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introduction
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Microglia can constitute up to 10% of cells in the central nervous system (CNS) and are distinctive from other CNS cells such as astrocytes and oligodendrocytes [>>1<<]. Distinguishing features of microglia are their “ramified” branches that emerge from the cell body that communicate with surrounding neurons and other glial cells.
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However, prolonged or excessive activation may result in pathological forms of inflammation that contribute to the progression of neurodegenerative and neoplastic diseases [>>2<<].
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Gene transcript clustering analysis reveals that microglia have close lineage relationship with bone-marrow-derived macrophages, indicating that these cells arise from the bone marrow and circulating monocytes/macrophages [>>3<<]. However, recent findings suggest that microglia originate from yolk sac macrophages that migrate into the CNS during early embryogenesis [4] (Figure 1).
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However, recent findings suggest that microglia originate from yolk sac macrophages that migrate into the CNS during early embryogenesis [>>4<<] (Figure 1).
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Further confounding the issue regarding the origin of CNS microglia are studies demonstrating the generation of microglia-like cells from a murine embryonal carcinoma cell line (P19) during neural differentiation [>>5<<]. Regardless of the origin, the microglia/macrophage population are usually the dominant glioma-infiltrating immune cells (5–30%) [6].
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Regardless of the origin, the microglia/macrophage population are usually the dominant glioma-infiltrating immune cells (5–30%) [>>6<<].
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Studies during the 90s demonstrated a positive correlation between the number of microglia/macrophage and glioma malignancy [>>7<<, 8]. Furthermore, microscopic analysis of microglia morphology in high-grade glioma revealed an activated state, described by amoeboid or spherical shape [9, 10].
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Studies during the 90s demonstrated a positive correlation between the number of microglia/macrophage and glioma malignancy [7, >>8<<]. Furthermore, microscopic analysis of microglia morphology in high-grade glioma revealed an activated state, described by amoeboid or spherical shape [9, 10].
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Furthermore, microscopic analysis of microglia morphology in high-grade glioma revealed an activated state, described by amoeboid or spherical shape [>>9<<, 10]. Morioka et al. have found that reactive microglia form a dense band that surround the tumor mass and can extend along the corpus callosum into the contralateral cerebral hemisphere [11]. These data would indicate that microglia
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Furthermore, microscopic analysis of microglia morphology in high-grade glioma revealed an activated state, described by amoeboid or spherical shape [9, >>10<<]. Morioka et al. have found that reactive microglia form a dense band that surround the tumor mass and can extend along the corpus callosum into the contralateral cerebral hemisphere [11]. These data would indicate that microglia react to
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Morioka et al. have found that reactive microglia form a dense band that surround the tumor mass and can extend along the corpus callosum into the contralateral cerebral hemisphere [>>11<<]. These data would indicate that microglia react to brain tumors; however, it remains to be determined whether this response represents an active anti-tumor defense mechanism or a tumor-supportive one. Likewise, microglia are commonly
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Hepatocyte growth factor (HGF)/scatter factor (SF), which plays a role in glioma motility and mitogenesis, may be one chemokine responsible for the microglia infiltration in malignant gliomas [>>12<<]. Additionally or alternatively, monocyte chemotactic protein-3 (MCP-3) was found to correlate with GAM infiltration [13] and to act as a chemokine. Furthermore, it has been reported that tumor necrosis factor (TNF) dependent action
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Additionally or alternatively, monocyte chemotactic protein-3 (MCP-3) was found to correlate with GAM infiltration [>>13<<] and to act as a chemokine.
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Furthermore, it has been reported that tumor necrosis factor (TNF) dependent action enhances macrophage/microglia recruitment in glioma [>>14<<]. Other chemoattractants that have been shown to stimulate microglia/macrophage migration into the tumor include colony stimulating factor-1 (CSF-1) [15, 16], macrophage colony-stimulating factor (M-CSF) [17], and glial-derived
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Other chemoattractants that have been shown to stimulate microglia/macrophage migration into the tumor include colony stimulating factor-1 (CSF-1) [>>15<<, 16], macrophage colony-stimulating factor (M-CSF) [17], and glial-derived neurotrophic factor (GDNF) [18].
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Other chemoattractants that have been shown to stimulate microglia/macrophage migration into the tumor include colony stimulating factor-1 (CSF-1) [15, >>16<<], macrophage colony-stimulating factor (M-CSF) [17], and glial-derived neurotrophic factor (GDNF) [18].
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Other chemoattractants that have been shown to stimulate microglia/macrophage migration into the tumor include colony stimulating factor-1 (CSF-1) [15, 16], macrophage colony-stimulating factor (M-CSF) [>>17<<], and glial-derived neurotrophic factor (GDNF) [18].
