Evidence map›Paper›PMID 16010587›Full record

ReviewCancer immunology, immunotherapy : CII2005

Tumor antigen-specific T helper cells in cancer immunity and immunotherapy.

K L Knutson, M L Disis

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04212377 (An Exploratory Study), which is not on this map. Cited by 307 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
307citing papers in PubMed, 4 pooled it
11.0field-weighted citation impact, top 1% 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.

NCT04212377 phase2completednot on this mapstarted 2019, after this paper: background citation

An Exploratory Study: Dendritic Cells for Immunotherapy of Metastatic Endometrial Cancer Patients

TypeinterventionalSponsorRadboud University Medical CenterRan2019 to 2021Enrolled8ConditionsEndometrial CancerArmsDendritic Cells for endometrial cancer
3 · Its place in the literature

Who cites it

307 citing papers in PubMed, 4 syntheses or guidelines pooled it, 675 citations in OpenAlex.

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  13. Bugs as drugs: parasite biomolecules as novel therapeutics against breast cancer.American journal of physiology. Cell physiology · 2026
    Review
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247 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

K L KnutsonDepartment of Immunology, Mayo Clinic College of Medicine, 342C Guggenheim Bldg., 200 First St. SW, Rochester, MN 55906, USA. knutson.keith@mayo.edu
M L Disis
Mayo Clinic · USUniversity of Washington · US

Funding

A Cancer Vaccine for Ovarian and Breast CancerR41CA107590 · NCI · IDM PHARMA, INC. · PI ISHIOKA, GLENN Y · 2004 to 2005
$605k
MIDCAREER INVESTIGATOR AWARD IN PATIENT ORIENTED RESEARCK24CA085218 · NCI · UNIVERSITY OF WASHINGTON · PI DISIS, MARY L. · 2000 to 2004
$571k
Tumor rejection antigens induced via epitope spreadingR21CA105270 · NCI · UNIVERSITY OF WASHINGTON · PI KNUTSON, KEITH L · 2004 to 2005
$271k
NCI NIH HHS K24 CA085218NCI NIH HHS K24CA85218NCI NIH HHS R21 CA105270NCI NIH HHS R21CA105270NCI NIH HHS R41 CA107590NCI NIH HHS R41CA107590
6 · The paper itself

Abstract

Historically, cancer-directed immune-based therapies have focused on eliciting a cytotoxic T cell (CTL) response, primarily due to the fact that CTL can directly kill tumors. In addition, many putative tumor antigens are intracellular proteins, and CTL respond to peptides presented in the context of MHC class I which are most often derived from intracellular proteins. Recently, increasing importance is being given to the stimulation of a CD4+ T helper cell (Th) response in cancer immunotherapy. Th cells are central to the development of an immune response by activating antigen-specific effector cells and recruiting cells of the innate immune system such as macrophages and mast cells. Two predominant Th cell subtypes exist, Th1 and Th2. Th1 cells, characterized by secretion of IFN-gamma and TNF-alpha, are primarily responsible for activating and regulating the development and persistence of CTL. In addition, Th1 cells activate antigen-presenting cells (APC) and induce limited production of the type of antibodies that can enhance the uptake of infected cells or tumor cells into APC. Th2 cells favor a predominantly humoral response. Particularly important during Th differentiation is the cytokine environment at the site of antigen deposition or in the local lymph node. Th1 commitment relies on the local production of IL-12, and Th2 development is promoted by IL-4 in the absence of IL-12. Specifically modulating the Th1 cell response against a tumor antigen may lead to effective immune-based therapies. Th1 cells are already widely implicated in the tissue-specific destruction that occurs during the pathogenesis of autoimmune diseases, such as diabetes mellitus and multiple sclerosis. Th1 cells directly kill tumor cells via release of cytokines that activate death receptors on the tumor cell surface. We now know that cross-priming of the tumor-specific response by potent APC is a major mechanism of the developing endogenous immune response; therefore, even intracellular proteins can be presented in the context of MHC class II. Indeed, recent studies demonstrate the importance of cross-priming in eliciting CTL. Many vaccine strategies aim to stimulate the Th response specific for a tumor antigen. Early clinical trials have shown that focus on the Th effector arm of the immune system can result in significant levels of both antigen-specific Th cells and CTL, the generation of long lasting immunity, and a Th1 phenotype resulting in the development of epitope spreading.

Indexed as

Antigen PresentationAntigens, NeoplasmCancer VaccinesCD4-Positive T-LymphocytesCytokinesEpitopes, T-LymphocyteHumansImmunity, CellularImmunotherapyNeoplasmsTh1 CellsAntigens, NeoplasmCancer VaccinesCytokinesEpitopes, T-Lymphocyte

Identifiers

PMID16010587
PMCPMC11032889
OpenAlexW2154203858

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.