Evidence map›Paper›PMID 40200271›Full record

ArticleCell communication and signaling : CCS2025

Toxoplasma gondii modulates immune responses and mitigates type 1 diabetes progression in a streptozotocin-induced rat model.

Kimia Moradi, Reyhaneh Moghaddami, Arshad Ghaffari-Nasab, Monir Khordadmehr, Abdol Sattar Pagheh, Hossein Mosajakhah, Sahar Rezaei, Esmaeil Gharepapagh, Mahdi Ahmadi, Mahbobeh Montazeri and 2 more

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

12 authors.

Kimia MoradiStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Reyhaneh MoghaddamiDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Arshad Ghaffari-NasabSchool of Nursing and Allied Medical Sciences, Maragheh University of Medical Sciences, Maragheh, Iran.
Monir KhordadmehrDepartment of Pathobiology, Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran.
Abdol Sattar PaghehInfectious Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran.
Hossein MosajakhahImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Sahar RezaeiDepartment of Nuclear Medicine, Medical School, Tabriz University of Medical Sciences, Tabriz, Iran.
Esmaeil GharepapaghDepartment of Nuclear Medicine, Medical School, Tabriz University of Medical Sciences, Tabriz, Iran.
Mahdi AhmadiSchool of Medical Sciences, Sarab Faculty of Medical Sciences, Sarab, Iran.
Mahbobeh MontazeriToxoplasmosis Research Center, Mazandaran University of Medical Sciences, Sari, Iran.
Hossein PazokiFaculty of Medicine, Department of Medical Microbiology, Infectious Diseases Research Center, Gonabad University of Medical Science, Gonabad, Iran.
Ehsan AhmadpourStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. ehsanahmadpour@gmail.com.

Funding

National Institute for Medical Research Development 4010301
6 · The paper itself

Abstract

Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by the destruction of insulin-producing β-cells in the pancreas. Emerging evidence suggests that infections, including Toxoplasma gondii (T. gondii), may modulate immune responses and influence disease outcomes. This study aimed to investigate the effects of T. gondii infection on the development of T1DM in a Streptozotocin (STZ)-induced rat model, with an emphasis on immune modulation, cytokine profiles, and organ inflammation. In rats experimentally infected with pathogenic and non-pathogenic Toxoplasma strains, diabetes was induced via STZ injection and compared to a control group. Blood glucose levels and the expression of IL-10, IL-1β, and TNF-α at both gene and protein levels were assessed. Histopathological examinations of the pancreas and kidneys were conducted, alongside small-animal PET scans to evaluate metabolic activity in these organs. The T. gondii-infected diabetic groups showed reduced blood glucose levels, increased IL-10, and decreased TNF-α and IL-1β levels compared to the STZ group. Histopathological and PET imaging analyses revealed improved pancreatic and renal tissues and reduced metabolic activity, indicating improvement effects associated with decreased inflammation and immune modulation. T. gondii infection seems to influence immune responses and slow the progression of T1DM in a rat model. These results suggest a potential therapeutic role for parasitic infections in autoimmune diseases, offering valuable insights into the complex relationship between infections, immune regulation, and metabolic health.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Disease ProgressionToxoplasmaToxoplasmosisAnimalsBlood GlucoseCytokinesDisease Models, AnimalKidneyMalePancreasRatsStreptozocinBlood GlucoseCytokinesStreptozocinCytokine profileImmune modulationSTZToxoplasmosisType 1 diabetes mellitus (T1DM)

Identifiers

PMID40200271
PMCPMC11980074

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.