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Generation and Immune Regulation of CD4+CD25-Foxp3) T Cells in Chronic Obstructive Pulmonary Disease
Open accessAbstract
The imbalance of CD4+Foxp3+ T cell subsets is reportedly involved in abnormal inflammatory immune responses in patients with chronic obstructive pulmonary disease (COPD). However, the possible role of CD4+CD25−Foxp3+ T cells in immune regulation in COPD remains to be investigated. In the current study, distribution and phenotypic characteristics of CD4+CD25−Foxp3+ T cells from peripheral blood were determined by flow cytometry; the origin, immune function and ultimate fate of CD4+CD25−Foxp3+ T cells were further explored in vitro. It was observed that circulating CD4+CD25−Foxp3+ T cells were significantly increased in stable COPD patients (SCOPD) and resembled central memory or effector memory T cells. Compared with peripheral CD4+CD25+Foxp3+ T cells, peripheral CD4+CD25−Foxp3+ T cells showed a lower expression of Foxp3, CTLA-4, HELIOS and TIGIT, but a higher expression of CD127 and KI-67, suggesting that CD4+CD25−Foxp3+ T cells lost the expression of Tregs-associated molecules following the reduction in CD25. Unexpectedly, our study found that transforming growth factor-β1 (TGFβ1) decreased CD25 expression and played a critical role in the generation of CD4+CD25−Foxp3+ T cells from CD4+CD25+Foxp3+ T cells. Phenotypic analysis further revealed that both inducible and peripheral CD4+CD25−Foxp3+ T cells exhibit the features of activated conventional T cells. Importantly, memory CD4+CD25−Foxp3+ T cells facilitated the proliferation and differentiation of naïve CD4+ T cells into Th17 cells in the presence of IL-1β, IL-6, IL-23 and TGFβ1. Finally, a fraction of CD4+CD25−Foxp3+ T cells, exhibiting instability and plasticity, were converted to Th17 cells when subjected to Th17 cell-polarizing condition. Taken together, we propose that TGFβ1 is responsible for the generation of CD4+CD25−Foxp3+ T cells, which functionally exert an auxiliary effect on Th17 cells generation and might perpetuate chronic inflammation in COPD.
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FOXP3+ AQP4-specific ThEx cells are not derived from an unstable thymic Treg precursor.
“indicating that they are not derived from an unstable thymic Treg precursor, as described in various AIDs 71,72 including NMOSD. 73-76”
From Autoantigen-specific CD4+ T cells acquire an exhausted phenotype and persist in human antigen-specific autoimmune diseases (2024) · cites this paper as [71]
The Introduction and Discussion address the origins and stability of CD4+CD25−Foxp3+ cells in COPD and mention other autoimmune diseases, but do not address AQP4-specific ThEx cells or NMOSD. Searches for AQP4, NMOSD, and thymic Treg precursors found no passage establishing whether those cells derive from an unstable thymic Treg precursor. (LLM, conf=0.77)
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Cites
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“An imbalance of circulating Th17 cells and Tregs results in immune dysfunction and the deterioration of pulmonary function in COPD (4, 15).”
BackgroundResultInduction of CD4 T cell memory by local cellular collectivity
Polonsky, M., Rimer, J., Kern-Perets, A., Zaretsky, I., Miller, S., Bornstein, C., David, E., Kopelman, N. M., Stelzer, G., Porat, Z., et al. (2018) · Science · doi:10.1126/science.aaj1853 · Cited by 78 · cited 1×
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“An imbalance of circulating Th17 cells and Tregs results in immune dysfunction and the deterioration of pulmonary function in COPD (4, 15).”
BackgroundImmune response in chronic obstructive pulmonary disease
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Background
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Research works printed but not linked: 2
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PD-L1 signaling selectively regulates T cell lymphatic transendothelial migration
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CD4+CD25-FoxP3+T cells: a distinct subset or a heterogeneous population?
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“In addition, iTregs gradually lose CD25 and FoxP3 expression.(41) Data from clinical studies further suggest the transformation of CD4þCD25–FoxP3– T cells into CD25–FoxP3þ T cells.”
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“Most studies have shown that compared with healthy controls, the proportion of Treg cells is decreased in patients with AECOPD [5, 6] and stable COPD (SCOPD) [7–10]; however, some studies have reported conflicting results [11, 12].”
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“interleukin-6 (IL-6).(6) Increasing evidence suggested that NF-κB (nuclear factor-kappa B) is closely relevant to COPD occurrence.”
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“An alternative to this conventional taxonomy would be a mechanism-based, unbiased approach that reflects the phenotypic heterogeneity and dynamic evolution of COPD.14 Celli argues that analogous to the definitions used for the different acute events in the course of coronary artery disease (CAD), the acute events of t…”
BackgroundMethodResultInfluentialSelf-citationT cell responses in respiratory viral infections and chronic obstructive pulmonary disease
Huang, S., He, Q., & Zhou, L. (2021) · Chinese Medical Journal · doi:10.1097/cm9.0000000000001388 · Cited by 13
“Following the reduction of CD25, CD4CD25 Foxp3 T cells appear to lose Treg-associated molecules and functions.([125]) Therefore, functional and cytokine measurements are essential to characterize Treg cells.”
