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Buerki et al. Neuroimmunol Neuroinflammation 2016;3:198-200 Neuroimmunology and
DOI: 10.20517/2347-8659.2016.41
Neuroinflammation

www.nnjournal.net
Editorial Open Access

Serum immuno-biomarkers in gliomas

Robin A. Buerki, Rimas V. Lukas

Department of Neurology, University of Chicago, Chicago, IL 60637, USA.
Correspondence to: Dr. Rimas V. Lukas, Department of Neurology, University of Chicago, 5841 S. Maryland Avenue, MC 2030, Chicago, IL
60637, USA. E-mail: rlukas@neurology.bsd.uchicago.edu
How to cite this article: Buerki RA, Lukas RV. Serum immuno-biomarkers in gliomas. Neuroimmunol Neuroinflammation 2016;3:198-200.
Article history: Received: 29-08-2016 Accepted: 31-08-2016 Published: 26-09-2016

Gliomas comprise the majority of malignant primary and survival and may be clinical indicators of which
brain tumors in adults and remain a devastating patients are likely to benefit in current and future
diagnosis. Despite therapeutic advances, median immunotherapeutic trials.
[1]
survival in the radiation and temozolamide era for
the most common and most aggressive tumor type, In the first article, a prospective, single-institution,
glioblastoma (GBM), is 14-20 months and tumor observational study of GBM patients treated with
recurrence is universal. A promising new direction tumor resection followed by chemotherapy and
[2]
[8]
to combat GBM is immunotherapy, which emerged radiation (under the Stupp regimen ) for up to 1
from intensive research revealing that although highly year, Alexiou et al. demonstrate a lower neutrophil-
[6]
immunogenic, GBM actively suppresses the host anti- to-lymphocyte ratio (NLR) to be an independent
tumoral immune response throughout a variety of prognostic predictor of survival. Using a cutoff value of
mechanisms (reviewed in and ). Current therapies NLR < 4.7, both overall survival (OS) and progression-
[3]
[4]
to abrogate tumor immunosuppression and unleash free survival (PFS) were significantly longer. This study
T-cell mediated killing of GBM include: inhibitors supports other work which also revealed NLR as an
[9]
of immune-checkpoints that are exploited by GBM independent prognostic predictor using a cut-off value
to enhance tumor survival (therapeutic antibodies of 4, and is consistent with other studies demonstrating
against CTLA-4 and PD-1, which are overexpressed the prognostic value of NLR in other tumor types.
in tumor-infiltrating lymphocytes, and against PD-L1, Importantly, both studies examined the NLR prior to
which is overexpressed on GBM cells and tumor- administration of corticosteroids as corticosteroid use
infiltrating immune cells); vaccination strategies is itself an independent negative prognostic indicator,
against single or multiple tumor-associated peptides; regardless of other chemo- or radiotherapy given. [10,11]
infusion of autologous adoptive CAR T-cells primed
against GBM-specific antigens; and inhibition of the Extensive work has explored the role of tumor-
immunomodulatory indoleamine 2,3-dioxygenase infiltrating lymphocytes (TILs) in glioma, both as
(IDO) pathway, which is also overexpressed in markers of tumor aggressiveness and with patient
GBM. [3,5] Recent work by Alexiou et al. [6,7] published in survival, namely that infiltration of cytotoxic CD8+ T
this journal contributes to the use of immune mediators lymphocytes are decreased and CD4+ and CD4+/
as prognostic surrogates of GBM aggressiveness CD25+/FoxP3+ (Treg) populations of T lymphocytes

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