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that have been shown to stimulate microglia/macrophage migration into the tumor include colony stimulating factor-1 (CSF-1) [15, 16], macrophage colony-stimulating factor (M-CSF) [17], and glial-derived neurotrophic factor (GDNF) [>>18<<]. However, recent studies have emphasized a predominant role of granulocyte-macrophage colony stimulating factor (GM-SCF) in microglia/macrophage attraction [19] which confirmed previous reports [20, 21].
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However, recent studies have emphasized a predominant role of granulocyte-macrophage colony stimulating factor (GM-SCF) in microglia/macrophage attraction [>>19<<] which confirmed previous reports [20, 21].
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However, recent studies have emphasized a predominant role of granulocyte-macrophage colony stimulating factor (GM-SCF) in microglia/macrophage attraction [19] which confirmed previous reports [20, >>21<<]. Nonetheless, the increased number of microglia/macrophages found in high-grade gliomas has suggested that they may have a pro-neoplastic role [8].
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Nonetheless, the increased number of microglia/macrophages found in high-grade gliomas has suggested that they may have a pro-neoplastic role [>>8<<].
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CD163, CD200, CD204, CD68, F4/80, and the lectin binding protein Iba-1 can be used as general markers of microglia/macrophages [>>22<<, 23]. P2X4R expression can define a distinct subset of GAMs [24]. Furthermore, allograft inflammatory factor-1 (AIF-1) and heme oxygenase-1 (HO-1) can also be used to define a distinct subset of GAMs in rat and human gliomas [25, 26].
n2:mentions
n3:17341475
Subject Item
_:vb24722878
rdf:type
n2:Context
rdf:value
CD163, CD200, CD204, CD68, F4/80, and the lectin binding protein Iba-1 can be used as general markers of microglia/macrophages [22, >>23<<]. P2X4R expression can define a distinct subset of GAMs [24]. Furthermore, allograft inflammatory factor-1 (AIF-1) and heme oxygenase-1 (HO-1) can also be used to define a distinct subset of GAMs in rat and human gliomas [25, 26].
n2:mentions
n3:11099416
Subject Item
_:vb24722879
rdf:type
n2:Context
rdf:value
P2X4R expression can define a distinct subset of GAMs [>>24<<]. Furthermore, allograft inflammatory factor-1 (AIF-1) and heme oxygenase-1 (HO-1) can also be used to define a distinct subset of GAMs in rat and human gliomas [25, 26].
n2:mentions
n3:15223238
Subject Item
_:vb24722880
rdf:type
n2:Context
rdf:value
Furthermore, allograft inflammatory factor-1 (AIF-1) and heme oxygenase-1 (HO-1) can also be used to define a distinct subset of GAMs in rat and human gliomas [>>25<<, 26]. However, the most commonly used criterion to distinguish CNS microglia from macrophages is the differential CD45 expression (CD45low for microglia and CD45high for macrophages) on CD11b+ CD11c+ cells [27–29]. The robustness of this
n2:mentions
n3:11056178
Subject Item
_:vb24722881
rdf:type
n2:Context
rdf:value
Furthermore, allograft inflammatory factor-1 (AIF-1) and heme oxygenase-1 (HO-1) can also be used to define a distinct subset of GAMs in rat and human gliomas [25, >>26<<]. However, the most commonly used criterion to distinguish CNS microglia from macrophages is the differential CD45 expression (CD45low for microglia and CD45high for macrophages) on CD11b+ CD11c+ cells [27–29]. The robustness of this is
n2:mentions
n3:11078219
Subject Item
_:vb24722882
rdf:type
n2:Context
rdf:value
However, the most commonly used criterion to distinguish CNS microglia from macrophages is the differential CD45 expression (CD45low for microglia and CD45high for macrophages) on CD11b+ CD11c+ cells [>>27<<–29]. The robustness of this is questionable.
n2:mentions
n3:1651506 n3:11455617
Subject Item
_:vb24722883
rdf:type
n2:Context
rdf:value
However, this is not an absolute since MDSCs isolated from mouse brain tumors, although expressing markers consistent with an immune suppressive phenotype (CCL17, CD206, and CD36), still express proinflammatory IL-1β, TNF-α, and CXCL10 [>>31<<]. Currently, there are two presumed MDSC populations: monocytic and granulocytic.
n2:mentions
n3:18285406
Subject Item
_:vb24722884
rdf:type
n2:Context
rdf:value
Specifically, MSDCs only weakly present glioma antigens to cytotoxic T cells and express FasL, which contributes to the local immunosuppressive milieu of malignant gliomas [>>32<<], similar immunological functions attributed to GAMs [33].
