Dynamics of factor VIII interactions determine its immunologic fate in hemophilia A Export

@article{citeulike:3054969, abstract = {Procoagulant factor VIII (FVIII) is either produced endogenously under physiologic conditions, or administered exogenously as a therapeutic hemostatic drug in patients with hemophilia A. In the circulation, FVIII interacts with a multitude of glycoproteins, and may be used for coagulation at the sites of bleeding, eliminated by scavenger cells, or processed by the immune system, either as a self-constituent or as a foreign antigen. The fate of FVIII is dictated by the immune status of the individual, the location of FVIII in the body at a given time point, and the inflammatory microenvironment. It also depends on the local concentration of FVIII and of each interacting partner, and on the affinity of the respective interactions. FVIII, by virtue of its promiscuity, thus constitutes the core of a dynamic network that links the coagulation cascade, cells of the immune system, and, presumably, the inflammatory compartment. We describe the different interactions that FVIII is prone to establish during its life cycle, with a special focus on players of the innate and adaptive immune response. Lessons can be learned from understanding the dynamics of FVIII interactions--lessons that should pave the way to the conception of long-lasting hemostatic drugs devoid of iatrogenic immunogenicity. 10.1182/blood-2008-02-124941}, author = {Lacroix-Desmazes, Sebastien and Navarrete, Ana-Maria and Andre, Sebastien and Bayry, Jagadeesh and Kaveri, Srinivas V. and Dasgupta, Suryasarathi}, citeulike-article-id = {3054969}, citeulike-linkout-0 = {http://dx.doi.org/10.1182/blood-2008-02-124941}, citeulike-linkout-1 = {http://bloodjournal.hematologylibrary.org/cgi/content/abstract/112/2/240}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/18469198}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=18469198}, day = {15}, doi = {10.1182/blood-2008-02-124941}, journal = {Blood}, keywords = {hemophilia}, month = {July}, number = {2}, pages = {240--249}, posted-at = {2008-07-29 01:25:59}, priority = {2}, title = {Dynamics of factor VIII interactions determine its immunologic fate in hemophilia A}, url = {http://dx.doi.org/10.1182/blood-2008-02-124941}, volume = {112}, year = {2008} }

TY - JOUR ID - citeulike:3054969 L3 - citeulike-article-id:3054969 N2 - Procoagulant factor VIII (FVIII) is either produced endogenously under physiologic conditions, or administered exogenously as a therapeutic hemostatic drug in patients with hemophilia A. In the circulation, FVIII interacts with a multitude of glycoproteins, and may be used for coagulation at the sites of bleeding, eliminated by scavenger cells, or processed by the immune system, either as a self-constituent or as a foreign antigen. The fate of FVIII is dictated by the immune status of the individual, the location of FVIII in the body at a given time point, and the inflammatory microenvironment. It also depends on the local concentration of FVIII and of each interacting partner, and on the affinity of the respective interactions. FVIII, by virtue of its promiscuity, thus constitutes the core of a dynamic network that links the coagulation cascade, cells of the immune system, and, presumably, the inflammatory compartment. We describe the different interactions that FVIII is prone to establish during its life cycle, with a special focus on players of the innate and adaptive immune response. Lessons can be learned from understanding the dynamics of FVIII interactions--lessons that should pave the way to the conception of long-lasting hemostatic drugs devoid of iatrogenic immunogenicity. 10.1182/blood-2008-02-124941 IS - 2 JF - Blood EP - 249 TI - Dynamics of factor VIII interactions determine its immunologic fate in hemophilia A VL - 112 SP - 240 KW - hemophilia AU - Lacroix-Desmazes, Sebastien AU - Navarrete, Ana-Maria AU - Andre, Sebastien AU - Bayry, Jagadeesh AU - Kaveri, Srinivas AU - Dasgupta, Suryasarathi PY - 2008/07/15/ UR - http://dx.doi.org/10.1182/blood-2008-02-124941 ER -