Systematic Discovery of TLR Signaling Components Delineates Viral-Sensing Circuits
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Deciphering the signaling networks that underlie normal and disease processes remains a major challenge. Here, we report the discovery of signaling components involved in the Toll-like receptor (TLR) response of immune dendritic cells (DCs), including a previously unkown pathway shared across mammalian antiviral responses. By combining transcriptional profiling, genetic and small-molecule perturbations, and phosphoproteomics, we uncover 35 signaling regulators, including 16 known regulators, involved in TLR signaling. In particular, we find that Polo-like kinases (Plk) 2 and 4 are essential components of antiviral pathways in vitro and in vivo and activate a signaling branch involving a dozen proteins, among which is Tnfaip2, a gene associated with autoimmune diseases but whose role was unknown. Our study illustrates the power of combining systematic measurements and perturbations to elucidate complex signaling circuits and discover potential therapeutic targets.
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Mouse bone marrow-derived dendritic cells are mostly post-mitotic, and LPS synchronizes them and triggers broad regulatory changes.
“DCs are mostly post-mitotic, and LPS synchronizes them (27) and causes dramatic regulatory changes from the expression of thousands of transcripts (22, 24, 25) to protein phosphorylation (26).”
From Dynamic profiling of the protein life cycle in response to pathogens (2015) · cites this paper as [26]
Only a handful of proteins (e.g., Tnfaip2) show peaked, transient protein expression within the time scale; all have very high basal degradation rates, which typically do not increase further.
“Only a handful of proteins (e.g., Tnfaip2 (26, 35, 36)), show peaked, transient protein expression within our time scale; all have very high basal degradation rates, which typically do not increase further.”
From Dynamic profiling of the protein life cycle in response to pathogens (2015) · cites this paper as [26]
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Self-citation
- Authors
- Chevrier, N., Mertins, P., Artyomov, M. N., Shalek, A. K., Iannacone, M., Ciaccio, M. F., Gat-Viks, I., Tonti, E., DeGrace, M. M., Clauser, K. R., Garber, M., Eisenhaure, T. M., Yosef, N., Robinson, J., Sutton, A., Andersen, M. S., Root, D. E., von Andrian, U., Jones, R. B., Park, H., Carr, S. A., Regev, A., Amit, I., & Hacohen, N.
- Affiliations
- Broad Institute (US)
- Harvard University (US)
- University of Chicago (US)
- Corresponding author
- Amit, Ido
- Hacohen, Nir
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2011-11
- Volume
- 147
- Issue
- 4
- Pages
- 853-867
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3809888
- OpenAlex
- W2136910340
- Cited by
- 179
- References
- 66
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 6 · 2023: 8 · 2022: 14 · 2021: 5 · 2020: 8 · 2019: 10 · 2018: 12 · 2017: 15 · 2016: 13 · 2015: 22 · 2014: 23 · 2013: 22 · 2012: 16
- FWCI
- 8.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 624 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc)
- MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (submittedVersion)
- Archivio Istituzionale della Ricerca - Università Vita-Salute San Raffaele (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (5rm1hg006193-10, 1dp2od002230-01)
- National Human Genome Research Institute (RM1‐HG006193, P50HG006193)
- National Cancer Institute (DP1CA174427)
- National Institute of General Medical Sciences (P50GM081892)
- National Institute of Allergy and Infectious Diseases (U54AI057159)
- National Center for Research Resources (S10RR026688)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- Toll-like receptor signaling, antiviral innate immunity, dendritic cells, PLK2, PLK4, TNFAIP2, phosphoproteomics, small molecule perturbations, gene expression profiling, signaling circuits, therapeutic target
- MeSH terms
- Animals, Dendritic Cells, Female, Humans, Interferons, Mice, Inbred C57BL, Viruses, Signal Transduction, Protein Serine-Threonine Kinases, Interferon Regulatory Factor-3, Toll-Like Receptors, Mice
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