activated monocytes. Peripheral T- and NK-cell depletion was observed after in vivo treatment with LO-CD2a/BTI322. Cytokine release (TNFalpha) was correlated with some side effects, but only after the first injection, and the effects were never severe or life threatening. CONCLUSION: The correlation between the in vitro and in vivo data suggests that T-cell depletion, especially of activated cells, and inhibition of cell activation after CD2 down-modulation are the main mechanisms of action of the LO-CD2a/BTI-322 mAb.