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B7-H4(B7x)-Mediated Cross-talk between Glioma-Initiating Cells and Macrophages via the IL6/JAK/STAT3 Pathway Lead to Poor Prognosis in Glioma Patients
Clinical cancer research, 2016-06, Vol.22 (11), p.2778-2790
Yao, Yu
Ye, Hongxing
Qi, Zengxin
Mo, Lianjie
Yue, Qi
Baral, Aparajita
Hoon, Dave S B
Vera, Juan Carlos
Heiss, John D
Chen, Clark C
Zhang, Jianmin
Jin, Kunlin
Wang, Ying
Zang, Xingxing
Mao, Ying
Zhou, Liangfu
2016
Volltextzugriff (PDF)
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Autor(en) / Beteiligte
Yao, Yu
Ye, Hongxing
Qi, Zengxin
Mo, Lianjie
Yue, Qi
Baral, Aparajita
Hoon, Dave S B
Vera, Juan Carlos
Heiss, John D
Chen, Clark C
Zhang, Jianmin
Jin, Kunlin
Wang, Ying
Zang, Xingxing
Mao, Ying
Zhou, Liangfu
Titel
B7-H4(B7x)-Mediated Cross-talk between Glioma-Initiating Cells and Macrophages via the IL6/JAK/STAT3 Pathway Lead to Poor Prognosis in Glioma Patients
Ist Teil von
Clinical cancer research, 2016-06, Vol.22 (11), p.2778-2790
Ort / Verlag
United States
Erscheinungsjahr
2016
Quelle
MEDLINE
Beschreibungen/Notizen
The objective of this study was to evaluate clinical significance and immunosuppressive mechanisms of B7-H4 (B7x/B7S1), a B7 family member, in glioma. B7-H4 levels in glioma tissue/cerebral spinal fluid (CSF) were compared between different grades of glioma patients. Survival data were analyzed with Kaplan-Meier to determine the prognostic value of B7-H4. Cytokines from CD133(+) cells to stimulate the expression of B7-H4 on human macrophages (Mφs) were investigated by FACS, neutralizing antibodies, and Transwell chemotaxis assay. shRNA, reporter vector, and chromatin immunoprecipitation were used to determine the binding of STAT3 to the B7-H4 promoter. The function of B7-H4(+) Mφs in vitro was evaluated through phagocytosis, T-cell proliferation/apoptosis, and cytokine production as well as in the xenografted model for in vivo analysis. We found that B7-H4 expression in tumors was associated with prognosis of human glioblastoma and correlated directly with malignant grades. Mechanistically, glioma initiating CD133(+) cells and Mφs/microglia cointeraction activated expression of B7-H4 via IL6 and IL10 in both tumor cells and microenvironment supporting cells. IL6-activated STAT3 bound to the promoter of B7-H4 gene and enhanced B7-H4 expression. Furthermore, CD133(+) cells mediated immunosuppression through B7-H4 expression on Mφs/microglia by silencing of B7-H4 expression on these cells, which led to increased microenvironment T-cell function and tumor regression in the xenograft glioma mouse model. We have identified B7-H4 activation on Mφs/microglia in the microenvironment of gliomas as an important immunosuppressive event blocking effective T-cell immune responses. Clin Cancer Res; 22(11); 2778-90. ©2016 AACR.
Sprache
Englisch
Identifikatoren
ISSN: 1078-0432
eISSN: 1557-3265
DOI: 10.1158/1078-0432.ccr-15-0858
Titel-ID: cdi_proquest_miscellaneous_1808666521
Format
–
Schlagworte
Adolescent
,
Adult
,
Aged
,
Animals
,
Brain Neoplasms - immunology
,
Brain Neoplasms - metabolism
,
Brain Neoplasms - mortality
,
Brain Neoplasms - pathology
,
Cell Line, Tumor
,
Female
,
Glioblastoma - immunology
,
Glioblastoma - metabolism
,
Glioblastoma - mortality
,
Glioblastoma - pathology
,
Humans
,
Interleukin-6 - physiology
,
Janus Kinases - metabolism
,
Kaplan-Meier Estimate
,
Lymphocyte Activation
,
Macrophages - metabolism
,
Male
,
Mice, Inbred C57BL
,
Middle Aged
,
Neoplasm Transplantation
,
Neoplastic Stem Cells - metabolism
,
Organ Specificity
,
Prognosis
,
Retrospective Studies
,
Signal Transduction
,
STAT3 Transcription Factor - metabolism
,
V-Set Domain-Containing T-Cell Activation Inhibitor 1 - physiology
,
Young Adult
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