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HVEM signalling at mucosal barriers provides host defence against pathogenic bacteria.

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Title: HVEM signalling at mucosal barriers provides host defence against pathogenic bacteria.
Authors: Shui, Jr-Wen, Larange, Alexandre, Kim, Gisen, Vela, Jose Luis, Zahner, Sonja, Cheroutre, Hilde, Kronenberg, Mitchell
Source: Nature. 8/9/2012, Vol. 488 Issue 7410, p222-225. 4p.
Subjects: Herpesviruses, Pathogenic bacteria, Immune response, Colitis, Escherichia coli diseases, Immunoglobulins, Laboratory mice, Patients
Abstract: The herpes virus entry mediator (HVEM), a member of the tumour-necrosis factor receptor family, has diverse functions, augmenting or inhibiting the immune response. HVEM was recently reported as a colitis risk locus in patients, and in a mouse model of colitis we demonstrated an anti-inflammatory role for HVEM, but its mechanism of action in the mucosal immune system was unknown. Here we report an important role for epithelial HVEM in innate mucosal defence against pathogenic bacteria. HVEM enhances immune responses by NF-?B-inducing kinase-dependent Stat3 activation, which promotes the epithelial expression of genes important for immunity. During intestinal Citrobacter rodentium infection, a mouse model for enteropathogenic Escherichia coli infection, Hvem?/? mice showed decreased Stat3 activation, impaired responses in the colon, higher bacterial burdens and increased mortality. We identified the immunoglobulin superfamily molecule CD160 (refs 7 and 8), expressed predominantly by innate-like intraepithelial lymphocytes, as the ligand engaging epithelial HVEM for host protection. Likewise, in pulmonary Streptococcus pneumoniae infection, HVEM is also required for host defence. Our results pinpoint HVEM as an important orchestrator of mucosal immunity, integrating signals from innate lymphocytes to induce optimal epithelial Stat3 activation, which indicates that targeting HVEM with agonists could improve host defence. [ABSTRACT FROM AUTHOR]
Copyright of Nature is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: HVEM signalling at mucosal barriers provides host defence against pathogenic bacteria.
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  Data: <searchLink fieldCode="AR" term="%22Shui%2C+Jr-Wen%22">Shui, Jr-Wen</searchLink><br /><searchLink fieldCode="AR" term="%22Larange%2C+Alexandre%22">Larange, Alexandre</searchLink><br /><searchLink fieldCode="AR" term="%22Kim%2C+Gisen%22">Kim, Gisen</searchLink><br /><searchLink fieldCode="AR" term="%22Vela%2C+Jose+Luis%22">Vela, Jose Luis</searchLink><br /><searchLink fieldCode="AR" term="%22Zahner%2C+Sonja%22">Zahner, Sonja</searchLink><br /><searchLink fieldCode="AR" term="%22Cheroutre%2C+Hilde%22">Cheroutre, Hilde</searchLink><br /><searchLink fieldCode="AR" term="%22Kronenberg%2C+Mitchell%22">Kronenberg, Mitchell</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Nature%22">Nature</searchLink>. 8/9/2012, Vol. 488 Issue 7410, p222-225. 4p.
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  Data: <searchLink fieldCode="DE" term="%22Herpesviruses%22">Herpesviruses</searchLink><br /><searchLink fieldCode="DE" term="%22Pathogenic+bacteria%22">Pathogenic bacteria</searchLink><br /><searchLink fieldCode="DE" term="%22Immune+response%22">Immune response</searchLink><br /><searchLink fieldCode="DE" term="%22Colitis%22">Colitis</searchLink><br /><searchLink fieldCode="DE" term="%22Escherichia+coli+diseases%22">Escherichia coli diseases</searchLink><br /><searchLink fieldCode="DE" term="%22Immunoglobulins%22">Immunoglobulins</searchLink><br /><searchLink fieldCode="DE" term="%22Laboratory+mice%22">Laboratory mice</searchLink><br /><searchLink fieldCode="DE" term="%22Patients%22">Patients</searchLink>
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  Data: The herpes virus entry mediator (HVEM), a member of the tumour-necrosis factor receptor family, has diverse functions, augmenting or inhibiting the immune response. HVEM was recently reported as a colitis risk locus in patients, and in a mouse model of colitis we demonstrated an anti-inflammatory role for HVEM, but its mechanism of action in the mucosal immune system was unknown. Here we report an important role for epithelial HVEM in innate mucosal defence against pathogenic bacteria. HVEM enhances immune responses by NF-?B-inducing kinase-dependent Stat3 activation, which promotes the epithelial expression of genes important for immunity. During intestinal Citrobacter rodentium infection, a mouse model for enteropathogenic Escherichia coli infection, Hvem?/? mice showed decreased Stat3 activation, impaired responses in the colon, higher bacterial burdens and increased mortality. We identified the immunoglobulin superfamily molecule CD160 (refs 7 and 8), expressed predominantly by innate-like intraepithelial lymphocytes, as the ligand engaging epithelial HVEM for host protection. Likewise, in pulmonary Streptococcus pneumoniae infection, HVEM is also required for host defence. Our results pinpoint HVEM as an important orchestrator of mucosal immunity, integrating signals from innate lymphocytes to induce optimal epithelial Stat3 activation, which indicates that targeting HVEM with agonists could improve host defence. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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