Diabetes can impact cellular immunity in solid tumors

Abstract

Cancer and type 2 diabetes (T2D) are prevalent diseases in both developed and developing countries, and many patients with T2D also develop solid tumors. Patients with diabetes and certain solid tumors show increased numbers of macrophages with a suppressive phenotype in their tumor tissue, in contrast to those without diabetes. T2D can also induce immunosuppressive properties in dendritic cells (DCs) and attract more myeloid-derived suppressor cells (MDSCs) to the tumor tissue. Effector CD8 + T cells and natural killer (NK) cells may display reduced activity and more suppressed phenotypes in the periphery and tumor tissues of diabetic patients and mice. T2D could increase the expression of CD8 + T cell exhaustion markers, which are associated with decreased antitumor immunity. Drugs prescribed for T2D, such as metformin, can positively influence antitumor therapies. We propose that examining the connections between T2D and tumor immunology may provide advantages for managing each condition, either separately or when treated together in the same patient. Tumors and type 2 diabetes (T2D) pose major global public health challenges. Recently, immunotherapy has considerably improved treatment outcomes for certain patients with cancer. Further progress has been possible due to a better understanding of immune mechanisms within the tumor microenvironment (TME). While we recognize that T2D patients face problems with immunity, we are beginning to uncover how diabetes can influence antitumor responses as well as the effectiveness of cancer immunotherapies. Cancer is increasingly prevalent worldwide, often coexisting with type 2 diabetes (T2D). Recent breakthroughs reveal the immune system’s pivotal role in eliminating tumors and how the metabolic environment, such as glucose availability, affects antitumor immunity. Diabetes is known to dysregulate both innate and adaptive immune responses, while cancer creates an immunosuppressive microenvironment. We hypothesize that diabetes in cancer subjects may exacerbate this immunosuppression. Here, we examine the current understanding of the interplay between T2D and solid tumors and the associated challenges. Despite inconsistencies in data from mouse models and human tissues, evidence suggests that T2D can impact the antitumor response. Possible mechanisms may involve myeloid cells, inducing local immunosuppression and impairing antigen presentation, and certain lymphoid cell populations, exhibiting exhaustion. Cancer is increasingly prevalent worldwide, often coexisting with type 2 diabetes (T2D). Recent breakthroughs reveal the immune system’s pivotal role in eliminating tumors and how the metabolic environment, such as glucose availability, affects antitumor immunity. Diabetes is known to dysregulate both innate and adaptive immune responses, while cancer creates an immunosuppressive microenvironment. We hypothesize that diabetes in cancer subjects may exacerbate this immunosuppression. Here, we examine the current understanding of the interplay between T2D and solid tumors and the associated challenges. Despite inconsistencies in data from mouse models and human tissues, evidence suggests that T2D can impact the antitumor response. Possible mechanisms may involve myeloid cells, inducing local immunosuppression and impairing antigen presentation, and certain lymphoid cell populations, exhibiting exhaustion.

Topics & Concepts