TR: What should public health administrators do with this information?
Drs. Yang & Tian: Public health administrators should collect data on health outcomes related to air pollution to identify vulnerable populations and high-risk areas, advocate for stricter air quality regulations, support policies that promote clean energy and allocate resources for community health initiatives focused on education and prevention related to air quality issues.
TR: What can’t this study tell us?
Drs. Yang & Tian: Our current study was an observational study. Given that a meaningful correlation analysis result does not imply a causal association, we can’t confirm the causal link between air pollution and incident SLE. Further studies underlying biological mechanisms linking air pollution exposure to SLE pathogenesis need to be explored.
TR: What would be your next steps in terms of future research?
Drs. Yang & Tian: We plan to conduct similar studies in different populations and areas, such as China. Because China has a relatively high prevalence of SLE and severe air pollution, exploring this association could further strengthen our current evidence from the U.K. Biobank and guide the development of more stringent air quality standards.
SLE: Driven by T Cell Imbalance
In July 2024, groundbreaking new research from labs at Northwestern and the Brigham and Woman’s Hospital was published in Nature.10 This work has also led us closer to understanding the pathogenesis of SLE. B cells and autoantibodies are likely what come to mind for most of us when we think about SLE, but this research points to certain B cell-helping helper T cells as one of the main drivers of the disease. If we can address a main driver of SLE, we may be able to better treat it.
Because basic science may feel far away for many (me included), let me break a few things down before moving on to the interview with the corresponding authors.
SLE is driven by inappropriate interactions between B cells and T cells. Certain types of helper T cells—T follicular helper (TFH) cells and T peripheral helper (TPH) cells—are expanded in patients with SLE. TFH cells help B cells within lymphoid follicles, and TPH help B cells within inflamed peripheral tissues. The investigators explain that “both activated B cells and T cells that help B cells [as above] are inappropriately expanded in people with SLE and correlate with disease activity.”10
The investigators demonstrated that the aryl hydrocarbon receptor (AHR) helps regulate the balance of TFH and TPH cells, and patients with SLE have an imbalance of chemicals (e.g., type I interferon) that suppress the aryl hydrocarbon pathway. When the AHR is suppressed, pathogenic TFH and TPH cells expand. Thus, if suppressing AHR leads to the T cell imbalance characteristic of SLE patients and other autoimmune diseases, perhaps stimulating it may correct the imbalance and reprogram the T cells to better treat SLE.
