Phenotypic consequences of an interleukin-4Rα/GP Ibα receptor on transgenic mouse platelets.

The IL-4Rα/GP Ibα coding sequence was placed immediately 3′ to a megakaryocytic-specific promoter, and the resultant DNA construct was injected into mice pronuclei to generate transgenic animals. Two different transgenic founders, Tg³³ and Tg⁵¹, were bred into the murine model of the Bernard-Soulier syndrome. After 2 generations of screening (described in “Materials and methods”), 2 colonies of mice were generated lacking their endogenous murine GP Ibα alleles but still expressing the IL-4Rα/GP Ibα transgene. (A) Shown is the fluorescence profile of platelets obtained from Tg³³ and Tg⁵¹ transgenic lines screened with an ^FITCanti–IL-4R mAb. Control platelets are shown from nontransgenic animals and GP Ibα–deficient animals. (B) Forward light scattering profiles from mouse platelets display the entire population of platelet sizes. The platelet population was identified using an antimouse CD41 (integrin α_IIb chain) monoclonal antibody. A total of 50 000 recorded events are presented for each genotype. A progressive shift to the left illustrates decreasing particle (platelet) size. The quantitation of this analysis from multiple animals is presented in Table 1.