ArticleCellular & molecular immunology2012
Cyclic adenosine monophosphate involvement in low-dose cyclophosphamide-reversed immune evasion in a mouse lymphoma model.
Article in Cellular & molecular immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- EngineeredMolecular therapy. Oncology · 2026Article
- Regulatory T cells: a promising new therapeutic target in ventricular remodeling after myocardial infarction.Frontiers in immunology · 2025Review
- Identification of a novel immune-related gene signature by single-cell and bulk sequencing for the prediction of the immune landscape and prognosis of breast cancer.Cancer cell international · 2024Article
- Identification of potential biomarkers associated with immune infiltration in papillary renal cell carcinoma.Journal of clinical laboratory analysis · 2021Article
- Combining low-dose or metronomic chemotherapy with anticancer vaccines: A therapeutic opportunity for lymphomas.Oncoimmunology · 2013Review
- A bystander cell-based GM-CSF secreting vaccine synergized with a low dose of cyclophosphamide presents therapeutic immune responses against murine hepatocellular carcinoma.Cellular & molecular immunology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lymphoma cells mobilize many mechanisms to evade the immune system. There is substantial evidence that CD4(+)CD25(+) regulatory T cells (Tregs) play a key role in the control of immune evasion. Tregs can transfer cyclic adenosine monophosphate (cAMP) to effector T cells, suggesting an association between Tregs' immune-evasion role and the intracellular cAMP pathway. In this study, we used A20 B-cell lymphoma mice as aggressive tumor models to investigate the mechanism of the depletion of Tregs by low-dose cyclophosphamide (CY, 20 mg/kg). The tumor-bearing mice had longer survival times and slower tumor growth rates following treatment with CY, but its effects were temporary. Along with the depletion of Tregs by low-dose CY treatment, the expression of interleukin-2 (IL-2) in T effector cells increased, and intracellular cAMP concentrations in immune cells decreased. Our study demonstrates the ability of low-dose CY to reverse Tregs-mediated immune evasion in a mouse model. The changes in intracellular cAMP concentrations correlated with the upregulation of effector T cells and the downregulation of Tregs, indicating the close association of cAMP analogs and low-dose CY in the immune therapy of B-cell lymphoma.
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