Fictions, Fault, and Forgiveness: Jury Nullification in a New Context

Recently, critics of the Anglo-American jury system have complained that juries in criminal trials have been ignoring the law, in favor of defendants who claim that they lack criminal responsibility because they are afflicted by the various victimization syndromes now popularized in the mass media. In this Article, Professors Dorfman and Iijima counter this characterization of the runaway jury and argue that juries are not ignoring the law, but rather, are exercising a primary power of the jury, to nullify the application of the law when such application to a particular defendant is unjust. The Authors trace the development of the jury nullification power from its beginnings in the late seventeenth century to the present. The Authors then counter the standard arguments against jury nullification. Finally, the Authors propose an explicit jury nullification instruction and accommodating adjustments to other trial procedures that would solve the deficiencies of the current manner in which juries exercise their nullification power

Fictions, Fault, and Forgiveness: Jury Nullification in a New Context

Recently, critics of the Anglo-American jury system have complained that juries in criminal trials have been ignoring the law, in favor of defendants who claim that they lack criminal responsibility because they are afflicted by the various victimization syndromes now popularized in the mass media. In this Article, Professors Dorfman and Iijima counter this characterization of the runaway jury and argue that juries are not ignoring the law, but rather, are exercising a primary power of the jury, to nullify the application of the law when such application to a particular defendant is unjust. The Authors trace the development of the jury nullification power from its beginnings in the late seventeenth century to the present. The Authors then counter the standard arguments against jury nullification. Finally, the Authors propose an explicit jury nullification instruction and accommodating adjustments to other trial procedures that would solve the deficiencies of the current manner in which juries exercise their nullification power

CD8+ T Cells Induce Fatal Brainstem Pathology during Cerebral Malaria via Luminal Antigen-Specific Engagement of Brain Vasculature

Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection that results in thousands of deaths each year, mostly in African children. The in vivo mechanisms underlying this fatal condition are not entirely understood. Using the animal model of experimental cerebral malaria (ECM), we sought mechanistic insights into the pathogenesis of CM. Fatal disease was associated with alterations in tight junction proteins, vascular breakdown in the meninges / parenchyma, edema, and ultimately neuronal cell death in the brainstem, which is consistent with cerebral herniation as a cause of death. At the peak of ECM, we revealed using intravital two-photon microscopy that myelomonocytic cells and parasite-specific CD8+ T cells associated primarily with the luminal surface of CNS blood vessels. Myelomonocytic cells participated in the removal of parasitized red blood cells (pRBCs) from cerebral blood vessels, but were not required for the disease. Interestingly, the majority of disease-inducing parasite-specific CD8+ T cells interacted with the lumen of brain vascular endothelial cells (ECs), where they were observed surveying, dividing, and arresting in a cognate peptide-MHC I dependent manner. These activities were critically dependent on IFN-γ, which was responsible for activating cerebrovascular ECs to upregulate adhesion and antigen-presenting molecules. Importantly, parasite-specific CD8+ T cell interactions with cerebral vessels were impaired in chimeric mice rendered unable to present EC antigens on MHC I, and these mice were in turn resistant to fatal brainstem pathology. Moreover, anti-adhesion molecule (LFA-1 / VLA-4) therapy prevented fatal disease by rapidly displacing luminal CD8+ T cells from cerebrovascular ECs without affecting extravascular T cells. These in vivo data demonstrate that parasite-specific CD8+ T cell-induced fatal vascular breakdown and subsequent neuronal death during ECM is associated with luminal, antigen-dependent interactions with cerebrovasculature