This investigation evaluated the effectiveness of a priming intervention to decrease the latency to mand for a five-year-old boy diagnosed with autism spectrum disorder. Parent participation in clinical applied behavior analytic intervention was increased by providing the family members with a home-and community-based priming technique to increase the efficacy of clinical treatment. Using a multiple-baseline design across settings, mand response latency was analyzed as a function of the verbal behavior priming intervention employed by two different caregivers. Results of the study indicate that the caregiver-implemented priming intervention was successful in reducing the child's latency to vocalize a request, allowing for more efficient use of instructional time.

Discoid lupus erythematosus (DLE) is a severely disfiguring and difficult to treat autoimmune skin disease for which no new therapies have been FDA-approved in over 60 years. One potential therapeutic target is cutaneous B cells. Though rare in healthy skin, B cells are prevalent in DLE lesions, comprising 10-20% of the robust lymphocytic infiltrate. However, the phenotype and function of this expanded B cell population have not been evaluated in detail and it is unknown whether cutaneous B cells play a role in DLE pathogenesis. We analyzed T cells (CD3), B cells (CD20), and plasma cells (CD138) by immunohistochemistry in skin biopsies from seventeen patients with a clinical and pathologic diagnosis of discoid lupus. Consistent with known literature, T cells predominated the infiltrate (180.3 cells/hpf, range 88-299). However, the number of B cells was not insignificant and comprised an average of 21% of the total lymphocytic infiltrate (39.3 cells/hpf, range 4-147). In contrast, very few plasma cells were noted in the biopsies (4.7 cells/hpf). The majority of the T and B cells analyzed were associated with one another in large perivascular and periadnexal clusters. Interestingly, the larger the total lymphocytic infiltrate, the greater the percentage of that infiltrate was comprised of B cells (p¼0.0185). This correlation with increased inflammation suggests that cutaneous B cells may be playing more than a bystander role in DLE pathogenesis. In support of this hypothesis, analysis of this B cell infiltrate by immunofluorescence microscopy revealed a greater number of class-switched memory B cells (IgG+) than naïve B cells (IgD+). This constitutes the first report of cutaneous memory B cells in DLE lesions. The potential role of these memory B cells in discoid lupus pathogenesis is unknown and warrants further investigation.