B cells and iBALT in TB immunity & pathogenesis – Research

Figure 1

Figure 1

Putative mechanism of iBALT formation in TB: 1) Mtb infection leads to chronic inflammation; 2) Persistent inflammation drives the release of pro-inflammatory cytokines, including TNF family members, IL-6, IL-17, and IL-22, which promote immune cell recruitment and tissue remodeling; 3) Inflammatory cytokines activate lung stromal cells, prompting them to function as lymphoid tissue organizer (LTo) cells by upregulating LTβR and VCAM expression on their surface. This transformation is critical for TLS formation; 4) Activated B cells express LTα/β, which binds to LTβR on stromal cells, initiating their function as lymphoid tissue inducer (LTi) cells and promoting lymphoid-like structures; 5) LTα/β-LTβR interactions drive the expression of CXCL13, CCL19, and CCL21, which recruit B cells, T cells, and dendritic cells (DCs) to the inflamed site, creating a localized immune niche; 6) Production of CCL19, CCL21, CXCL12, and CXCL13, ensures the persistence of inducible bronchus-associated lymphoid tissue (iBALT) and reinforces local immune response; 7) A positive feedback loop amplifies the secretion of these critical chemokines and cytokines, stabilizing the iBALT structure and supporting its function as a persistent immune hub; 8) iBALT structures may develop germinal center-like formations, where T and B cells interact, leading to the generation of high-affinity antibodies against Mtb antigens, enhancing immune defense against infection. The image was created using