Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (657 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A subset of helper-inducer T-lymphocytes which synthesize and secrete the interleukins il-4; IL-5; IL-6; and il-10. These cytokines influence B-cell development and antibody production as well as augmenting humoral responses.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Th2 Cell; Cells, Th2; Cell, Th2; T Helper2 Cell; Cells, T Helper2; Cell, T Helper2; TH-2 Cell; Cells, TH-2.
Where it fits in the MeSH classification
- Broader topics
- T-Lymphocytes, Helper-Inducer
Related concepts
- Interleukins Il-4
- Il-10
Research landscape
PubMed indexes 19,429 records tagged with the MeSH heading “Th2 Cells” (counts retrieved 2026-10-31). 2,492 of them (12.8%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 7,834 records.
Reviews account for 2,999 records (15.4%) and meta-analyses for 25. Randomized controlled trials number 215 (1.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,259 |
| 2000-2009 | 7,834 |
| 2010-2019 | 6,844 |
| 2020 onward | 2,492 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,999 | 15.4% |
| Meta-analyses | 25 | 0.1% |
| Randomized controlled trials | 215 | 1.1% |
Method: PubMed query "Th2 Cells"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Type 2 immunity in allergic diseases | 2025 | Review article Design not recorded in structured metadata | 331 | cc by PMID 39962262 · DOI · PMC11868591 |
| B. adolescentis ameliorates chronic colitis by regulating Treg/Th2 response and gut microbiota remodeling | 2021 | Research article Design not recorded in structured metadata | 203 | cc by PMID 33557671 · DOI · PMC7889144 |
| Lung mesenchymal stromal cells influenced by Th2 cytokines mobilize neutrophils and facilitate metastasis by producing complement C3 | 2021 | Research article Design not recorded in structured metadata | 144 | cc by PMID 34707103 · DOI · PMC8551331 |
Type 2 immunity in allergic diseases [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Significant advancements have been made in understanding the cellular and molecular mechanisms of type 2 immunity in allergic diseases such as asthma, allergic rhinitis, chronic rhinosinusitis, eosinophilic esophagitis (EoE), food and drug allergies, and atopic dermatitis (AD).
- Closing excerpt
- Recent biologics targeting the pathways and effector functions of IL4/IL13, IL-5, and IgE have shown promising results for almost all ages, although some patients with severe allergic diseases do not respond to these therapies, highlighting the unmet need for a more detailed and personalized approach.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (254 words)
Significant advancements have been made in understanding the cellular and molecular mechanisms of type 2 immunity in allergic diseases such as asthma, allergic rhinitis, chronic rhinosinusitis, eosinophilic esophagitis (EoE), food and drug allergies, and atopic dermatitis (AD). Type 2 immunity has evolved to protect against parasitic diseases and toxins, plays a role in the expulsion of parasites and larvae from inner tissues to the lumen and outside the body, maintains microbe-rich skin and mucosal epithelial barriers and counterbalances the type 1 immune response and its destructive effects. During the development of a type 2 immune response, an innate immune response initiates starting from epithelial cells and innate lymphoid cells (ILCs), including dendritic cells and macrophages, and translates to adaptive T and B-cell immunity, particularly IgE antibody production. Eosinophils, mast cells and basophils have effects on effector functions. Cytokines from ILC2s and CD4+ helper type 2 (Th2) cells, CD8 + T cells, and NK-T cells, along with myeloid cells, including IL-4, IL-5, IL-9, and IL-13, initiate and sustain allergic inflammation via T cell cells, eosinophils, and ILC2s; promote IgE class switching; and open the epithelial barrier. Epithelial cell activation, alarmin release and barrier dysfunction are key in the development of not only allergic diseases but also many other systemic diseases. Recent biologics targeting the pathways and effector functions of IL4/IL13, IL-5, and IgE have shown promising results for almost all ages, although some patients with severe allergic diseases do not respond to these therapies, highlighting the unmet need for a more detailed and personalized approach.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39962262 · DOI · PMC11868591
B. adolescentis ameliorates chronic colitis by regulating Treg/Th2 response and gut microbiota remodeling [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Inflammatory bowel disease (IBD) is defined as an immune dysregulation disease with poor prognosis.
