Identification of Co-inhibitory Receptors PD-1 and TIM-3 on T Cells from Gastric Cancer Patients

Immunogenetics: Open Access is the Journal that discuss the branch of medical genetics that explores the relationship between the immune system and genetics. Here we explaining about gastric cancer patients from the study of researchers.

Gastric cancer (GC) is the second leading cause of cancer-related deaths worldwide, causing approximately 700,000 deaths annually. The five-year overall survival rates of advanced gastric cancer patients are still very poor when multimodal treatment strategies involving surgery, perioperative chemotherapy, and radiation are used. It has been demonstrated that a high density of cytotoxic T cells and memory T cells infiltrating the tumor is associated with a better disease outcome for gastric cancer patients. Adjuvant adoptive cell transfer (ACT) immunotherapy using autologous cytokine-induced killer (CIK) cells for gastric cancer patients is better than traditional chemotherapy alone. However, immunosuppression remains serious after surgery, chemotherapy and immunotherapy for gastric cancer. Tumor cells can induce increased expression of co-inhibitory receptors on TILs, leading to TIL exhaustion and decreasing the tumor-specific response. Thus, not all gastric cancer patients receiving ACT immunotherapy have an overall response. The co-inhibitory molecules upregulated on TILs in gastric cancer can be targeted to augment the host immune system, leading to improved survival [3]. Regrettably, until now, no systematically analysed data have shown a leading role for any particular co-inhibitory molecule in gastric cancer. Therefore, a comprehensive study of co-inhibitory molecule expression in gastric cancer is important both for fully understanding this disease and as a basis for developing new treatment options.

Over two decades of study, a class of immune checkpoint proteins, including cytotoxic T lymphocyte antigen-4 (CTLA-4), programmed death-1 (PD-1), T-cell immunoglobulin and mucin protein-3 (TIM-3), T cell Ig and ITIM domain (TIGIT), has been found to be crucial for regulating the responses of T cells. In the normal physiological state, immune checkpoints are critical for the maintenance of self-tolerance and for protecting normal tissues from damage by the immune system. Long term contact with tumor cells in the tumor micro-environment can induce tumor- specific lymphocytes to dysregulate the expression of certain immune checkpoint proteins, resulting in lymphocyte dysfunction [10]. Preclinical findings have shown that antibodies that block the inhibitory signals of checkpoint proteins enhance antigenspecific T cell responses. Thus, immune checkpoint proteins are potential targets for human anti-tumor immune therapy.

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