Evidence map›Paper›PMID 35979362›Full record

ArticleFrontiers in immunology2022

CTLA-4 silencing in dendritic cells loaded with colorectal cancer cell lysate improves autologous T cell responses

Farid Ghorbaninezhad, Javad Masoumi, Mohammad Bakhshivand, Amir Baghbanzadeh, Ahad Mokhtarzadeh, Tohid Kazemi, Leili Aghebati-Maleki, Siamak Sandoghchian Shotorbani, Mahdi Jafarlou, Oronzo Brunetti and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

Farid GhorbaninezhadImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Javad MasoumiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammad BakhshivandImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Amir BaghbanzadehImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Ahad MokhtarzadehImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Tohid KazemiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Leili Aghebati-MalekiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Siamak Sandoghchian ShotorbaniImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mahdi JafarlouImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Oronzo BrunettiMedical Oncology Unit, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Istituto Tumori "Giovanni Paolo II" of Bari, Bari, Italy.
Mariacarmela SantarpiaMedical Oncology Unit, Department of Human Pathology "G. Barresi", University of Messina, Messina, Italy.
Behzad BaradaranImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Nicola SilvestrisMedical Oncology Unit, Department of Human Pathology "G. Barresi", University of Messina, Messina, Italy.
Tabriz University of Medical Sciences · IRUniversity of Messina · ITIstituto Tumori Bari · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic cell (DC)-based immunotherapy has increased interest among anti-cancer immunotherapies. Nevertheless, the immunosuppressive mechanisms in the tumor milieu, e.g., inhibitory immune checkpoint molecules, have been implicated in diminishing the efficacy of DC-mediated anti-tumoral immune responses. Therefore, the main challenge is to overcome inhibitory immune checkpoint molecules and provoke efficient T-cell responses to antigens specifically expressed by cancerous cells. Among the inhibitory immune checkpoints, cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) expression on DCs diminishes their maturation and antigen presentation capability. Accordingly, we hypothesized that the expression of CTLA-4 on DCs inhibits the T cell-mediated anti-tumoral responses generated following the presentation of tumor antigens by DCs to T lymphocytes. In this study, we loaded colorectal cancer (CRC) cell lysate on DCs and inhibited the expression of CTLA-4 by small interfering RNA (siRNA) in them to investigate the DCs' functional and phenotypical features, and T-cell mediated responses following DC/T cell co-culture. Our results demonstrated that blockade of CTLA-4 could promote stimulatory properties of DCs. In addition, CTLA-4 silenced CRC cell lysate-loaded DCs compared to the DCs without CTLA-4 silencing resulted in augmented T cell proliferation and cytokine production, i.e., IFN-γ and IL-4. Taken together, our findings suggest CTLA-4 silenced CRC cell lysate-loaded DCs as a promising therapeutic approach however further studies are needed before this strategy can be used in clinical practice.

Indexed as

Colorectal NeoplasmsT-LymphocytesCTLA-4 AntigenDendritic CellsHumansImmune Checkpoint ProteinsCTLA-4 AntigenImmune Checkpoint Proteinscancer immunotherapycolorectal cancerCTLA-4dendritic cellT lymphocytetumor cell lysate

Identifiers

PMID35979362
PMCPMC9376327
OpenAlexW4289130620

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.