The intersection of systemic lupus erythematosus with social and occupational environments among black adults: A qualitative study.

Background: Black people have disproportionately high morbidity and mortality due to systemic lupus erythematosus (SLE). Features of social and occupational environments can protect against poor health outcomes.

Objective: We aimed to characterize how SLE intersects with interpersonal relationships and employment among Black adults to inform tailored care approaches and public policies that could alleviate racial inequities in SLE.

A qualitative study on opportunities to improve research engagement and inclusion of Black adults with systemic lupus erythematosus.

In response to racial inequities in systemic lupus erythematosus (SLE), we aimed to identify practical recommendations for increasing engagement and inclusion of Black adults in SLE research. We used a qualitative, interpretive description approach and recruited 30 Black adults diagnosed with SLE in Michigan to participate in semi-structured interviews. Theme development focused on factors influenced research perceptions and research did not meet participant needs and expectations.

Recommendations for Improving Systemic Lupus Erythematosus Care From Black Adults: A Qualitative Study.

Importance: Racial inequities in incidence, morbidity, and mortality are a defining feature of systemic lupus erythematosus (SLE). Health care systems are integral to addressing these inequities. However, qualitative evidence that highlights Black SLE care experiences is limited.

Endothelial ACKR1 is induced by neutrophil contact and down-regulated by secretion in extracellular vesicles.

Atypical chemokine receptor-1 (ACKR1), previously known as the Duffy antigen receptor for chemokines, is a widely conserved cell surface protein that is expressed on erythrocytes and the endothelium of post-capillary venules. In addition to being the receptor for the parasite causing malaria, ACKR1 has been postulated to regulate innate immunity by displaying and trafficking chemokines. Intriguingly, a common mutation in its promoter leads to loss of the erythrocyte protein but leaves endothelial expression unaffected.