Table 3.

Immunosenescence, inflammaging and cancer

Description	References
Chronic exposure to IL-1β, IL-6 and TNFα support tumor growth and metastasis spread	[177–179]
Senescent immune cells directly promote SASP	[180]
SASP promotes tumorigenesis and immunosuppressive behavior of immune cells	[182–184]
Essential factors for MDSC expansion, infiltration and activation (e.g., CSFs, CCL2, IL-1β) are increased in elderly	[186, 187]
Age-related expansion of immunosuppressive MDSCs impairs the clearance of senescent and cancerous cells, leading to tumor immune escape	[185]
Aged TAMs defect in anti-tumoral cytokine production and antigen presentation	[188–191]
N2 TANs resemble aged neutrophils for their reduced chemotactic and phagocytic capacity, and their impaired free radical production and apoptosis	[52, 193–196]
Several SASP molecules remodel the ECM, favoring immune and cancer cell trafficking and dissemination	[199, 200]
Aged immunosuppressive myeloid cells alter the ECM composition	[201]

IL interleukin, TNF tumor necrosis factor, SASP senescence-associated secretory phenotype, CSF colony-stimulating factor, CCL2 C–C motif chemokine ligand 2, MDSC myeloid-derived suppressor cell, TAM tumor-associated macrophage, TAN tumor-associated neutrophil, ECM extracellular matrix