Neonatal Regulatory B Cells Impair B Cell Activation and Enhance Inflammatory T Cell Responses During RSV Infection 9082

Abstract Description Respiratory syncytial virus (RSV) is the 2nd leading cause of infant deaths worldwide. The complexity of the infant immune response to RSV has significantly hindered the development of an effective pediatric vaccine. A recently identified subset of B cells, termed neonatal regulatory B cells (nBregs), has been linked to the severity of RSV disease, though their precise role in disease progression is not well understood. In this study, we utilized a murine model of RSV infection to explore how nBregs influence the immune response. nBregs were isolated from 5-7 d old BALB/cJ mice and adoptively transferred into adult mice 2 h before RSV infection. Lung tissue was collected 6 d post-infection to assess B cell activation and CD4+ T cell profiles by flow cytometry. The results showed that the transfer of nBregs into adult mice prior to RSV infection led to a reduction in the expression of key B cell activation markers (CD40, BAFF-R, and TACI). Unexpectedly, this transfer also resulted in an increase in Th1 and Th17 cells, indicating an enhanced inflammatory response. These findings suggest that nBregs impair B cell activation, reducing the capacity for effective antibody production, while simultaneously promoting inflammation and increasing lung damage. Future experiments will focus on the long-term effects of nBregs, including their impact on RSV-specific IgA production and memory responses during subsequent virus encounters. Funding Sources NIH R01 AI090059 Topic Categories Viral Immunology (VIR)