Evidence map›Paper›PMID 32313211›Full record

ArticleCellular & molecular immunology2021

Glutamate triggers the expression of functional ionotropic and metabotropic glutamate receptors in mast cells.

Md Abdul Alim, Mirjana Grujic, Paul W Ackerman, Per Kristiansson, Pernilla Eliasson, Magnus Peterson, Gunnar Pejler

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Paradoxical Expression of Ionotropic Glutamate Receptors in Leucocytes.Clinical reviews in allergy & immunology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
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  12. Article
  13. Article
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  15. Article
  16. Review
  17. Neuronal-Immune Cell Units in Allergic Inflammation in the Nose.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Md Abdul AlimDepartment of Public Health and Caring Sciences, General Medicine and Preventive Medicine, Uppsala University, Uppsala, Sweden.
Mirjana GrujicDepartment of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden.
Paul W AckermanDepartment of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-5520-169X
Per KristianssonDepartment of Public Health and Caring Sciences, General Medicine and Preventive Medicine, Uppsala University, Uppsala, Sweden.
Pernilla EliassonDepartment of Orthopedics and Sports Medicine, Linköping University, Linköping, Sweden.
Magnus PetersonDepartment of Public Health and Caring Sciences, General Medicine and Preventive Medicine, Uppsala University, Uppsala, Sweden. magnus.peterson@pubcare.uu.se.
Gunnar PejlerDepartment of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden. gunnar.pejler@imbim.uu.se.
Uppsala University · SEKarolinska Institutet · SELinköping University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mast cells are emerging as players in the communication between peripheral nerve endings and cells of the immune system. However, it is not clear the mechanism by which mast cells communicate with peripheral nerves. We previously found that mast cells located within healing tendons can express glutamate receptors, raising the possibility that mast cells may be sensitive to glutamate signaling. To evaluate this hypothesis, we stimulated primary mast cells with glutamate and showed that glutamate induced the profound upregulation of a panel of glutamate receptors of both the ionotropic type (NMDAR1, NMDAR2A, and NMDAR2B) and the metabotropic type (mGluR2 and mGluR7) at both the mRNA and protein levels. The binding of glutamate to glutamate receptors on the mast cell surface was confirmed. Further, glutamate had extensive effects on gene expression in the mast cells, including the upregulation of pro-inflammatory components such as IL-6 and CCL2. Glutamate also induced the upregulation of transcription factors, including Egr2, Egr3 and, in particular, FosB. The extensive induction of FosB was confirmed by immunofluorescence assessment. Glutamate receptor antagonists abrogated the responses of the mast cells to glutamate, supporting the supposition of a functional glutamate-glutamate receptor axis in mast cells. Finally, we provide in vivo evidence supporting a functional glutamate-glutamate receptor axis in the mast cells of injured tendons. Together, these findings establish glutamate as an effector of mast cell function, thereby introducing a novel principle for how cells in the immune system can communicate with nerve cells.

Indexed as

Glutamic AcidReceptors, Metabotropic GlutamateMast CellsNeuronsReceptors, GlutamateGlutamic AcidReceptors, GlutamateReceptors, Metabotropic GlutamateGlutamateGlutamate receptorsMast cellsNMDA receptorsTryptase

Identifiers

PMID32313211
PMCPMC8484602
OpenAlexW3016522653

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.