Evidence map›Paper›PMID 40305198›Full record

ReviewBiomolecules2025

Neutrophils in Type 1 Diabetes: Untangling the Intricate Web of Pathways and Hypothesis.

Laura Nigi, Erika Pedace, Francesco Dotta, Guido Sebastiani

Abstract readReview
In one paragraph

Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. (TCRαβCells · 2025
    Review
  7. 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

4 authors.

Laura NigiDiabetes Unit, Department of Medicine, Surgery and Neurosciences, University of Siena, 53100 Siena, Italy.ORCID 0000-0002-6251-3069
Erika PedaceDiabetes Unit, Department of Medicine, Surgery and Neurosciences, University of Siena, 53100 Siena, Italy.ORCID 0000-0002-0131-8534
Francesco DottaDiabetes Unit, Department of Medicine, Surgery and Neurosciences, University of Siena, 53100 Siena, Italy.
Guido SebastianiDiabetes Unit, Department of Medicine, Surgery and Neurosciences, University of Siena, 53100 Siena, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils are increasingly recognized as key contributors to the pathogenesis of Type 1 Diabetes (T1D), yet their precise mechanistic role in disease onset and progression remains incompletely understood. While these innate immune cells reside in pancreatic tissue and support tissue homeostasis under physiological conditions, they can also drive tissue damage by triggering innate immune responses and modulating inflammation. Within the inflammatory milieu, neutrophils establish complex, bidirectional interactions with various immune cells, including macrophages, dendritic cells, natural killer cells, and lymphocytes. Once activated, they may enhance the innate immune response through direct or indirect crosstalk with immune cells, antigen presentation, and β-cell destruction or dysfunction. These mechanisms underscore the multifaceted and dynamic role of neutrophils in T1D, shaped by their intricate immunological interactions. Further research into the diverse functional capabilities of neutrophils is crucial for uncovering novel aspects of their involvement in T1D, potentially revealing new therapeutic targets to modulate disease progression.

Indexed as

Diabetes Mellitus, Type 1NeutrophilsAnimalsHumansImmunity, InnateInflammationautoimmune diseasesinnate immunityneutrophilstype 1 diabetes

Identifiers

PMID40305198
PMCPMC12025241

What OpenQuestion holds

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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.