CD8+CD57+ T cells exhibit distinct features in human non-small cell lung cancer

• DOI: 10.1136/jitc-2020-000639
• Publication Date: 2020-06-30T20:00:54Z
• Authors: Bing Huang; Rong Liu; Peiliang Wang; Zhiwei Yuan; Jianjian Yang; Hui Xiong; Ni Zhang; Qi Huang; Xiangning Fu; Wei Sun; Lequn Li
• Keywords: Interleukin-15; 0301 basic medicine; Lung Neoplasms; Programmed Cell Death 1 Receptor; Neoplasms. Tumors. Oncology. Including cancer and carcinogens; Basic Tumor Immunology; Cell Differentiation; CD8-Positive T-Lymphocytes; T-Lymphocytes, Regulatory; 3. Good health; Interferon-gamma; 03 medical and health sciences; Lymphocytes, Tumor-Infiltrating; Phenotype; CD28 Antigens; Carcinoma, Non-Small-Cell Lung; Case-Control Studies; Tumor Microenvironment; Humans; Lymph Nodes; Immunologic Memory; RC254-282

The repetitive antigen stimulation during chronic infection often leads to the accumulation of CD8+CD57+ T cells. These cells express high levels interferon-γ, granzyme B and perforin with elevated cytolytic effect, are considered as most potent for combating chronical viral infection. status in non-small cell lung cancer (NSCLC) has not been well defined. We used flow cytometry undertook a systemic approach examine frequency, immunophenotyping functional properties peripheral blood, tumor tissue corresponding normal tissue, draining lymph nodes, patients NSCLC. CD57+ expressed programmed death-1 (PD-1) all tested compartments were predominantly CD8+ blood displayed terminally differentiated phenotype defined by loss CD27 CD28 while expressing KLRG1. exhibited enhanced cytotoxic potencies impaired proliferative capability. Unlike significant proportion primary tumors CD28. lacked activity. activity these was also impaired. tissues shared similarities their counterparts rather than tumors. vast majority nodes positive unable produce B, but preserved. an inferior response PD-1 blockade compared CD8+CD57- counterparts. Interleukin (IL)-15 preferentially restored effector function Additionally, IL-15 able restore blood. Our data indicate that failure immune system fight progression could be result T-cell maturation into fully within microenvironment. Boosting might promote tumor-reactive preserving