{
  "abstract": "Introduction: Acyl CoA binding protein (ACBP, encoded by the gene diazepam binding inhibitor, DBI) is a tissue stress hormone involved in pathological aging that mediates immunosuppression. The antibody-mediated neutralization of ACBP/DBI enhances anticancer immune responses in the context of chemoimmunotherapy. ACBP/DBI inhibition also upregulates the expression of the anti-aging gene Lmna coding for Lamin A in tumor-infiltrating T lymphocytes. This study was designed to explore the role of Lmna in the anticancer effects of ACBP/DBI neutralization. Methods: We generated mice lacking Lmna expression in T lymphocytes due to a conditional knockout. Mice bearing orthotopic (cutaneous) MCA205 fibrosarcomas were treated with an anti-ACBP/DBI monoclonal antibody in the context of chemoimmuntherapy (oxaliplatin combined with a PD-1 blocking antibody), and tumor growth was monitored. Results: As compared to immunocompetent control mice, in which ACBP/DBI neutralization plus chemoimmunotherapy was highly efficient in reducing MCA205 growth, mice lacking ACBP/DBI in T cells largely failed to respond to the therapeutic intervention. This result was undistinguishably observed in both female and male mice. Discussion: Altogether, these results indicate that Lmna expression by T lymphocytes is required for the anticancer effects of the combination of chemoimmunotherapy and ACBP/DBI neutralization. We conclude that lamin A, a factor required for optimal T cell activation, is causally involved in the immunostimulatory effects of ACBP/DBI neutralization.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 5,
  "authors": [
    {
      "name": "Sijing Li"
    },
    {
      "name": "Carlos López-Otín"
    },
    {
      "name": "Maria Chiara Maiuri"
    },
    {
      "name": "Isabelle Martins"
    },
    {
      "name": "Guido Kroemer"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/0e86wjz4d9fv9.bib",
  "cited_by": 0,
  "doi": "10.2147/itt.s604318",
  "fulltext_url": null,
  "id": "0e86wjz4d9fv9",
  "issns": [
    "2253-1556"
  ],
  "landing_url": "https://hal.science/hal-05801081v1",
  "language": "en",
  "licence": "CC-BY-NC-4.0",
  "licence_label": "CC BY-NC 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "hal",
      "0.sdv"
    ],
    [
      "openalex",
      "2730|Cancer Immunotherapy and Biomarkers"
    ]
  ],
  "openalex": "W7213534369",
  "pdf_url": "https://hal.science/hal-05801081/document",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-18",
  "publisher": "Dove Medical Press",
  "ris": "https://research.draconitic.com/paper/0e86wjz4d9fv9.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:57Z",
      "native_id": "hal-05801081",
      "source": "hal",
      "url": "https://hal.science/hal-05801081v1"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2730|Cancer Immunotherapy and Biomarkers",
      "subfield": "oncology"
    }
  ],
  "title": "ACBP/DBI Neutralization Stimulates Anticancer Immune Responses by Upregulating Lamin A in T Cells",
  "title_text": "ACBP/DBI Neutralization Stimulates Anticancer Immune Responses by Upregulating Lamin A in T Cells",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:57Z",
  "url": "https://research.draconitic.com/paper/0e86wjz4d9fv9",
  "venue": "ImmunoTargets and Therapy",
  "versions": []
}