Targeting Immune Modulators in Glioma While Avoiding Autoimmune Conditions.
Lynn BitarUlrike SchumannRenate KönigFrauke ZippMirko H H SchmidtPublished in: Cancers (2021)
Communication signals and signaling pathways are often studied in different physiological systems. However, it has become abundantly clear that the immune system is not self-regulated, but functions in close association with the nervous system. The neural-immune interface is complex; its balance determines cancer progression, as well as autoimmune disorders. Immunotherapy remains a promising approach in the context of glioblastoma multiforme (GBM). The primary obstacle to finding effective therapies is the potent immunosuppression induced by GBM. Anti-inflammatory cytokines, induction of regulatory T cells, and the expression of immune checkpoint molecules are the key mediators for immunosuppression in the tumor microenvironment. Immune checkpoint molecules are ligand-receptor pairs that exert inhibitory or stimulatory effects on immune responses. In the past decade, they have been extensively studied in preclinical and clinical trials in diseases such as cancer or autoimmune diseases in which the immune system has failed to maintain homeostasis. In this review, we will discuss promising immune-modulatory targets that are in the focus of current clinical research in glioblastoma, but are also in the precarious position of potentially becoming starting points for the development of autoimmune diseases like multiple sclerosis.
Keyphrases
- multiple sclerosis
- regulatory t cells
- papillary thyroid
- immune response
- clinical trial
- squamous cell
- dendritic cells
- signaling pathway
- small molecule
- young adults
- binding protein
- white matter
- lymph node metastasis
- transcription factor
- multidrug resistant
- stem cells
- toll like receptor
- childhood cancer
- epithelial mesenchymal transition
- cell therapy
- squamous cell carcinoma
- pi k akt
- cancer therapy