Flagellin & Toll-like receptor 5 (TLR-5)

Flagellin stimulates Toll-like receptor 5 (TLR-5) or evades Toll-like receptor 5 (TLR-5) by lack of recognition. There are silent flagellins that are weak TLR-5 agonists despite being recognized by TLR-5.
Clasen et al. 2023 Science Immunology 8(79): https://doi.org/10.1126/sciimmunol.abq7001

It has been reported that flagellin serves to activate phosphatidylinositol-3-kinase (PI3K)/AKT signaling pathway in the gut epithelium via a Toll-like receptor 5 (TLR-5)-dependent mechanism
Hayashi et al. 2001 Nature 410: 1099-103
Song et al. 2017 Sci Rep. 7: 40878

The rapid activation of the PI3K pathway by TLR5 can limit the MAPK signaling pathway, thereby limiting the expression of pro-inflammatory genes and inhibiting inflammation
Song et al. 2017 Sci Rep. 7: 40878

Some TLRs respond to their ligands when the integrity of the intestinal epithelium is compromised, as in the interaction of bacterial flagellin with TLR5 expressed basolaterally in IEC
Rhee et al. 2005 Proc Natl Acad Sci USA 102: 13610-13615

Toll-like receptor 5 (TLR-5) is important because it helps the body recognize flagellin. When TLR-5 detects flagellin, it starts a chain reaction inside the cell. This reaction leads to the creation of Interferon beta (IFN-beta) and other similar proteins, using a specific pathway that involves Myeloid Differentiation Primary Response 88 (MYD88). Once Interferon beta (IFN-beta) is produced, it interacts with the interferon receptor (IFNAR). This interaction is essential for the immune system to effectively switch to producing specific antibodies, like anti-flagellin IgA and IgG2c, in B cells.
Kang et al. 2020b Mol Cells 43(3): 251-263

see also:
Gut microbiota & Metabolic Syndrome (MetS)
Toll-like receptor 5 (TLR-5) / MYD88 / NFKB signaling pathway