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Peer-reviewedCC BY 4.0Cancers

Immunosenescence and Inflammaging in the Pathogenesis of Non-Melanoma Skin Cancer

  • Martina Mihalj1,2
  • Nika Filipović Mioč3
  • Iva Sabljić4
  • Zdenka Šitum Čeprnja5
  • Stana Tokić6
  • Marija Buljan2,7
7 affiliations
  1. 1Department of Dermatology and Venereology, Osijek University Hospital, J. Huttlera 4, HR-31000 Osijek, Croatia
  2. 2Department of Dermatovenereology, Faculty of Medicine Josip Juraj Strossmayer University of Osijek, J. Huttlera 4, HR-31000 Osijek, Croatia
  3. 3Department of Dermatology and Venereology, Sestre Milosrdnice University Hospital Centre, Vinogradska 29, HR-10000 Zagreb, Croatia
  4. 4Department of dermatology and venereology, Vinkovci County General Hospital, Zvonarska ul. 57, HR-32100, Vinkovci, Croatia
  5. 5Department of dermatology and venereology, University Hospital Split, Šoltanska 2, HR-21000 Split, Croatia
  6. 6Department of Laboratory Medicine and Pharmacy, Faculty of Medicine, Josip Juraj Strossmayer University of Osijek, J. Huttlera 4, HR-31000 Osijek, Croatia
  7. 7School of Dental Medicine, University of Zagreb, Gundulićeva 5, HR-10000 Zagreb, Croatia
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Abstract

Non-melanoma skin cancer (NMSC) is the most frequently diagnosed malignancy worldwide, and its incidence rises disproportionately with age. While cumulative ultraviolet (UV) exposure is the dominant recognised risk factor, it does not fully account for the steep age-associated increase in NMSC, suggesting that additional, underrecognised mechanisms operate in older skin. This review synthesises evidence that immune senescence (the age-related remodelling of innate and adaptive immunity) is a central and partly modifiable driver of NMSC aetiopathogenesis. We first outline the classical risk factors and the epidemiological and economic burden of NMSC, and revisit the proposal to regard recurrent NMSC as a chronic disease. We then examine four interlocking, age-associated processes: the accumulation of senescent cells and their pro-inflammatory secretory phenotype (“inflammaging”) in the skin microenvironment; UV-induced suppression of cutaneous immune function; age-related dysbiosis of the skin microbiome and its impact on antitumour immunity; and the systemic decline of T-cell-mediated tumour immunosurveillance. We integrate these processes into a framework in which immune senescence contributes to the progression of accumulated cutaneous damage to overt malignancy, and consider the implications for prevention (including senotherapeutics, microbiome modulation, and immune-stratified surveillance) that extend beyond UV-directed measures alone.

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Cite

BibTeXRIS
BibTeX
@article{mihalj2026immunosenescence,
  title = {{Immunosenescence and Inflammaging in the Pathogenesis of Non-Melanoma Skin Cancer}},
  author = {Martina Mihalj and Nika Filipović Mioč and Iva Sabljić and Zdenka Šitum Čeprnja and Stana Tokić and Marija Buljan},
  journal = {Cancers},
  year = {2026},
  month = oct,
  doi = {10.3390/cancers18213481},
  url = {https://www.mdpi.com/2072-6694/18/21/3481},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Immunosenescence and Inflammaging in the Pathogenesis of Non-Melanoma Skin Cancer
AU  - Martina Mihalj
AU  - Nika Filipović Mioč
AU  - Iva Sabljić
AU  - Zdenka Šitum Čeprnja
AU  - Stana Tokić
AU  - Marija Buljan
PY  - 2026
DA  - 2026/10/28
JO  - Cancers
DO  - 10.3390/cancers18213481
UR  - https://www.mdpi.com/2072-6694/18/21/3481
AB  - Non-melanoma skin cancer (NMSC) is the most frequently diagnosed malignancy worldwide, and its incidence rises disproportionately with age. While cumulative ultraviolet (UV) exposure is the dominant recognised risk factor, it does not fully account for the steep age-associated increase in NMSC, suggesting that additional, underrecognised mechanisms operate in older skin. This review synthesises evidence that immune senescence (the age-related remodelling of innate and adaptive immunity) is a central and partly modifiable driver of NMSC aetiopathogenesis. We first outline the classical risk factors and the epidemiological and economic burden of NMSC, and revisit the proposal to regard recurrent NMSC as a chronic disease. We then examine four interlocking, age-associated processes: the accumulation of senescent cells and their pro-inflammatory secretory phenotype (“inflammaging”) in the skin microenvironment; UV-induced suppression of cutaneous immune function; age-related dysbiosis of the skin microbiome and its impact on antitumour immunity; and the systemic decline of T-cell-mediated tumour immunosurveillance. We integrate these processes into a framework in which immune senescence contributes to the progression of accumulated cutaneous damage to overt malignancy, and consider the implications for prevention (including senotherapeutics, microbiome modulation, and immune-stratified surveillance) that extend beyond UV-directed measures alone.
SN  - 2072-6694
ER  -