Evidence map›Paper›PMID 35657353›Full record

ArticleThe Journal of experimental medicine2022

CD4+ T helper 2 cells suppress breast cancer by inducing terminal differentiation.

Margherita Boieri, Anna Malishkevich, Ranya Guennoun, Emanuela Marchese, Sanne Kroon, Kathryn E Trerice, Mary Awad, Jong Ho Park, Sowmya Iyer, Johannes Kreuzer and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 91 citations in OpenAlex.

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  9. Peritumoral macrophages recruit eosinophils to promote antitumor immune responses in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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 1 institution in 1 country.

Margherita Boieri *Center for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0002-9416-0536
Anna Malishkevich *Center for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0002-5287-7408
Ranya GuennounCenter for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0001-5383-228X
Emanuela MarcheseCenter for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0001-6960-8581
Sanne KroonCenter for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0002-5722-0763
Kathryn E TrericeCenter for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0003-1119-6734
Mary AwadCenter for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0001-7072-4192
Jong Ho ParkCenter for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0002-0488-7791
Sowmya IyerCenter for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0002-8058-7942
Johannes KreuzerCenter for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0003-4716-2843
Wilhelm HaasCenter for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0001-8225-9099
Miguel N RiveraCenter for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0002-3636-2113
Shadmehr DemehriCenter for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.ORCID 0000-0002-7913-2641
Harvard University · US

Funding

Epithelium-derived alarmins role in breast cancer immunopreventionU01CA233097 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DEMEHRI, SHADMEHR · 2018 to 2022
$4.0M
THE MECHANISM OF TSLP ANTI-TUMOR EFFECTS IN THE SKINDP5OD021353 · OD · MASSACHUSETTS GENERAL HOSPITAL · PI DEMEHRI, SHADMEHR · 2015 to 2019
$2.2M
American Cancer SocietyBreast Cancer AllianceBurroughs Wellcome FundDebra & Claudio Del Vecchio and The Alexander Bodini FoundationESSCO MGH Breast Cancer Research FundNCI NIH HHS U01 CA233097NIH HHS DP5 OD021353The American-Italian Cancer FoundationWalgreens Boots Alliance
6 · The paper itself

Abstract

Cancer immunology research is largely focused on the role of cytotoxic immune responses against advanced cancers. Herein, we demonstrate that CD4+ T helper (Th2) cells directly block spontaneous breast carcinogenesis by inducing the terminal differentiation of the cancer cells. Th2 cell immunity, stimulated by thymic stromal lymphopoietin, caused the epigenetic reprogramming of the tumor cells, activating mammary gland differentiation and suppressing epithelial-mesenchymal transition. Th2 polarization was required for this tumor antigen-specific immunity, which persisted in the absence of CD8+ T and B cells. Th2 cells directly blocked breast carcinogenesis by secreting IL-3, IL-5, and GM-CSF, which signaled to their common receptor expressed on breast tumor cells. Importantly, Th2 cell immunity permanently reverted high-grade breast tumors into low-grade, fibrocystic-like structures. Our findings reveal a critical role for CD4+ Th2 cells in immunity against breast cancer, which is mediated by terminal differentiation as a distinct effector mechanism for cancer immunoprevention and therapy.

Indexed as

Breast NeoplasmsCancer VaccinesCarcinogenesisCD4-Positive T-LymphocytesCell DifferentiationCytokinesFemaleHumansImmunotherapyTh1 CellsTh2 CellsCancer VaccinesCytokines

Identifiers

PMID35657353
PMCPMC9170526
OpenAlexW4281761354

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.