Table 2.

Factors related to the efficacy of ICBs.

Classification	Biomarkers	Influence
Clinical-relevant factors	Age	The elderly patients lack response to ICBs.
	Gender	Male patients respond better to ICBs.
	Diet	Obesity and improved FA catabolism improve anti-PD therapy.
	Viral infection	MCV and EBV infected patients respond better to anti-PD therapy.
Tumor autonomous mechanisms	Tumor mutational/neoantigen load	High mutational/neoantigen loads improve efficacy of ICBs
	PD-L1 expression	High PD-L1 expression improves anti-PD therapy
Tumor microenvironment	Cells	Increased TILs improve response to ICBs, while Tregs and MDSCs impair the efficacy.
	Immunoregulatory pathways	Inhibition of TH1 chemokines, CD28/B7, IFN and activation of TGFβ, TIM3 lead to resistance to PD blockades.
Host-related factors	Peripheral blood markers	Increased eosinophils, lymphocytes, monocytes and low LDH levels improve response to PD blockades.
	MHC class I	Impaired MHC class I molecules lead to resistance to anti-PD therapy
	TCR repertoire	Less diverse T cell repertoire improves response to anti-PD
	The gut microbiota	Bacteroides species facilitate anti-CTLA, more diversified bacteria, such as Bifidobacterium, Akkermansia muciniphila, Ruminococcaceae bacteria, facilitate anti-PD.