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Biotech / Medical : HuMAB companies -- Ignore unavailable to you. Want to Upgrade?

To: nigel bates who wrote (127)	2/27/2001 4:05:52 PM
From: scaram(o)uche	Respond to of 1022

biospace.com Now for an interesting science tidbit. A recent report in Science helped define the mechanism by which high dose intravenous immunoglobulin globulin (IVIGg), the most common form of human antibodies, help autoimmune diseases such as ITP (idiopathic thrombocytopenic purpura)-a condition in which the body makes antibodies against its own platelets (part of the clotting mechanism). Patients with this condition are at high risk for serious bleeding as their platelet level drops. One of the emergency treatments is the administration of huge quantities of IVIGg (in the range of 20-30 grams daily for a few days-a very expensive treatment). I just had a patient-a 30 year-old woman about to deliver who was discovered to have this condition -and with a dangerously low platelet count. The auto-antibodies coating the platelets just set them up to be recognized by cells with receptors to the tail of the antibody. This tail is known as the Fc portion (the tail is common to the whole class of antibodies-it is the head portion or the V region which gives an antibody its specificity). Once the Fc portion becomes bound to the receptors (Fc?R 3) the attached platelet is engulfed and destroyed. Recently another receptor that binds the Fc has been characterized (Fc?R 2b) and acts to inhibit the engulfment and destruction. It turns out that giving large doses of IVIGg causes the Fc?R 2b receptor to be up regulated on the surface of the destructive cells thus mitigating the destructive process. Now that we have our hands on the likely mechanism of our empiric therapy we have the opportunity to design more specific and much cheaper therapies. For example, the Science article demonstrated that using the isolated Fc fragment worked as well as the whole antibody (and much cheaper to produce). The researchers also showed that using a monoclonal antibody designed to block the Fc?R 2b receptor was also effective. This article represents a clear case of the immediate impact of basic science on our ability to treat patients.