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IL-17 and immunologically induced senescence regulate response to injury in osteoarthritis
Open accessAbstract
Senescent cells (SnCs) are implicated in the pathogenesis of age-related diseases including osteoarthritis (OA), in part via expression of a senescence-associated secretory phenotype (SASP) that includes immunologically relevant factors and cytokines. In a model of posttraumatic OA (PTOA), anterior cruciate ligament transection (ACLT) induced a type 17 immune response in the articular compartment and draining inguinal lymph nodes (LNs) that paralleled expression of the senescence marker p16INK4a (Cdkn2a) and p21 (Cdkn1a). Innate lymphoid cells, γδ+ T cells, and CD4+ T cells contributed to IL-17 expression. Intra-articular injection of IL-17-neutralizing antibody reduced joint degeneration and decreased expression of the senescence marker Cdkn1a. Local and systemic senolysis was required to attenuate tissue damage in aged animals and was associated with decreased IL-17 and increased IL-4 expression in the articular joint and draining LNs. In vitro, we found that Th17 cells induced senescence in fibroblasts and that SnCs skewed naive T cells toward Th17 or Th1, depending on the presence of TGF-β. The SASP profile of the inflammation-induced SnCs included altered Wnt signaling, tissue remodeling, and cell-cycle pathways not previously implicated in senescence. These findings provide molecular targets and mechanisms for senescence induction and therapeutic strategies to support tissue healing in an aged environment.
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“in a mouse model of osteoarthritis, a combination of UBX0101 with N was necessary to restore aged joint structure131.”
From Cellular senescence and senolytics: the path to the clinic (2022) · cites this paper as [131]
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Metadata
- Authors
- Faust, H. J., Zhang, H., Han, J., Wolf, M. T., Jeon, O. H., Sadtler, K., Peña, A. N., Chung, L., Maestas, D. R., Tam, A. J., Pardoll, D. M., Campisi, J., Housseau, F., Zhou, D., Bingham, C. O., & Elisseeff, J. H.
- Affiliations
- Johns Hopkins University (US)
- Korea University (KR)
- Buck Institute for Research on Aging (US)
- University of Florida (US)
- Corresponding author
- Elisseeff, Jennifer H.
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2020-09-21
- Volume
- 130
- Issue
- 10
- Pages
- 5493-5507
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC7524483
- OpenAlex
- W3087504560
- Cited by
- 260
- References
- 80
- Citations by year
- 2026: 33 · 2025: 56 · 2024: 57 · 2023: 46 · 2022: 43 · 2021: 24 · 2020: 1
- FWCI
- 21.64
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- other-oa
- Locations
- Journal of Clinical Investigation (publishedVersion, other-oa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense (W81XWH-17-1-0627, W81XWH-14-1-0285)
- National Institutes of Health (R01CA211963, R01CA219836)
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- osteoarthritis, senescence-associated secretory phenotype, senescence, IL-17, Th17 cells, post-traumatic osteoarthritis, anterior cruciate ligament transection, senolysis, p16INK4a, p21, innate lymphoid cells, γδ T cells, CD4+ T cells, TGF-beta, Wnt signaling, joint degeneration, aging, tissue repair
- MeSH terms
- Aging, Animals, Arthritis, Experimental, Disease Models, Animal, Humans, Immunity, Innate, Male, Mice, Inbred C57BL, Osteoarthritis, Cellular Senescence, Mice, Knockout, Receptors, Interleukin-4, Interleukin-17, Regenerative Medicine, Mice, Adaptive Immunity, Th17 Cells
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