期刊
FUTURE ONCOLOGY
卷 4, 期 3, 页码 433-442出版社
FUTURE MEDICINE LTD
DOI: 10.2217/14796694.4.3.433
关键词
CD25; CTLA-4; cytotoxic T-lymphocyte antigen 4; Foxp3; GITR; glioblastoma multiforme; glioma; glucocorticoid-induced tumor necrosis factor receptor-related protein; immunosuppression; regulatory T cells; TGF-beta; transforming growth factor-beta
类别
资金
- NATIONAL CANCER INSTITUTE [P50CA108786, R21CA132891] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS067980] Funding Source: NIH RePORTER
- NCI NIH HHS [P50 CA108786, R21 CA132891, R01 CA235612] Funding Source: Medline
- NINDS NIH HHS [R21 NS067980] Funding Source: Medline
Despite maximal therapy, malignant gliomas have a very poor prognosis. Patients with glioma express significant immune defects, including CD4 lymphopenia, increased fractions of regulatory T cells in peripheral blood and shifts in cytokine profiles from Th1 to Th2. Recent studies have focused on ways to combat immunosuppression in patients with glioma as well as in animal models for glioma. We concentrate on two specific ways to combat immunosuppression: inhibition of TGF-beta signaling and modulation of regulatory T cells. TGF-beta signaling can be interrupted by antisense oligonucleotide technology, TGF-beta receptor I kinase inhibitors, soluble TGF-beta receptors and antibodies against TGF-beta. Regulatory T cells have been targeted with antibodies against T-cell markers, such as CD25, CTLA-4 and GITR. In addition, vaccination against Foxp3 has been explored. The results of these studies have been encouraging; combating immunosuppression may be one key to improving prognosis in malignant glioma.
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