TY - JOUR
T1 - Understanding the Immune-Stroma Microenvironment in B Cell Malignancies for Effective Immunotherapy
AU - Apollonio, Benedetta
AU - Ioannou, Nikolaos
AU - Papazoglou, Despoina
AU - Ramsay, Alan G.
N1 - Publisher Copyright:
© Copyright © 2021 Apollonio, Ioannou, Papazoglou and Ramsay.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2021/3/25
Y1 - 2021/3/25
N2 - Cancers, including lymphomas, develop in complex tissue environments where malignant cells actively promote the creation of a pro-tumoral niche that suppresses effective anti-tumor effector T cell responses. Research is revealing that the tumor microenvironment (TME) differs between different types of lymphoma, covering inflamed environments, as exemplified by Hodgkin lymphoma, to non-inflamed TMEs as seen in chronic lymphocytic leukemia (CLL) or diffuse-large B-cell lymphoma (DLBCL). In this review we consider how T cells and interferon-driven inflammatory signaling contribute to the regulation of anti-tumor immune responses, as well as sensitivity to anti-PD-1 immune checkpoint blockade immunotherapy. We discuss tumor intrinsic and extrinsic mechanisms critical to anti-tumor immune responses, as well as sensitivity to immunotherapies, before adding an additional layer of complexity within the TME: the immunoregulatory role of non-hematopoietic stromal cells that co-evolve with tumors. Studying the intricate interactions between the immune-stroma lymphoma TME should help to design next-generation immunotherapies and combination treatment strategies to overcome complex TME-driven immune suppression.
AB - Cancers, including lymphomas, develop in complex tissue environments where malignant cells actively promote the creation of a pro-tumoral niche that suppresses effective anti-tumor effector T cell responses. Research is revealing that the tumor microenvironment (TME) differs between different types of lymphoma, covering inflamed environments, as exemplified by Hodgkin lymphoma, to non-inflamed TMEs as seen in chronic lymphocytic leukemia (CLL) or diffuse-large B-cell lymphoma (DLBCL). In this review we consider how T cells and interferon-driven inflammatory signaling contribute to the regulation of anti-tumor immune responses, as well as sensitivity to anti-PD-1 immune checkpoint blockade immunotherapy. We discuss tumor intrinsic and extrinsic mechanisms critical to anti-tumor immune responses, as well as sensitivity to immunotherapies, before adding an additional layer of complexity within the TME: the immunoregulatory role of non-hematopoietic stromal cells that co-evolve with tumors. Studying the intricate interactions between the immune-stroma lymphoma TME should help to design next-generation immunotherapies and combination treatment strategies to overcome complex TME-driven immune suppression.
KW - CAR T
KW - anti-PD1
KW - immunotherapy
KW - interferon
KW - lymphoma
KW - stroma
KW - T cells
KW - tumor microenviroment
UR - http://www.scopus.com/inward/record.url?scp=85103779384&partnerID=8YFLogxK
U2 - 10.3389/fonc.2021.626818
DO - 10.3389/fonc.2021.626818
M3 - Review article
AN - SCOPUS:85103779384
SN - 2234-943X
VL - 11
JO - Frontiers in oncology
JF - Frontiers in oncology
M1 - 626818
ER -