Evidence map›Paper›PMID 32438408›Full record

ArticleThe Journal of experimental medicine2020

Talin1 controls dendritic cell activation by regulating TLR complex assembly and signaling.

Thomas Jun Feng Lim, Maegan Bunjamin, Christiane Ruedl, I-Hsin Su

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Targeting Talin1 to reprogram dendritic cell activation landscapes: A mechanistically grounded cell therapy for multiple sclerosis model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  4. Talin 1 plays a significant role in the development of tolerogenic dendritic cells, which may contribute to the progression of multiple sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Regulation of myeloid-cell activation.Current opinion in immunology · 2021
    Review
  10. Review
  11. Talin1 sets the stage for dendritic cell activation.The Journal of experimental medicine · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Thomas Jun Feng LimLaboratory of Molecular Immunology & Cell Signalling, School of Biological Sciences, College of Science, Nanyang Technological University, Singapore, Republic of Singapore.
Maegan BunjaminLaboratory of Molecular Immunology & Cell Signalling, School of Biological Sciences, College of Science, Nanyang Technological University, Singapore, Republic of Singapore.
Christiane RuedlLaboratory of Immunology, School of Biological Sciences, College of Science, Nanyang Technological University, Singapore, Republic of Singapore.
I-Hsin SuLaboratory of Molecular Immunology & Cell Signalling, School of Biological Sciences, College of Science, Nanyang Technological University, Singapore, Republic of Singapore.
Nanyang Technological University · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Talin critically controls integrin-dependent cell migration, but its regulatory role in skin dendritic cells (DCs) during inflammatory responses has not been investigated. Here, we show that talin1 regulates not only integrin-dependent Langerhans cell (LC) migration, but also MyD88-dependent Toll-like receptor (TLR)-stimulated DC activation. Talin1-deficient LCs failed to exit the epidermis, resulting in reduced LC migration to skin-draining lymph nodes (sdLNs) and defective skin tolerance induction, while talin1-deficient dermal DCs unexpectedly accumulated in the dermis despite their actomyosin-dependent migratory capabilities. Furthermore, talin1-deficient DCs exhibited compromised chemotaxis, NFκB activation, and proinflammatory cytokine production. Mechanistically, talin1 was required for the formation of preassembled TLR complexes in DCs at steady state via direct interaction with MyD88 and PIP5K. Local production of PIP2 by PIP5K then recruited TIRAP to the preassembled complexes, which were required for TLR signalosome assembly during DC activation. Thus, talin1 regulates MyD88-dependent TLR signaling pathways in DCs through a novel mechanism with implications for antimicrobial and inflammatory immune responses.

Indexed as

Immune ToleranceAnimalsChemotaxisCytokinesLangerhans CellsMembrane GlycoproteinsMiceMice, KnockoutMyeloid Differentiation Factor 88NF-kappa BPhosphotransferases (Alcohol Group Acceptor)Receptors, Interleukin-1Signal TransductionSkinTalinToll-Like Receptors1-phosphatidylinositol-4-phosphate 5-kinaseCytokinesMembrane GlycoproteinsMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BPhosphotransferases (Alcohol Group Acceptor)Receptors, Interleukin-1TalinTIRAP protein, mouseTln1 protein, mouseToll-Like Receptors

Identifiers

PMID32438408
PMCPMC7398162
OpenAlexW3028398765

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.