Pattern recognition receptor pathways activated by Bacillus Calmette–Guérin

The entry refers to a set of innate immune sensing pathways rather than a single molecule or receptor: BCG components are detected by multiple pattern-recognition receptors including Toll-like receptors—particularly TLR2 and TLR4 on the surface and TLR9 in endosomes—C-type lectins such as DC-SIGN, complement receptors CR3 and CR4, and NOD-like receptors such as NOD2 recognizing muramyl dipeptide. Their coordinated activation in monocytes, macrophages, neutrophils, and dendritic cells initiates reactive oxygen species and NF-κB signaling, inducing a first wave of cytokines and chemokines, which is then amplified via autocrine/paracrine signaling through cytokine receptors (IL-6R, IL-1R, TNFR) and JAK-dependent pathways. BCG also induces trained immunity, a durable enhancement of innate responses mediated by NOD2-dependent epigenetic reprogramming (e.g., H3K4me3) and increased PRR expression, conferring nonspecific protection against unrelated pathogens and contributing to its clinical effects in infection and cancer settings.

Other names

Pattern-recognition receptors activated by BCGPRR pathways engaged by BCGInnate immune sensing pathways of BCGBCG-activated PRRs

Engagement of Toll-like receptors (TLR2, TLR4, TLR9) by BCG lipoglycans/lipids and CpG DNA to trigger innate activation and cytokine production. Recognition by C-type lectins (e.g., DC-SIGN), complement receptors (CR3, CR4), and NOD-like receptors (notably NOD2 binding muramyl dipeptide), leading to downstream inflammatory signaling and trained immunity. Induction of NF-κB signaling and ROS, followed by autocrine/paracrine amplification via cytokine receptors (IL-6R, IL-1R, TNFR) and JAK-mediated pathways.