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TLR5: beyond the recognition of flagellin

Cellular & Molecular Immunology volume 14, pages 1017–1019 (2017)Cite this article

The innate immune system plays an essential role in the host defense against infections by initially sensing and recognizing diverse microbial pathogens and directing adaptive immune responses to their infections. How does the innate immune system sense and recognize pathogens? The identification of pattern recognition receptors (PRRs) during the past decades has brought us into a new era to explore this fundamental question. PRRs are an array of germline-encoded multifunctional proteins that do not recognize specific pathogens but rather recognize conserved molecular patterns associated with various classes of pathogens, leading to pathogen-associated molecular patterns (PAMPs).1 Among the PRRs, there is a family of Toll-like receptors (TLRs), including TLR5, that recognize a wide variety of PAMPs and elicit innate immune responses. TLR5 is known to specifically sense and recognize flagellin, the major structural protein of bacterial flagella.2 It is conceivable that the immune system is equipped with TLR5 for the detection of flagellin in different cells, tissues and organs. However, the fundamental functions of TLR5 beyond the recognition of flagellin are only beginning to be appreciated. Studies on TLR5 in recent years have revealed different scenarios after the recognition of flagellin by TLR5 in the respiratory tract, gastrointestinal tract, liver or even in the dorsal root ganglion neurons.

TLR5 is expressed constitutively in epithelial cells and immune cells, such as monocytes and immature DCs. TLR5 is preferentially expressed on the apical side of respiratory epithelia in both mice and humans.3, 4 Thus, TLR5 can induce early signaling dedicated to protective innate immune responses against respiratory infection. For example, airway epithelium TLR5 can sense Pseudomonas aeruginosa and initiate an early host inflammatory reaction to clear the invading pathogen.5 Moreover, the early clearance of P. aeruginosa from the airways depends on flagellin-TLR5-MyD88-dependent signaling in respiratory epithelial cells.6

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Acknowledgements

This work was supported by grants from the National Natural Science Foundation of China (Nos. 31300717 and 81461130019) and the Grants of Deutsche Forschungsgemeinschaft (TRR60 and GK1949).

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  1. Mucosal Immunity Research Group, State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, Hubei, China

    Jingyi Yang & Huimin Yan

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Correspondence to Huimin Yan.

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Yang, J., Yan, H. TLR5: beyond the recognition of flagellin. Cell Mol Immunol 14, 1017–1019 (2017). https://doi.org/10.1038/cmi.2017.122

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