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Negative regulation of TLR signaling in myeloid cells--implications for autoimmune diseases
Hamerman JA, Pottle J, Ni M, He Y, Zhang ZY, Buckner JH.. Immunological reviews, 2016-01-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Toll-like receptors (TLR) are transmembrane pattern recognition receptors that recognize microbial ligands and signal for production of inflammatory cytokines and type I interferon in macrophages and dendritic cells (DC). Whereas TLR-induced inflammatory mediators are required for pathogen clearance, many are toxic to the host and can cause pathological inflammation when over-produced. This is demonstrated by the role of TLR-induced cytokines in autoimmune diseases, such as rheumatoid arthritis, inflammatory bowel disease, and systemic lupus erythematosus.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Hamerman, J. A., Pottle, J., Ni, M., He, Y., Zhang, Z. Y., & Buckner, J. H. (2016). Negative regulation of TLR signaling in myeloid cells--implications for autoimmune diseases. Immunological reviews. https://doi.org/10.1111/imr.12381
Vancouver
Hamerman JA, Pottle J, Ni M, He Y, Zhang ZY, Buckner JH. Negative regulation of TLR signaling in myeloid cells--implications for autoimmune diseases. Immunological reviews. 2016. doi:10.1111/imr.12381. PMID: 26683155.
BibTeX
@article{hamerman2016-26683155,
author = {Hamerman, J. A. and Pottle, J. and Ni, M. and He, Y. and Zhang, Z. Y. and Buckner, J. H.},
title = {{Negative regulation of TLR signaling in myeloid cells--implications for autoimmune diseases}},
journal = {Immunological reviews},
year = {2016},
doi = {10.1111/imr.12381},
pmid = {26683155},
url = {https://doi.org/10.1111/imr.12381}
}
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Key findings
- Whereas TLR-induced inflammatory mediators are required for pathogen clearance, many are toxic to the host and can cause pathological inflammation when over-produced.
- This is demonstrated by the role of TLR-induced cytokines in autoimmune diseases, such as rheumatoid arthritis, inflammatory bowel disease, and systemic lupus erythematosus.
- Because of the potent effects of TLR-induced cytokines, we have diverse mechanisms to dampen TLR signaling.
- Here, we highlight three pathways that participate in inhibition of TLR responses in macrophages and DC, and their implications in autoimmunity; A20, encoded by the TNFAIP3 gene, Lyp encoded by the PTPN22 gene, and the BCAP/PI3K pathway.
Why it matters
This review describes how the body dampens Toll-like receptor signaling to avoid excessive inflammation, using examples from autoimmune diseases such as rheumatoid arthritis and lupus. It is about immune regulation in general and does not report any Alzheimer's treatment, cure or prevention findings.
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Study details
- Evidence strengthLow
How this study scored 44/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Immunological reviews) |
| Journal's citation record | 3 / 4 | Immunological Reviews: journal h-index 320 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2016 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 110 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 9.2 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 1 / 6 | Cited 0.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 2 / 4 | Cited 19 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Jane Hoyt Buckner: h-index 67 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | University of Washington: institution h-index 3,540 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 26683155) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 44 / 100 | — |
What each of these 20 components measures, and what this score is not →
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