Table 5.

Impact of the antigen presenting pathway and T cell receptor (TCR) repertoire on clinical outcome with immune-checkpoint inhibitors (ICI).

Reference	Author	Tumor Entity	Findings
[122]	McGranahan et al.	NSCLC, melanoma	↑ PFS/OS with high clonal neoantigen burden + low intratumoral neoantigen heterogeneity
[152]	Gettinger et al.	NSCLC	β2m loss drives resistance to ICI
[153]	Sade-Feldman et al.	melanoma	β2m LOH drives resistance to ICI
[16]	Chowell et al.	solid tumors	↑ OS with maximal heterozygosity at HLA-I loci
[17]	Goodman et al.	solid tumors	↑ ORR/PFS/OS prediction by MHC I genotype analysis among TMBhigh tumors
[159]	Hopkins et al.	pancreatic ductal adenocarcinoma	↑ OS with low baseline TCR clonality before anti-CTLA-4 Tx ↑ OS with higher number of expanded TCR clones following anti-CTLA-4 Tx
[161]	Hogan et al.	melanoma	↑ ORR/PFS with low baseline TCR clonality in anti-CTLA-4 treated patients ↑ ORR/PFS with high baseline TCR clonality in anti-PD-1 treated patients
[162]	Ghorani et al.	NSCLC, melanoma	↑ PFS/OS prediction by assessment of differential binding affinity of mutated peptides for MHC I compared to TMB or tumor neoantigen burden
[147]	Luksza et al.	NSCLC, melanoma	OS discrimination based on neoantigen MHC I binding affinity and T cell recognition
[165]	Snyder et al.	melanoma	OS prediction based on neoantigen MHC I binding probability, TCR binding probability, HLA genotype and epitope-homology analysis

PFS: progression-free survival; OS: overall survival; MHC: major histocompatibility complex; TCR: T cell receptor; HLA: human leukocyte antigen; ORR: overall response rate; NSCLC: non-small cell lung cancer; β2m: beta-2 microglobulin; ICI: immune-checkpoint inhibitor; LOH: loss of heterzygosity; TMB: tumor mutational burden; CTLA-4: cytotoxic T-lymphocyte protein 4; Tx: therapy; PD-1: programmed cell death protein 1;.