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Triggering receptor expressed on myeloid cells-1 (TREM-1): a new player in antiviral immunity?
The triggering receptor expressed on myeloid cells (TREM) family of protein receptors is rapidly emerging as a critical regulator of a diverse array of cellular functions, including amplification of inflammation. Although the ligand(s) for TREM have not yet been fully identified, circumstantial evid...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4244588/ https://www.ncbi.nlm.nih.gov/pubmed/25505454 http://dx.doi.org/10.3389/fmicb.2014.00627 |
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author | Roe, Kelsey Gibot, Sébastien Verma, Saguna |
author_facet | Roe, Kelsey Gibot, Sébastien Verma, Saguna |
author_sort | Roe, Kelsey |
collection | PubMed |
description | The triggering receptor expressed on myeloid cells (TREM) family of protein receptors is rapidly emerging as a critical regulator of a diverse array of cellular functions, including amplification of inflammation. Although the ligand(s) for TREM have not yet been fully identified, circumstantial evidence indicates that danger- and pathogen-associated molecular patterns (DAMPs and PAMPs) can induce cytokine production via TREM-1 activation. The discovery of novel functions of TREM, such as regulation of T-cell proliferation and activation of antigen-presenting cells, suggests a larger role of TREM proteins in modulation of host immune responses to microbial pathogens, such as bacteria and fungi. However, the significance of TREM signaling in innate immunity to virus infections and the underlying mechanisms remain largely unclear. The nature and intensity of innate immune responses, specifically production of type I interferon and inflammatory cytokines is a crucial event in dictating recovery vs. adverse outcomes from virus infections. In this review, we highlight the emerging roles of TREM-1, including synergy with classical pathogen recognition receptors. Based on the literature using viral PAMPs and other infectious disease models, we further discuss how TREM-1 may influence host-virus interactions and viral pathogenesis. A deeper conceptual understanding of the mechanisms associated with pathogenic and/or protective functions of TREM-1 in antiviral immunity is essential to develop novel therapeutic strategies for the control of virus infection by modulating innate immune signaling. |
format | Online Article Text |
id | pubmed-4244588 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-42445882014-12-10 Triggering receptor expressed on myeloid cells-1 (TREM-1): a new player in antiviral immunity? Roe, Kelsey Gibot, Sébastien Verma, Saguna Front Microbiol Microbiology The triggering receptor expressed on myeloid cells (TREM) family of protein receptors is rapidly emerging as a critical regulator of a diverse array of cellular functions, including amplification of inflammation. Although the ligand(s) for TREM have not yet been fully identified, circumstantial evidence indicates that danger- and pathogen-associated molecular patterns (DAMPs and PAMPs) can induce cytokine production via TREM-1 activation. The discovery of novel functions of TREM, such as regulation of T-cell proliferation and activation of antigen-presenting cells, suggests a larger role of TREM proteins in modulation of host immune responses to microbial pathogens, such as bacteria and fungi. However, the significance of TREM signaling in innate immunity to virus infections and the underlying mechanisms remain largely unclear. The nature and intensity of innate immune responses, specifically production of type I interferon and inflammatory cytokines is a crucial event in dictating recovery vs. adverse outcomes from virus infections. In this review, we highlight the emerging roles of TREM-1, including synergy with classical pathogen recognition receptors. Based on the literature using viral PAMPs and other infectious disease models, we further discuss how TREM-1 may influence host-virus interactions and viral pathogenesis. A deeper conceptual understanding of the mechanisms associated with pathogenic and/or protective functions of TREM-1 in antiviral immunity is essential to develop novel therapeutic strategies for the control of virus infection by modulating innate immune signaling. Frontiers Media S.A. 2014-11-26 /pmc/articles/PMC4244588/ /pubmed/25505454 http://dx.doi.org/10.3389/fmicb.2014.00627 Text en Copyright © 2014 Roe, Gibot and Verma. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology Roe, Kelsey Gibot, Sébastien Verma, Saguna Triggering receptor expressed on myeloid cells-1 (TREM-1): a new player in antiviral immunity? |
title | Triggering receptor expressed on myeloid cells-1 (TREM-1): a new player in antiviral immunity? |
title_full | Triggering receptor expressed on myeloid cells-1 (TREM-1): a new player in antiviral immunity? |
title_fullStr | Triggering receptor expressed on myeloid cells-1 (TREM-1): a new player in antiviral immunity? |
title_full_unstemmed | Triggering receptor expressed on myeloid cells-1 (TREM-1): a new player in antiviral immunity? |
title_short | Triggering receptor expressed on myeloid cells-1 (TREM-1): a new player in antiviral immunity? |
title_sort | triggering receptor expressed on myeloid cells-1 (trem-1): a new player in antiviral immunity? |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4244588/ https://www.ncbi.nlm.nih.gov/pubmed/25505454 http://dx.doi.org/10.3389/fmicb.2014.00627 |
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