Aging type | Changes in phenotypes | Potential consequences |
---|---|---|
Innate immunity | (1) decrease chemotaxis; (2) decrease phagocytosis of debris; (3) decrease antigen presentation ability | (1) inhibit the activation of tumor-specific CD8 + cytotoxic T cells; (2) decrease the diversity of tumor-specific CD8 + cytotoxic T cells |
Immunosenescence | Â | Â |
B cells | (1) increase precursor cells; (2) increase proinflammatory B cells (TNF-α +): (3) inhibit antibody production, diversity and avidity | (1) decrease antibody production and diversity; (2) inhibit response to novel tumor antigens; (3) promote inflammation and autoantibody production; (4) increase the possibility of immune-related AEs |
T cells | (1) increase naive T cells; (2) increase Tregs; (3) decrease T-cell repertoire | (1) decrease recognition and responses to novel tumor antigen; (2) increase antigen recall due to large amount of memory T cells |
Bone marrow | (1) increase myeloid lymphoid progenitors; (2) inhibit B-cell maturation | decrease potential adoptive immune response to novel tumor antigens |
Thymus | (1) increase epithelial cell attrition; (2) reduce IL-7; (3) decrease mature T-cell production | (1) decrease the amount of naive T cells; (2) decrease the possibility to recognize novel tumor antigens |
Cellular senescence | (1) decrease telomere length; (2) inhibit cell proliferation; (3) increase expression of cell cycle inhibitors (p16INK4a and P21CIP/KIP); (4) increase proinflammatory cytokine and matrix remodeling factors | (1) decrease the amount of responding B and T cells; (2) promote cancer metastasis; (3) increase the recruitment of immunosuppressive cells (Tregs, MDSCs) |
Inflammaging | (1) increase chronic inflammation; (2) increase the level of IL-6, IL-8, IL-18, TNF-α, CRP | (1) increase tumor mutagenesis via inflammatory mediators; (2) inhibit cytokine production in response to tumor antigens |