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Review ARticleThe tumor microenvironment comprises of multiple distinct immune cells and checkpoint markers, which includes: CTLA-4, dendritic cells (DC), indoleamine 2,3-dioxygenase (IDO), interleukin (IL), lymphocyte activation gene 3 (LAG3), major histocompatibility complex (MHC), PD-1, PD-L1, PD-L2, T cell receptor (TCR), tumor necrosis factor (TNF), T cell and immunoglobulin mucin domain-3 (TIM-3), regulatory T cells (Treg), macrophages, natural killer (NK) cells, neutrophils, B lymphocytes, myeloid-derived suppressor cells (MDSCs), extracellular matrix (ECM), pericytes, and adipocytes. 7 Immune checkpoints can enhance antitumor immunity by their ability to control the interactions between antigen-presenting cells, T cells, or tumor cells.Their therapeutic aim is to overcome immune suppression within the TME and restore the cytotoxic T-cell response necessary for tumor destruction. 7 Regulatory T cells (Tregs) modulate these processes and help maintain immune homeostasis, although they can also limit antitumor responses. 8 Immune checkpoints, such as PD-1 and CTLA-4, function to prevent autoimmunity but can also be utilized by tumor cells to avoid immune destruction.Tumors expressing PD-L1 can deactivate T cells by binding to PD-1 receptors, forming a pathway that can be targeted by current immunotherapeutic drugs. 9
Obiekwe et al. (Fri,) studied this question.