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Levels of moral condemnation often vary with outcome severity (e.g., extreme destruction is morally worse than moderate damage), but this is not always true. We investigated whether judgments of purity transgressions are more or less sensitive to variation in dosage than judgments of harm transgressions. In three studies, adults ( N = 426) made moral evaluations of harm and purity transgressions that systematically varied in dosage (frequency or magnitude). Pairs of low-dosage and high-dosage transgressions were presented such that the same sets of modifiers (e.g., "occasionally" vs. "regularly," "small" vs. "large") or amounts (e.g., "millimeter" vs. "centimeter") were reused across moral domains. Statistical interactions between domain and dosage indicated robust distinctions between the perceived wrongness of high-dosage and low-dosage harms, whereas moral evaluations of impure acts were considerably less influenced by dosage. Our findings support the existence of a cognitive distinction between purity-based and harm-based morals and challenge current wisdom regarding relationships between intentions and outcomes in moral judgment.

The mammalian immune system is remarkable in that it can respond to an essentially infinite number of foreign antigens. The ability to mount a long-lasting (adaptive) immune response against foreign antigen requires the participation of cells selected from an enormously diverse population of B and T cells. Because the B and T cell receptors expressed by these cells are generated at random, a significant percentage of B and T cells are invariably directed against self-antigen. Under normal circumstances, autoreactive B and T cells are eliminated, reprogrammed, or inactivated in the primary and secondary lymphoid organs. Despite these checks and balances, a small but significant number of people and animals still develop autoimmune disease. One such autoimmune disease-systemic lupus erythematosus-is characterized by the loss of B- and T-cell tolerance to self-antigens (principally nuclear), culminating in multisystemic inflammation. Multiple genetic defects, drug exposure, infectious agents, and environmental factors can contribute to the pathogenesis of the disease. Loss of B- and T-cell tolerance precipitates activation of plasmacytoid and myeloid dendritic cells; collectively, these cells cooperate to form a complex positive feedback loop, continually stimulated by the persistence of self-antigen. Novel treatment strategies now focus on specific inhibition of various aspects of the feedback loop. These specific inhibitors have the potential to be more effective and lack the side effects associated with generalized immunosuppression.

Veterinary pathologists engaged in basic research use a variety of methods to study disease pathogenesis at the light microscopic and submicroscopic (protein and mRNA) levels. The ribonuclease protection assay is a sensitive and accurate method to measure mRNA expression. The major advantages of the assay are that multiple mRNA species can be measured simultaneously in a single total RNA sample and that the assay has relatively high throughput. The major disadvantage is that the assay requires moderate technical skill.

Leukocyte homing is a complex, multistep process involving the coordinated expression of adhesion molecules and certain chemotactic cytokines, termed chemokines. Although chemokines initially burst into the literature as potent inflammatory mediators, it is now clear that they are involved in a variety of processes including lymphocyte maturation, angiogenesis, and tumor growth. Furthermore, a variety of important pathogens manipulate various chemokine/receptor pathways to infect the host and evade the immune system.

Inbred strains of rats and mice have long been used to study basic mechanisms of human disease. Our knowledge of the rodent and human immune systems has increased in recent years, largely because of the availability of reagents and techniques specific for these species. In contrast, outbred animals, including domestic companion and food animals, have not been used routinely as experimental models for human disease, largely because reagents and assays necessary for basic research in immunology and physiology have not been available. Here, using consensus cytokine nucleic acid sequences, we adapt a previously described reverse transcription-quantitative competitive polymerase chain reaction technique to measure interleukin 2 (IL2), IL4, IL6, IL10, IL12, interferon, gamma tumor necrosis factor alpha, and glyceraldehyde-3-phosphate dehydrogenase mRNA expression in the cow, cat, dog, horse, and pig. We demonstrate that the assay is sensitive, accurate, and reproducible.