IL-6-mediated environmental conditioning of defective Th1 differentiation dampens antitumour immune responses in old age
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Decline in immune function and inflammation concomitantly develop with ageing. Here we focus on the impact of this inflammatory environment on T cells, and demonstrate that in contrast to successful tumour elimination in young mice, replenishment of tumour-specific CD4+ T cells fails to induce tumour regression in aged hosts. The impaired antitumour effect of CD4+ T cells with their defective Th1 differentiation in an aged environment is restored by interleukin (IL)-6 blockade or IL-6 deficiency. IL-6 blockade also restores the impaired ability of CD4+ T cells to promote CD8+ T-cell-dependent tumour elimination in aged mice, which requires IFN-γ. Furthermore, IL-6-stimulated production of IL-4/IL-21 through c-Maf induction is responsible for impaired Th1 differentiation. IL-6 also contributes to IL-10 production from CD4+ T cells in aged mice, causing attenuated responses of CD8+ T cells. These findings suggest that IL-6 serves as an extrinsic factor counteracting CD4+ T-cell-mediated immunity against tumour in old age.
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Systemic low-grade chronic inflammation that develops with age, referred to as inflammaging, appears to affect the phenotype and function of CD4 T cells.
“In addition, systemic low-grade chronic inflammation that develops with age, referred to as “inflammaging”, also appears to affect the phenotype and function of CD4 T cells (14, 15).”
From Aging promotes reorganization of the CD4 T cell landscape toward extreme regulatory and effector phenotypes (2019) · cites this paper as [14]
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Additional file 1 of Telomerase deficiency reflects age-associated changes in CD4+ T cells
Matthe, D. M., Thoma, O.-M., Sperka, T., Neurath, M. F., & Waldner, M. J. (2022) · Figshare · doi:10.6084/m9.figshare.19408073
- Authors
- Tsukamoto, H., Senju, S., Matsumura, K., Swain, S. L., & Nishimura, Y.
- Affiliations
- Kumamoto University (JP)
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Tsukamoto, Hirotake
- Nishimura, Yasuharu
- Venue
- Nature Communications
- Published
- 2015-04-07
- Volume
- 6
- Issue
- 1
- Pages
- 6702-6702
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4396369
- OpenAlex
- W2020612723
- Cited by
- 104
- References
- 55
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 9 · 2023: 11 · 2022: 12 · 2021: 8 · 2020: 12 · 2019: 8 · 2018: 6 · 2017: 11 · 2016: 4 · 2015: 3
- FWCI
- 3.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Yasuda Memorial Medical Foundation
- Japan Society for the Promotion of Science (15H04311, 26430165, 24700994)
- National Institute on Aging (P01AG021600)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- interleukin-6, aging, Th1 differentiation, CD4+ T cells, antitumor immunity, tumor surveillance, IL-6 inhibition, IL-10, c-Maf, interferon-gamma, CD8+ T cells, immunosenescence, tumor-specific T cells
- MeSH terms
- Interleukin-21, Aging, Animals, Cell Differentiation, Fibrosarcoma, Immunity, Cellular, Interferon-gamma, Interleukins, Mice, Inbred C57BL, Neoplasm Transplantation, CD4-Positive T-Lymphocytes, Interleukin-4, Interleukin-6, Interleukin-10, CD8-Positive T-Lymphocytes, Th1 Cells, Tumor Escape, Proto-Oncogene Proteins c-maf, Mice
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