BackgroundXue, H., Chen, J., & Fan, W. (2024) · Journal of Affective Disorders · doi:10.1016/j.jad.2024.04.006 · Cited by 8
TIGIT Regulates T Cell Inflammation in Airway Inflammatory Diseases
Ke, J., Huang, S., He, Z., Lei, S., Lin, S., & Duan, M. (2024) · Inflammation · doi:10.1007/s10753-024-02045-y · Cited by 8
“Conversely, hypermethylation of the TIGIT locus is linked to airflow limitation in COPD [49], with increased TIGIT expression on CD4 and CD8 + T cells in COPD patients [50].”
Hou, J., Wang, X., Su, C., Ma, W., Zheng, X., Ge, X., & Duan, X. (2022) · Respiratory Research · doi:10.1186/s12931-022-02099-2 · Cited by 8
“5E, F) revealed no differences in the frequency of circulating Tregs in patients with COPD compared to smokers and never-smokers, confirming prior research [25, 26].”
ResultPereira, L. M. S., Madureira, M. W. D. S., de Castro, R. B. H., Abreu, I. N., Conde, S. R. S. D. S., Demachki, S., de Sousa, M. S., Queiroz, M. A. F., da Silva, A. N. M. R., Lima, S. S., et al. (2020) · BMC Immunology · doi:10.1186/s12865-020-00387-4 · Cited by 7
“The impact of Treg frequency on the progression of chronic diseases is important because these cells mediate the inflammatory balance in an immunologically polarized environment [2].”
BackgroundJalalvand, M., Tahermohammadi, H., Madreseh, E., Varahram, M., Sharifi, H., Akhtari, M., & Jamaati, H. (2025) · Respiratory Medicine · doi:10.1016/j.rmed.2025.108104 · Cited by 5
Liu, C., Tian, Y., Lu, R., Yue, C., Xie, Y., Zhang, T., Li, J., & Guan, Q. (2025) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2025.120126 · Cited by 5
Zhang, L., Nie, X., Luo, Z., Wei, B., & teng, G. (2020) · Medical Science Monitor · doi:10.12659/msm.928051 · Cited by 5
“In addition, CD4+ CD25+ FoxP3+ frequency in the peripheral blood of AECOPD patients was elevated compared with that of patients with stable COPD [14,15].”
BackgroundResultXue, T., Dong, F., Gao, J., & Zhong, X.-N. (2024) · Scientific Reports · doi:10.1038/s41598-024-62758-w · Cited by 4
“Some evidence has emerged to suggest that TGFβ partcipates in the chronic inflammatory process of COPD by inducing Th17 cell formationby producing CD4+ CD25-Foxp3 + T cells 13,14 .”
BackgroundCD4+CD25+ regulatory T cell therapy in neurological autoimmune diseases
Yuan, G., Liu, Y., Wang, H., Yang, T., & Liu, G.-Z. (2025) · PeerJ · doi:10.7717/peerj.19450 · Cited by 3
“This type of CD4 CD25 Foxp3 Tregs has been extensively studied ( Amini et al., 2022 ; Jeyamogan et al., 2023 ; Wu et al., 2019 ; Zhao, Liao & Kang, 2017 ).”
Guan, T., Qin, Y., Qu, N., & Pan, Y. (2024) · International Journal of COPD · doi:10.2147/copd.s460342 · Cited by 2
Xiong, X., Zhu, M., Wu, H., Fan, L., & Cheng, D. (2021) · Research Square · doi:10.21203/rs.3.rs-829435/v1
Self-citationXiong, X., Zhu, M., Wu, H.-X., Fan, L.-L., & Cheng, D.-Y. (2022) · Figshare · doi:10.6084/m9.figshare.19918918
Self-citationHou, J., Wang, X., Su, C., Ma, W., Zheng, X., Ge, X., & 段相国 (2022) · Figshare · doi:10.6084/m9.figshare.20222564
Metadata
- Authors
- Wu, J.-H., Zhou, M., Jin, Y., Meng, Z.-J., Xiong, X.-Z., Sun, S.-W., Miao, S.-Y., Han, H.-L., & Tao, X.-N.
- Affiliations
- Huazhong University of Science and Technology (CN)
- Corresponding author
- Xiong, Xian-Zhi
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2019-02-20
- Volume
- 10
- Pages
- 220-220
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC6392103
- OpenAlex
- W2916218771
- Cited by
- 26
- References
- 68
- Citations by year
- 2025: 3 · 2024: 5 · 2023: 2 · 2022: 6 · 2021: 2 · 2020: 6 · 2019: 2
- FWCI
- 1.60
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Natural Science Foundation of China (81370146, 81570032)
- Health and Family Planning Commission of Hubei Province
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- regulatory T cells, TGF-β1, Th17 cells, T cell plasticity, CD25 expression, immune regulation, chronic inflammation, central memory T cells, effector memory T cells, T cell differentiation
- MeSH terms
- Cells, Cultured, Female, Humans, Immunologic Memory, Lymphocyte Activation, Male, Middle Aged, CD4-Positive T-Lymphocytes, T-Lymphocyte Subsets, Pulmonary Disease, Chronic Obstructive, T-Lymphocytes, Regulatory, Forkhead Transcription Factors, Transforming Growth Factor beta1, Immunomodulation
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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