Cited by 262Osteoarthritis Treatment and MechanismsTelomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model Organisms

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IL-17 and immunologically induced senescence regulate response to injury in osteoarthritis

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Faust, Heather J., Zhang, Hong, Han, Jin, Wolf, Matthew T., Jeon, Ok Hee, Sadtler, Kaitlyn, Peña, Alexis N., Chung, Liam, Maestas, David R., Tam, Ada J., Pardoll, Drew M., Campisi, Judith, Housseau, Franck, Zhou, Daohong, Bingham, Clifton O., Elisseeff, Jennifer H.·2020·Journal of Clinical Investigation

DOI 10.1172/jci134091PMC PMC7524483

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Abstract

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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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: Faust, Heather J.
Zhang, Hong
Han, Jin
Wolf, Matthew T.
Jeon, Ok Hee
Sadtler, Kaitlyn
Peña, Alexis N.
Chung, Liam
Maestas, David R.
Tam, Ada J.
Pardoll, Drew M.
Campisi, Judith
Housseau, Franck
Zhou, Daohong
Bingham, Clifton O.
Elisseeff, Jennifer H.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2020-09-21
Volume: 130
Issue: 10
Pages: 5493-5507
ISSN: 0021-9738 (ISSN-L)
1558-8238
DOI: 10.1172/jci134091
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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IL-17 and immunologically induced senescence regulate response to injury in osteoarthritis

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