 |
Journal of IMAB - Annual Proceeding (Scientific Papers)
Publisher: Peytchinski, Gospodin Iliev
ISSN: 1312 773X (Online)
Issue: 2010, vol. 16, book 3
Subject Collection: Medicine
Page: 17 - 19
DOI: 10.5272/jimab.1632010_17-19
Online date: July 21, 2010
J of IMAB 2010; 16(3):17-19
IMMUNE RESPONSE IN MALIGNANT GLIOMA
Iliyan Koev1, E. Slavov2, D. Staykov1, K. Halacheva2, Sarafian V.1,
1) Clinic of Neurosurgery; Department of General and Clinical pathology, Department of Biology, Medical University-Plovdiv, Bulgaria;
2) Department of Molecular Biology, Medical genetics and Immunology, Trakia University, Stara Zagora, Bulgaria
ABSTRACT:
Objective: Malignant gliomas are primary brain tumors with excessive mortality and high resistance to chemotherapy and radiotherapy. The survival time for glioblastoma multiforme is about 6-12 months. As key pathogenetic mechanisms are recognized the massive necrosis, angiogenesis and hypoxia within the tumor, as well as the resistance to apoptosis. It is also suspected that altered immune response might contribute to the fatal clinical outcome.
The aim of the present study was to determine the immune status of patients with malignant gliomas.
Material and methods: Peripheral blood lymphocytes were collected preoperatively from 9 patients (aged 57-76) diagnosed as anaplastic astrocytoma grade III (n=4) and glioblastoma multiforme (n=5). The following lymphocyte populations were analyzed by flow cytometry: CD19+, CD3+, CD3+CD4+, CD3+CD8+, CD3-CD56+, CD3+CD56+, CD3+CD25+, CD8-CD11b+, CD8+CD11b+, CD8+CD11b-. The results obtained were compared to reference values for each cell population.
Results: No significant alterations were detected in CD19+, CD3+, CD3+CD4+, CD3+CD8+ cells, but the CD4/CD8 ratio was below the reference range in some cases. No obvious decrease in (CD3-CD56+) NK cells and (CD3-CD56+) NKT cells was observed in most patients. A reproducible phenomenon of increased CD8+CD11b+ and decreased CD8+CD11b- cells was noticed.
These preliminary results suggest that the immune response in patients with malignant glioma is seriously disregulated. The rapid clinical deterioration, relapses and high mortality could be at least partially explained with the suppressed activity of NK-cells which are the major cytotoxic antitumoral cells. The increase in the population of activated suppressor-effector cells also contributes to the unfavourable outcome in malignant brain tumors.
Conclusion: This pilot study reveals the presence of altered immune response in malignant gliomas and opens possibilities for prospective investigations concerning immune status and clinical outcome.
Key words: glioma, immune response, immune suppression.
- Download FULL TEXT /PDF 190 KB/
Please cite this article as: Koev I, Slavov E, Staykov D, Halacheva K, Sarafian V. IMMUNE RESPONSE IN MALIGNANT GLIOMA. J of IMAB. 2010; 16(3):17-19. doi: 10.5272/jimab.1632010_17-19.
REFERENCES:
1. Sathornsumetee S, Rich JN. New treatment strategies for malignant gliomas. Expert Rev Anticancer Ther, 2006; 6 : 1087-104. [ PubMed ]
2. Dix AR, Brooks WH, Roszman TL et al. Immune defects observed in patients with primary malignant brain tumors. J Neuroimmunol, 1999; 100:216-232.
3. Gustafson MP, Lin Y, New KC et al. Systemic immune suppression in glioblastoma: the interplay between CD14 +HLA-DRlo/neg monocytes, tumor factors, and dexamethasone. Neuro Oncol, 2010 Feb 23.
4. Chiu TL, Lin SZ, Hsieh WH et al. AAV2-mediated interleukin-12 in the treatment of malignant brain tumors through activation of NK cells. Int J Oncol, 2009; 35: 1361-1367.
5. Castriconi R, Daga A, Dondero A et al. NK cells recognize and kill human glioblastoma cells with stem cell-like properties. J Immunol, 2009;182:3530-3539. [CrossRef ]
6. Wei J, Barr J, Kong LY et al. Glioblastoma cancer-initiating cells inhibit T-cell proliferation and effector responses by the signal transducers and activators of transcription 3 pathway. Mol Cancer Ther, 2010; 9: 67-78. [ PubMed ]
7. Kempuraj D, Devi RS, Madhappan B et al. T lymphocyte subsets and immunoglobulins in intracranial tumor patients before and after treatment, and based on histological type of tumors. Int J Immunopathol Pharmacol, 2004; 17 : 57-64.
8. Waziri A. Glioblastoma-derived mechanisms of systemic immunosuppression. Neurosurg Clin N Am, 2010; 21: 31-42. [ PubMed ]
9. Ichinose M, Masuoka J, Shiraishi T et al. Fas ligand expression and depletion of T-cell infiltration in astrocytic tumors. Brain Tumor Pathol, 2001; 18 : 37-42. [ PubMed ]
10. Parsa AT, Waldron JS, Panner A et al. Loss of tumor suppressor PTEN function increases B7-H1 expression and immunoresistance in glioma. Nat Med, 2007; 13 : 84-88. [ CrossRef ]