Table 1 Age-related immune phenotypes and potential therapeutic 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

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