Objective. The Gullah population of the Sea Islands of South Carolina is a unique group of African Americans who, due to geographic and cultural factors, remained isolated with minimal genetic admixture until the 1950s. Because of the unique homogeneous nature of the Gullah, we sought to define the genetic and environmental factors contributing to systemic lupus erythematosus (SLE) in this population.Methods. Using data from our ongoing cohort study of lupus in the Gullah population, which we established in 2003, disease characteristics and serologic profiles were summarized for 184 patients with SLE, 144 unaffected first-degree relatives, and 144 matched unrelated, unaffected control subjects. These findings were compared with those in 2 other large cohorts of African Americans with SLE.Results. In the Gullah cohort, we observed a high prevalence of SLE multiplex families (26.6%), malar rash (56.0%), discoid rash (34.2%), photosensitivity (60.9%), and oral/nasal ulcerations (43.5%), but a lower prevalence of hematologic and pleuropericardial disease than has been reported in other African American cohorts. Overall renal and central nervous system involvement, number of American College of Rheumatology disease criteria met, and SLE Damage Index scores were similar to those reported in other cohorts. Of interest, male and female first-degree relatives and male and female control subjects in this cohort had similar rates of antinuclear antibody positivity, whereas lupusspecific antibodies were more prevalent in the women than in the men.Conclusion. These data indicate that the severity of lupus in the Gullah population is similar to that in other African American populations, whereas skin disease and familial disease prevalence are increased in the Gullah. These findings suggest that there is an increased genetic influence on overall disease in this cohort compared with that in other African American cohorts, which confirms the unique nature of this cohort.African Americans have a 3-fold increased prevalence of systemic lupus erythematosus (SLE), develop SLE at an earlier age, and have increased SLE-related morbidity and mortality compared with Caucasians (1-5). Multiple factors, including genetic, environmental, and socioeconomic factors, likely underlie the ethnic disparity in SLE. Socioeconomic and genetic differences alone, however, cannot explain the significant increase in prevalence of SLE in the last 20 years or the gradient of SLE between West Africa, where it is a rare disease (6-9), and the United States, where it is prevalent. These latter findings suggest that environmental factors play a key role in inducing lupus and influencing disease severity.

This study evaluates the effectiveness of a culturally relevant intervention, delivered over 12 months on knowledge of colorectal cancer and participation in fecal occult blood testing. An experimental, repeated measures design was used. Free fecal occult blood testing was offered to the participants. Fifteen senior centers were randomly selected and assigned to the Cultural and Self-Empowerment Group, the Modified Cultural Group, or the Traditional Group. Their mean age was 73.83 years, and their average educational level was 8.8 years. The majority was African American, female, and reported annual incomes < or = 10,000 dollars. Data were collected at baseline, at 6 months, and at 12 months. Participants in the Cultural and Self-Empowerment Group had a significantly greater increase in their knowledge of colorectal cancer over time. Group membership and knowledge of colorectal cancer were significant predictors of participation in colorectal cancer screening. Participants in the Cultural and Self-Empowerment Group and those with greater knowledge of colorectal cancer were more likely to participate in fecal occult blood testing at the end of the 12-month period. Similar strategies may be implemented in community settings and health care agencies to inform elders about colorectal cancer.

Type I interferons (IFN) causes inflammatory responses to pathogens, and can be elevated in autoimmune diseases such as systemic lupus erythematosus (SLE). We previously reported unexpected associations of increased numbers of B lymphocytes expressing the DNA-binding protein ARID3a with both IFN alpha (IFNα) expression and increased disease activity in SLE. Here, we determined that IFNα producing low density neutrophils (LDNs) and plasmacytoid dendritic cells (pDCs) from SLE patients exhibit strong associations between ARID3a protein expression and IFNα production. Moreover, SLE disease activity indices correlate most strongly with percentages of ARID3a+ LDNs, but were also associated, less significantly, with IFNα expression in LDNs and pDCs. Hierarchical clustering and transcriptome analyses of LDNs and pDCs revealed SLE patients with low ARID3a expression cluster with healthy controls and identified gene profiles associated with increased proportions of ARID3a- and IFNα-expressing cells of each type. These data identify ARID3a as a potential transcription regulator of IFNα-related inflammatory responses and other pathways important for SLE disease activity.

Systemic lupus erythematosus (SLE) is a devastating and heterogeneous autoimmune disease that affects multiple organs, and for which the underlying causes are unknown. The majority of SLE patients produce autoantibodies, have increased levels of type-I inflammatory cytokines, and can develop glomerulonephritis. Recent studies indicate an unexpected but strong association between increased disease activity in SLE patients and the expression of the DNA-binding protein ARID3a (A + T rich interaction domain protein 3a) in a number of peripheral blood cell types. ARID3a expression was first associated with autoantibody production in B cells; however, more recent findings also indicate associations with expression of the inflammatory cytokine interferon alpha in SLE plasmacytoid dendritic cells and low-density neutrophils. In addition, ARID3a is expressed in hematopoietic stem cells and some adult kidney progenitor cells. SLE cells expressing enhanced ARID3a levels show differential gene expression patterns compared with homologous healthy control cells, identifying new pathways potentially regulated by ARID3a. The associations of ARID3a expression with increased disease severity in SLE, suggest that it, or its downstream targets, may provide new therapeutic targets for SLE.