title: Immune checkpoint receptors in cancer: redundant by design?
abstract: Co-inhibitory receptors expressed on activated immune cells function to regulate T cell tolerance to self-antigens, also serving by tumor cells to escape from eradication by the host immune system. Therefore, blockade of immune checkpoint receptors (ICR) has become a promising immunotherapeutic strategy for treatment of a wide variety of cancers. However, blockade of one of the immune checkpoint receptors alone is often not sufficiently effective; co-blockade shows synergic effects in reversing immunosuppression. In this article, we summarize the expression patterns, mechanisms of action of different ICRs as well as the stages and sites they function in, and discuss how they execute non-redundant suppressive effects in anti-tumor immunity.
authors.affiliation: Institute for Immunology and School of Medicine, Tsinghua University, Beijing 100084, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.affiliation: Institute for Immunology and School of Medicine, Tsinghua University, Beijing 100084, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Ni
authors.affiliation: Institute for Immunology and School of Medicine, Tsinghua University, Beijing 100084, China. Electronic address: chendong@tsinghua.edu.cn.
authors.forename: Chen
authors.initials: C
authors.lastname: Dong
mesh_terms: D000818:Animals; D006801:Humans; D007108:Immune Tolerance; D007111:Immunity, Cellular; D009369:Neoplasms / Q000276:immunology* / Q000473:pathology; D011971:Receptors, Immunologic / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology* / Q000473:pathology
chemical_list: D011971:Receptors, Immunologic