Evidence map›Paper›PMID 10049945›Full record

ArticleThe Journal of experimental medicine1999

Cytotoxic T lymphocytes to an unmutated tumor rejection antigen P1A: normal development but restrained effector function in vivo.

S Sarma, Y Guo, Y Guilloux, C Lee, X F Bai, Y Liu

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
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  5. Neoantigen: A Long March toward Cancer Immunotherapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
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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

6 authors at 2 institutions in 1 country.

S SarmaDepartment of Pathology and Kaplan Comprehensive Cancer Center, New York University Medical Center, New York 10016, USA.
Y Guo
Y Guilloux
C Lee
X F Bai
Y Liu
The Ohio State University Wexner Medical Center · USThe Ohio State University · US

Funding

TRAINING PROGRAM IN MOLECULAR ONCOLOGY &IMMUNOLOGYT32CA009161 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CARROLL, WILLIAM L., LEVY, DAVID E · 1985 to 2020
$13.3M
Tumor burden and T cell immunityR01CA058033 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, YANG · 1992 to 2013
$3.3M
RECEPTORS FOR B7-MEDIATED T CELL EFFECTOR FUNCTIONSR01CA069091 · NCI · OHIO STATE UNIVERSITY · PI LIU, YANG · 1996 to 2003
$1.3M
NCI NIH HHS CA09161NCI NIH HHS CA58033NCI NIH HHS CA69091NCI NIH HHS R01 CA058033NCI NIH HHS T32 CA009161
6 · The paper itself

Abstract

Unmutated tumor antigens are chosen as primary candidates for tumor vaccine because of their expression on multiple lineages of tumors. A critical issue is whether unmutated tumor antigens are expressed in normal cells, and if so, whether such expression imposes special restrictions on cytotoxic T lymphocyte (CTL) responses. In this study, we use a transgenic approach to study the development and effector function of T cells specific for P1A, a prototypical unmutated tumor antigen. We report here that although P1A is expressed at low levels in normal tissues, including lymphoid tissues, the P1A-specific transgenic T cells develop normally and remain highly responsive to the P1A antigen. The fact that transgenic expression of P1A antigen in the thymus induces T cell clonal deletion demonstrates that normal hematopoietic cells can process and present the P1A antigen and that P1A-specific T cells are susceptible to clonal deletion. By inference, P1A-specific T cells must have escaped clonal deletion due to low expression of P1A in the thymus. Interestingly, despite the fact that an overwhelming majority of T cells in the T cell receptor for antigen (TCR)-transgenic mice are specific for P1A, these mice are no more resistant to a P1A-expressing plasmocytoma than nontransgenic littermates. Moreover, when the same TCR-transgenic mice were challenged simultaneously with B7-1(+) and B7-1(-) tumors, only B7-1(+) tumors were rejected. Therefore, even though P1A can be a tumor rejection antigen, the effector function of P1A-specific CTL is restrained in vivo. These results have important implications for the strategy of tumor immunotherapy.

Indexed as

AnimalsAntigens, NeoplasmClonal DeletionHematopoietic Stem CellsMiceMice, Inbred BALB CMice, Inbred C3HMice, Inbred C57BLMice, TransgenicReceptors, Antigen, T-CellRNA, MessengerThymus GlandTissue DistributionT-Lymphocytes, CytotoxicAntigens, NeoplasmReceptors, Antigen, T-CellRNA, Messengertumor rejection antigen P815A, mouse

Identifiers

PMID10049945
PMCPMC2192944
OpenAlexW2131407015

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY-NC-SA
Read underepoch 390

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 OpenQuestion graph.