Figure 3.

The sketch illustrates the intricate interaction between beneficial microbiota and the host immune system through Toll-like receptors (TLRs) on dendritic cells. The binding of microbial components to TLRs triggers a cascade of immune responses. Pattern recognition receptors (PRRs), such as endocytic PRRs, recognize microbial molecules, leading to the activation of dendritic cells. This activation involves upregulation of co-stimulatory molecules like CD80/86, which interact with CD28 on naive T cells through the major histocompatibility complex II (MHC-II) and T cell receptor (TCR) interactions. The dendritic cells release interleukin-12 (IL-12), a key cytokine that promotes the differentiation of naive T cells into T helper cells. Depending on the cytokine environment, T cells differentiate into various subtypes, including Th1 cells, which produce pro-inflammatory cytokines like interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α), driving cell-mediated immunity. Alternatively, T cells may differentiate into other subtypes producing anti-inflammatory cytokines such as IL-4, IL-5, IL-10, and IL-13, which modulate immune responses. This mechanism underlines the potential for modulating gut microbiota to influence systemic immunity and the potential therapeutic implications for inflammatory diseases. Created with BioRender.com