Evidence map›Paper›PMID 36252475›Full record

ReviewInternational immunopharmacology2022

Role of CCL2/CCR2 axis in the pathogenesis of COVID-19 and possible Treatments: All options on the Table.

Mitra Ranjbar, Ali Rahimi, Zeinab Baghernejadan, Atousa Ghorbani, Hossein Khorramdelazad

Open access · greenAbstract readReview
In one paragraph

Review in International immunopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. COVID-19 and Lung Cancer Interactions: A Literature Review.Medical sciences (Basel, Switzerland) · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. SARS-CoV-2 XBB.1.5 infects wild-type C57BL/6 mice and induces a protective CD4Frontiers in cellular and infection microbiology · 2025
    Article
  19. A20 as a Potential Therapeutic Target for COVID-19.Immunity, inflammation and disease · 2025
    Review
  20. Observational
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

5 authors at 2 institutions in 1 country.

Mitra RanjbarDepartment of Infectious Disease, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Ali RahimiDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Zeinab BaghernejadanDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Atousa GhorbaniDepartment of Biology, East Tehran Branch, Islamic Azad University, Tehran, Iran.
Hossein KhorramdelazadDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran; Department of Immunology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Electronic address: Khorramdelazad@gmail.com.
Iran University of Medical Sciences · IRIslamic Azad University South Tehran Branch · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is cause of the novel coronavirus disease (COVID-19). In the last two years, SARS-CoV-2 has infected millions of people worldwide with different waves, resulting in the death of many individuals. The evidence disclosed that the host immune responses to SARS-CoV-2 play a pivotal role in COVID-19 pathogenesis and clinical manifestations. In addition to inducing antiviral immune responses, SARS-CoV-2 can also cause dysregulated inflammatory responses characterized by the noticeable release of proinflammatory mediators in COVID-19 patients. Among these proinflammatory mediators, chemokines are considered a subset of cytokines that participate in the chemotaxis process to recruit immune and non-immune cells to the site of inflammation and infection. Researchers have demonstrated that monocyte chemoattractant protein-1 (MCP-1/CCL2) and its receptor (CCR2) are involved in the recruitment of monocytes and infiltration of these cells into the lungs of patients suffering from COVID-19. Moreover, elevated levels of CCL2 have been reported in the bronchoalveolar lavage fluid (BALF) obtained from patients with severe COVID-19, initiating cytokine storm and promoting CD163

Indexed as

Chemokine CCL2COVID-19 Drug TreatmentCytokine Release SyndromeHumansMonocytesReceptors, CCR2SARS-CoV-2CCL2 protein, humanCCR2 protein, humanChemokine CCL2Receptors, CCR2CCL2CCR2COVID-19CXCL17ImmunotherapyMDSCs

Identifiers

PMID36252475
PMCPMC9561120
OpenAlexW4306166189

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.