- Closing excerpt
- adolescentis regularly treatment might improve the therapeutic effects for inflammatory bowel disease.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (256 words)
Inflammatory bowel disease (IBD) is defined as an immune dysregulation disease with poor prognosis. Various therapies based on gut microbe modulation have been proposed. In this study, we aim to explore the therapeutic effect of B. adolescentis on IBD, as well as the immune and microecology mechanism of B. adolescentis in IBD. The fecal level of B. adolescentis was decreased in the IBD patients compared with the normal people in our cohort and the GMrepo database. To further clarify the role of B. adolescentis in IBD, we induced chronic colitis with three cycles of dextran sulfate sodium (DSS). We found B. adolescentis gavage exhibited protective effects as evidenced by the significantly decreased diarrhea score, spleen weight, and increased colon length. Accordingly, the cumulative histological grading was decreased in the B. adolescentis administration group. In addition, tight junction protein and mucin family were enhanced after B. adolescentis treatment. Furthermore, distinct effects were found with decreased pro-inflammatory cytokines such as TNF-α, IL-6, IL-1β, IL-18, IL-22, IL-9 and increased anti-inflammatory cytokines IL-10, IL-4, IL-5. Importantly, the colon lamina propria in the B. adolescentis group consisted of more Treg and Th2 cells, which inhibited extreme gut inflammation. Additionally, 16srRNA sequencing showed an evident increase in the B:F ratio in the B. adolescentis group. In particular, B. adolescentis application inhibited the excessive growth of Akkermansia and Escherichia-Shigella in genus level. In conclusion, B. adolescentis refined the DSS-induced chronic colitis by stimulating protective Treg/Th2 response and gut microbiota remodeling. B. adolescentis regularly treatment might improve the therapeutic effects for inflammatory bowel disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33557671 · DOI · PMC7889144
Lung mesenchymal stromal cells influenced by Th2 cytokines mobilize neutrophils and facilitate metastasis by producing complement C3 [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Pre-metastatic niche formation is critical for the colonization of disseminated cancer cells in distant organs.
- Closing excerpt
- Our results suggest that targeting the Th2-STAT6-C3-NETs cascade may reduce breast cancer metastasis to the lungs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (147 words)
Pre-metastatic niche formation is critical for the colonization of disseminated cancer cells in distant organs. Here we find that lung mesenchymal stromal cells (LMSCs) at pre-metastatic stage possess potent metastasis-promoting activity. RNA-seq reveals an upregulation of complement 3 (C3) in those LMSCs. C3 is found to promote neutrophil recruitment and the formation of neutrophil extracellular traps (NETs), which facilitate cancer cell metastasis to the lungs. C3 expression in LMSCs is induced and sustained by Th2 cytokines in a STAT6-dependent manner. LMSCs-driven lung metastasis is abolished in Th1-skewing Stat6-deficient mice. Blockade of IL-4 by antibody also attenuates LMSCs-driven cancer metastasis to the lungs. Consistently, metastasis is greatly enhanced in Th2-skewing T-bet-deficient mice or in nude mice adoptively transferred with T-bet-deficient T cells. Increased C3 levels are also detected in breast cancer patients. Our results suggest that targeting the Th2-STAT6-C3-NETs cascade may reduce breast cancer metastasis to the lungs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34707103 · DOI · PMC8551331
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article CD4⁺T cells: differentiation and functions [4]
- Research article Type 2 immunity in tissue repair and fibrosis [5]
- Research article TH2, allergy and group 2 innate lymphoid cells [6]
- Research article TH2 cell development and function [7]
- Research article The immunology of atopic dermatitis and its reversibility with broad-spectrum and targeted therapies [8]
- Research article The many paths to asthma: phenotype shaped by innate and adaptive immunity [9]
References
- Ogulur I, Mitamura Y, Yazici D, Pat Y, Ardicli S, Li M, et al.. Type 2 immunity in allergic diseases. . 2025. PMID 39962262 · DOI · PMC11868591
- Fan L, Qi Y, Qu S, Chen X, Li A, Hendi M, et al.. B. adolescentis ameliorates chronic colitis by regulating Treg/Th2 response and gut microbiota remodeling. . 2021. PMID 33557671 · DOI · PMC7889144
- Zheng Z, Li YN, Jia S, Zhu M, Cao L, Tao M, et al.. Lung mesenchymal stromal cells influenced by Th2 cytokines mobilize neutrophils and facilitate metastasis by producing complement C3. . 2021. PMID 34707103 · DOI · PMC8551331
- Luckheeram RV, Zhou R, Verma AD, Xia B. CD4⁺T cells: differentiation and functions. Clin Dev Immunol. 2012. PMID 22474485 · DOI · PMC3312336
- Gieseck RL, Wilson MS, Wynn TA. Type 2 immunity in tissue repair and fibrosis. Nat Rev Immunol. 2018. PMID 28853443 · DOI
- Licona-Limón P, Kim LK, Palm NW, Flavell RA. TH2, allergy and group 2 innate lymphoid cells. Nat Immunol. 2013. PMID 23685824 · DOI
- Walker JA, McKenzie ANJ. TH2 cell development and function. Nat Rev Immunol. 2018. PMID 29082915 · DOI
- Brunner PM, Guttman-Yassky E, Leung DY. The immunology of atopic dermatitis and its reversibility with broad-spectrum and targeted therapies. J Allergy Clin Immunol. 2017. PMID 28390479 · DOI · PMC5405702
- Kim HY, DeKruyff RH, Umetsu DT. The many paths to asthma: phenotype shaped by innate and adaptive immunity. Nat Immunol. 2010. PMID 20562844 · DOI · PMC3114595
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.