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Human Toll-like receptor-dependent induction of interferons in protective immunity to viruses.
Immunol Rev 2007; 220:225-36IR

Abstract

Five of the 10 human Toll-like receptors (TLRs) (TLR3, TLR4, TLR7, TLR8, and TLR9), and four of the 12 mouse TLRs (TLR3, TLR4, TLR7, TLR9) can trigger interferon (IFN)-alpha, IFN-beta, and IFN-lambda, which are critical for antiviral immunity. Moreover, TLR3, TLR7, TLR8, and TLR9 differ from TLR4 in two particularly important ways for antiviral immunity: they can be activated by nucleic acid agonists mimicking compounds produced during the viral cycle, and they are typically present within the cell, along the endocytic pathway, where they sense viral products in the intraluminal space. Investigations in mice have demonstrated that the TLR7/9-IFN and TLR3-IFN pathways are different and critical for protective immunity to various experimental viral infections. Investigations in humans with interleukin-1 receptor-associated kinase-4 (IRAK-4) deficiency (unresponsive to TLR7, TLR8, and TLR9), UNC-93B deficiency (unresponsive to TLR3, TLR7, TLR8, and TLR9), and TLR3 deficiency have recently shed light on the role of these two pathways in antiviral immunity in natural conditions. UNC-93B- and TLR3-deficient patients appear to be specifically prone to herpes simplex virus 1 (HSV-1) encephalitis, although clinical penetrance is incomplete, whereas IRAK-4-deficient patients appear to be normally resistant to most viruses, including HSV-1. These experiments of nature suggest that the TLR7-, TLR8-, and TLR9-dependent induction of IFN-alpha, IFN-beta, and IFN-lambda is largely redundant in human antiviral immunity, whereas the TLR3-dependent induction of IFN-alpha, IFN-beta, and IFN-lambda is critical for primary immunity to HSV-1 in the central nervous system in children but redundant for immunity to most other viral infections.

Authors+Show Affiliations

Laboratory of Human Genetics of Infectious Diseases, Institut National de la Santé et de la Recherche Médicale, Paris, France, EU.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

17979850

Citation

Zhang, Shen-Ying, et al. "Human Toll-like Receptor-dependent Induction of Interferons in Protective Immunity to Viruses." Immunological Reviews, vol. 220, 2007, pp. 225-36.
Zhang SY, Jouanguy E, Sancho-Shimizu V, et al. Human Toll-like receptor-dependent induction of interferons in protective immunity to viruses. Immunol Rev. 2007;220:225-36.
Zhang, S. Y., Jouanguy, E., Sancho-Shimizu, V., von Bernuth, H., Yang, K., Abel, L., ... Casanova, J. L. (2007). Human Toll-like receptor-dependent induction of interferons in protective immunity to viruses. Immunological Reviews, 220, pp. 225-36.
Zhang SY, et al. Human Toll-like Receptor-dependent Induction of Interferons in Protective Immunity to Viruses. Immunol Rev. 2007;220:225-36. PubMed PMID: 17979850.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Human Toll-like receptor-dependent induction of interferons in protective immunity to viruses. AU - Zhang,Shen-Ying, AU - Jouanguy,Emmanuelle, AU - Sancho-Shimizu,Vanessa, AU - von Bernuth,Horst, AU - Yang,Kun, AU - Abel,Laurent, AU - Picard,Capucine, AU - Puel,Anne, AU - Casanova,Jean-Laurent, PY - 2007/11/6/pubmed PY - 2008/1/18/medline PY - 2007/11/6/entrez SP - 225 EP - 36 JF - Immunological reviews JO - Immunol. Rev. VL - 220 N2 - Five of the 10 human Toll-like receptors (TLRs) (TLR3, TLR4, TLR7, TLR8, and TLR9), and four of the 12 mouse TLRs (TLR3, TLR4, TLR7, TLR9) can trigger interferon (IFN)-alpha, IFN-beta, and IFN-lambda, which are critical for antiviral immunity. Moreover, TLR3, TLR7, TLR8, and TLR9 differ from TLR4 in two particularly important ways for antiviral immunity: they can be activated by nucleic acid agonists mimicking compounds produced during the viral cycle, and they are typically present within the cell, along the endocytic pathway, where they sense viral products in the intraluminal space. Investigations in mice have demonstrated that the TLR7/9-IFN and TLR3-IFN pathways are different and critical for protective immunity to various experimental viral infections. Investigations in humans with interleukin-1 receptor-associated kinase-4 (IRAK-4) deficiency (unresponsive to TLR7, TLR8, and TLR9), UNC-93B deficiency (unresponsive to TLR3, TLR7, TLR8, and TLR9), and TLR3 deficiency have recently shed light on the role of these two pathways in antiviral immunity in natural conditions. UNC-93B- and TLR3-deficient patients appear to be specifically prone to herpes simplex virus 1 (HSV-1) encephalitis, although clinical penetrance is incomplete, whereas IRAK-4-deficient patients appear to be normally resistant to most viruses, including HSV-1. These experiments of nature suggest that the TLR7-, TLR8-, and TLR9-dependent induction of IFN-alpha, IFN-beta, and IFN-lambda is largely redundant in human antiviral immunity, whereas the TLR3-dependent induction of IFN-alpha, IFN-beta, and IFN-lambda is critical for primary immunity to HSV-1 in the central nervous system in children but redundant for immunity to most other viral infections. SN - 0105-2896 UR - https://www.unboundmedicine.com/medline/citation/17979850/Human_Toll_like_receptor_dependent_induction_of_interferons_in_protective_immunity_to_viruses_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0105-2896&date=2007&volume=220&spage=225 DB - PRIME DP - Unbound Medicine ER -