Summary. Immune responses to the factor IX protein pose problems for hemophilia B patients who develop antibodies against factor IX and for potential future treatment with gene therapy. To better define the response to human factor IX, we analyzed T-cell responses to human factor IX in factor IX knockout mice on BALB/c and C57BL/6 (B6) backgrounds, both strains having CD4þ T cells that proliferate in response to human factor IX. Surprisingly, wild-type mice have similar factor IX-recognizing CD4þ T cells. We defined a dominant CD4þ epitope for each strain (CVETGVKITVVAGEH for BALB/c and LLELDEPLVLNSYVTPIC for B6) that was recognized by both factor IX knockout and wild-type mice. While human factor IX did not cross-react with the mouse homologs of these epitopes, immunization with peptides from murine factor IX stimulated proliferation in factor IX knockout mice and wild-type mice, demonstrating a failure to delete murine factor IX-specific T cells in normal mice.

Promote radiation oncology in various capacities; American College of Radiology. Organizing refresher courses in radiation oncology in RSNA annual meeting; Radiological Society of North America (RSNA). Establishing appropriateness criteria for radiotherapy for bone metastases; American College of Radiology. S.G. Soltys: Consultant; Inovio Pharmaceuticals.