作者: Terhi Karpanen , Johanna Olweus
关键词: Minor histocompatibility antigen 、 T cell 、 Cancer immunotherapy 、 Immunotherapy 、 Myeloid leukemia 、 Human leukocyte antigen 、 Priming (immunology) 、 Donor lymphocyte infusion 、 Immunology 、 Medicine
摘要: T cells can recognize peptides encoded by mutated genes, but analysis of tumor-infiltrating lymphocytes suggests that very few neoantigens spontaneously elicit T-cell responses. This may be an important reason why immune checkpoint inhibitors are mainly effective in tumors with a high mutational burden. Reasons for clinically insufficient responses to might inefficient priming, inhibition, or deletion the cognate cells. Responses dramatically improved cancer immunotherapy such as often temporary effects. By contrast, from human leukocyte antigen (HLA)-matched donors cure diseases chronic myeloid leukemia. The therapeutic effect is mediated donor recognizing polymorphic which and patient disparate, presented on self-HLA. Donor repertoires unbiased immunosuppressive environment tumor. A recent study demonstrated healthy individuals able respond ignored melanoma patients. In this review, we discuss possible reasons escape host how these limitations overcome utilization donor-derived facilitate rational design neoantigen-targeted immunotherapy.