Evidence map›Paper›PMID 31126693›Full record

ArticleImmunobiology2019

Human β-defensin 2 is involved in CCR2-mediated Nod2 signal transduction, leading to activation of the innate immune response in macrophages.

Ju Kim, Ye Lin Yang, Yong-Suk Jang

Open access · greenAbstract read
In one paragraph

Article in Immunobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Antimicrobial Peptide Signaling in Skin Diseases.JID innovations : skin science from molecules to population health · 2025
    Review
  4. Review
  5. Structure-activity relationship in NOD2 agonistic muramyl dipeptides.European journal of medicinal chemistry · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. The seven constitutive respiratory defense barriers against SARS-CoV-2 infection.Revista da Sociedade Brasileira de Medicina Tropical · 2021
    Review
  20. NOD2-dependent BCG-induced trained immunity: A way to regulate innate responses to SARS-CoV2?International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2020
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ju KimDepartment of Molecular Biology and the Institute for Molecular Biology and Genetics, Chonbuk National University, 54896, South Korea.
Ye Lin YangDepartment of Bioactive Material Sciences and Institute of Bioactive Materials, Chonbuk National University, Jeonju, 54856, South Korea.
Yong-Suk JangDepartment of Molecular Biology and the Institute for Molecular Biology and Genetics, Chonbuk National University, 54896, South Korea; Department of Bioactive Material Sciences and Institute of Bioactive Materials, Chonbuk National University, Jeonju, 54856, South Korea. Electronic address: yongsuk@jbnu.ac.kr.
Jeonbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beta-defensins contribute to host innate defense against various pathogens, including viruses, although the details of their roles in innate immune cells are unclear. We previously reported that human β-defensin 2 (HBD 2) activates primary innate immunity against viral infection and suggested that it plays a role in the induction of the adaptive immune response. We analyzed the mechanisms by which HBD 2 primes innate antiviral immunity and polarized activation of macrophage-like THP-1 cells using the receptor-binding domain (RBD) of Middle East respiratory syndrome coronavirus (MERS-CoV) spike protein (S RBD) as a model antigen. The expression of nucleotide-binding oligomerization domain containing 2 (Nod2), type I interferons, (IFNs), and proinflammatory mediators was enhanced in S RBD-HBD 2-treated THP-1 cells. S RBD-HBD 2 treatment also enhanced phosphorylation and activation of receptor-interacting serine/threonine-protein kinase 2 and IFN regulatory factor 3 compared to S RBD alone. Finally, HBD 2-conjugated S RBD interacted with C-C chemokine receptor 2 (CCR2), and Nod2 was involved in HBD 2-mediated CCR2 signaling, which was associated with the activation and M1 polarization of THP-1 cells. Therefore, HBD 2 promotes CCR2-mediated Nod2 signaling, which induces production of type I IFNs and an inflammatory response, and enhances primary innate immunity leading to an effective adaptive immune response to HBD 2-conjugated antigen.

Indexed as

Immunity, InnateSignal TransductionAnimalsbeta-DefensinsChlorocebus aethiopsCytokinesHost-Pathogen InteractionsHumansMacrophage ActivationMacrophagesNod2 Signaling Adaptor ProteinReceptors, CCR2THP-1 CellsVero Cellsbeta-DefensinsCCR2 protein, humanCytokinesDEFB4A protein, humanNOD2 protein, humanNod2 Signaling Adaptor ProteinReceptors, CCR2Adaptive immunityDefensinInnate immunitySignalingVirus

Identifiers

PMID31126693
PMCPMC7114636
OpenAlexW2946050253

What OpenQuestion holds

Textmetadata
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.