Evidence map›Paper›PMID 42161270›Full record

ArticleImmunity2026

Interleukin-4-producing type 2 innate lymphoid cells in the lymph node promote proallergic Tfh13 cell differentiation.

DongUk Lee, Meng-Ping Lu, Priya Rajamanimuthu, Mrinmoy Das, Enxhi Ferraj, Courtney Fisher, Peri Matatia, Chun-Wei Chen, Raif S Geha, Caroline L Sokol and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

11 authors.

DongUk LeeDepartment of Pathology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Meng-Ping LuDepartment of Pathology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Priya RajamanimuthuDepartment of Pathology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Mrinmoy DasDivision of Immunology, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA.
Enxhi FerrajDepartment of Pathology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Courtney FisherDepartment of Pathology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Peri MatatiaCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Department of Immunology, Harvard Medical School, Boston, MA, USA.
Chun-Wei ChenDepartment of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Raif S GehaDivision of Immunology, Department of Pediatrics, Boston Children's Hospital, Boston, MA, USA.
Caroline L SokolCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Uthaman GowthamanDepartment of Pathology, University of Massachusetts Chan Medical School, Worcester, MA, USA. Electronic address: gowthaman.uthaman@umassmed.edu.

Funding

Generation & Regulation of Tfh13 cells that drive Pathogenic IgE in AllergyR01AI187460 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GOWTHAMAN UTHAMAN · 2025 to 2026
$1.2M
NIAID NIH HHS R01 AI187460
6 · The paper itself

Abstract

Proallergic T follicular helper 13 (Tfh13) cells are obligatory for generating high-affinity, anaphylactic immunoglobulin E (IgE) responses to allergens. Unlike Tfh2 cells, which are induced by vaccination and most type 2 immune responses, Tfh13 cells are primarily elicited during allergic disease states. However, the cellular and molecular determinants governing Tfh13 cell differentiation remain unclear. Using orthogonal genetic and bone marrow chimera approaches, we identified a critical role for group 2 innate lymphoid cells (ILC2s) within draining lymph nodes (dLNs) in promoting Tfh13 cell differentiation. During allergen sensitization, ILC2s trafficked into dLNs in a chemokine receptor CCR8-dependent manner and produced interleukin (IL)-4, a factor necessary for Tfh13-but not for Tfh2-cell induction. These findings uncover a mechanism by which ILC2s selectively drive pathogenic Tfh13 responses, underscoring the distinct regulatory requirements for Tfh2 and Tfh13 cell differentiation in allergic immunity.

Indexed as

Cell DifferentiationHypersensitivityImmunity, InnateInterleukin-4Lymph NodesLymphocytesT Follicular Helper CellsAllergensAnimalsImmunoglobulin EInterleukin-13MiceMice, Inbred C57BLMice, KnockoutTh2 CellsAllergensImmunoglobulin EInterleukin-13Interleukin-4allergyanaphylaxisCCR8group 2 innate lymphoid cellsIgEIL-4ILC2sTfh13 cellsTfh cells

Identifiers

PMID42161270
PMCPMC13244145

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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.