Overview of Cellular Immunotherapy for Patients with Glioblastoma

Abstract

High grade gliomas (HGG) including glioblastomas (GBM) are the most common and devastating primary brain tumours. Despite important progresses in GBM treatment that currently includes surgery combined to radio- and chemotherapy, GBM patients' prognosis remains very poor. Immunotherapy is one of the new promising therapeutic approaches that can specifically target tumour cells. Such an approach could also maintain long term antitumour responses without inducing neurologic defects. Since the past 25 years, adoptive and active immunotherapies using lymphokine-activated killer cells, cytotoxic T cells, tumour-infiltrating lymphocytes, autologous tumour cells, and dendritic cells have been tested in phase I/II clinical trials with HGG patients. This paper inventories these cellular immunotherapeutic strategies and discusses their efficacy, limits, and future perspectives for optimizing the treatment to achieve clinical benefits for GBM patients.

Stereotaxic administrations of allogeneic human Vγ9Vδ2 T cells efficiently control the development of human glioblastoma brain tumors

“…8 Using orthotopic xenograft mouse models of human GBM cells from either commercially available cell lines or primary GBM cells, our study indicates that stereotaxic administrations of allogeneic ex vivo-amplified human Vg9Vd2 T cell effectors plus zoledronate efficiently eradicate brain tumors.…”

“…In this context, immunotherapies represent effective therapeutic options with minimal toxicities. 8 Cellular immunotherapies have been explored 9 and could allow the elimination of deep brain infiltrative tumor cells. GBM-specific tumor antigens (Ag) recognized by ab T cells, 10 stress-induced molecules activating gd T cells or specific surface molecules that can trigger ADCC have been identified and proposed for effective immunotherapies in GBM.…”

The therapeutic potential of natural killer cells to target medulloblastoma

“…Some central nervous system (CNS) tumors such as glioblastoma multiforme highly express MHC class I molecules; thus, NK cells cannot recognize tumor cells by inhibitory receptors because of the presence of inhibitory signals [18]. MB cells downregulate MHC class I molecule expression, however, resulting in the absence of inhibitory signals mediated by KIRs expressed by NK cells.…”

The Effects of All-Trans Retinoic Acid on Vasculogenic Mimicry Formation Ability in CD133+ Glioma Stem Cells and Its Mechanisms

“…However, the majority of glioblastoma patients, particularly the elderly, succumb to the disease within a year [3], and this is not satisfactory. Thus, more effective treatment strategies which contain molecularly targeted therapies [4], immunotherapy [5], and gene therapy [6] are under investigation for patients with glioma [7].…”