Immune checkpoint inhibitors (ICIs) are widely sought after for the treatment of different types of cancers. Unfortunately, only 20%–30% patients with cancer respond to ICI treatment. Although the factors that influence the positive or negative response to ICI treatment are poorly understood, the strength of the ICIs' antitumor response by TILs is thought to play a key role. Hence, investigating the antitumor response induced by ICIs might provide insights into their underlying mechanisms.
tumor-infiltrating T-lymphocytes are the primary effector cells that lead to antitumor response. TILs are composed of various T-cell clones that are determined by their unique T-cell receptor genes. A diverse TCR repertoire can indicate the existence of TIL population that can recognize multiple tumor-antigens. However, the way that the diversity of tumor-reactive clones influences their antitumor effects remains unclear.
First, the team analyzed the TCR repertoire of B16F10 and Lewis lung carcinoma tumor bearing mice, treated with the ICIs—anti-PD-L1 anti-CD4, and a combination of both antibodies. They observed that the antibodies increased the mobilization of overlapping T-cell clones in draining lymph nodes and tumors.
The team further found that increase of the polyclonal fraction of OL repertoire due to ICI administration was correlated with the tumor volume after treatment, a parameter reflecting an antitumor effect. Moreover, single-cell RNA and TCR sequencing exhibited that the polyclonal dLN-tumor OL clones were rich in progenitor exhausted T cells .
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