n2:mentions
n3:11694315
Subject Item
_:vb24722885
rdf:type
n2:Context
rdf:value
Specifically, MSDCs only weakly present glioma antigens to cytotoxic T cells and express FasL, which contributes to the local immunosuppressive milieu of malignant gliomas [32], similar immunological functions attributed to GAMs [>>33<<]. Furthermore, the MDSCs have been shown to inhibit T cell activity by NO production [34]; however, this immune suppression was postulated to be distinct from CNS microglia.
n2:mentions
n3:16775224
Subject Item
_:vb24722886
rdf:type
n2:Context
rdf:value
Furthermore, the MDSCs have been shown to inhibit T cell activity by NO production [>>34<<]; however, this immune suppression was postulated to be distinct from CNS microglia.
n2:mentions
n3:20452681
Subject Item
_:vb24722887
rdf:type
n5:Section
dc:title
summary
n5:contains
_:vb24722888
Subject Item
_:vb24722888
rdf:type
n2:Context
rdf:value
In the early stages of gliomagenesis, innate responses mediated by microglia may be beneficial and involve the activation of effective surveillance by adaptive immunity resulting in the elimination of these cells [>>136<<]. However, in the context of progressive malignancy, when tumor cells have escaped immune editing, the smoldering inflammation orchestrated by GAMs, may promote tumor progression. Therapeutic strategies targeting macrophages should take
n2:mentions
n3:16730260
Subject Item
_:vb24722889
rdf:type
n5:Section
dc:title
the m1/m2 continuum
n5:contains
_:vb24722890 _:vb24722891 _:vb24722892 _:vb24722893 _:vb24722894 _:vb24722895 _:vb24722896 _:vb24722897 _:vb24722898 _:vb24722899 _:vb24722900 _:vb24722901 _:vb24722902 _:vb24722903 _:vb24722904 _:vb24722905 _:vb24722906 _:vb24722907 _:vb24722908 _:vb24722909 _:vb24722910
Subject Item
_:vb24722890
rdf:type
n2:Context
rdf:value
The M1 cell is capable of stimulating anti-tumor immune responses by presenting antigen to adaptive immune cells, producing pro-inflammatory cytokines and phagocytosing tumor cells [>>35<<] (Figure 3).
n2:mentions
n3:17981560
Subject Item
_:vb24722891
rdf:type
n2:Context
rdf:value
Whereas the alternatively activated pathway, M2, is characterized by the expression of surface CD163 and CD204, expression of intracellular STAT-3 and the production of arginase [>>36<<, 37] (Figure 2).
n2:mentions
n3:14708027
Subject Item
_:vb24722892
rdf:type
n2:Context
rdf:value
M2 polarization prevents the production of cytokines required to support tumor-specific CD8+ T cells, and CD4+ T helper 1 (Th1) and promotes the function of CD4+ regulatory T cells, and are therefore tumor supportive [>>38<<, 39] (Figure 4).
n2:mentions
n3:20068105
Subject Item
_:vb24722893
rdf:type
n2:Context
rdf:value
Glioma cells secrete a wide variety of factors that suppress immune cells, such as IL-10, IL-4, IL-6, M-CSF, macrophage inhibitory factor (MIF), TGFβ, and prostaglandin E2 (PGE2) [>>17<<, 40–43]. These cytokines are known to promote a M2 phenotype and/or to suppress the M1 phenotype.
n2:mentions
n3:18553315
Subject Item
_:vb24722894
rdf:type
n2:Context
rdf:value
Glioma cells secrete a wide variety of factors that suppress immune cells, such as IL-10, IL-4, IL-6, M-CSF, macrophage inhibitory factor (MIF), TGFβ, and prostaglandin E2 (PGE2) [17, >>40<<–43]. These cytokines are known to promote a M2 phenotype and/or to suppress the M1 phenotype.
n2:mentions
n3:21446047 n3:21088899 n3:17289164 n3:19326434
Subject Item
_:vb24722895
rdf:type
n2:Context
rdf:value
For example, TGFβ inhibits microglia cell proliferation and the production of proinflammatory cytokines in vitro [>>44<<]. IL-4, IL-6 and IL-10 have been shown to polarize microglia to an M2-like phenotype [45]. Other immunosuppressive mechanisms such as the downregulation ICAM-1 and expression of immune inhibitory molecules such as B7-H1 can also dismantle
n2:mentions
n3:20667896
Subject Item
_:vb24722896
rdf:type
n2:Context
rdf:value
IL-4, IL-6 and IL-10 have been shown to polarize microglia to an M2-like phenotype [>>45<<]. Other immunosuppressive mechanisms such as the downregulation ICAM-1 and expression of immune inhibitory molecules such as B7-H1 can also dismantle the microglia-T cell combined immune recognition and clearance of gliomas [46].
n2:mentions
n3:16520032
Subject Item
_:vb24722897
rdf:type
n2:Context
rdf:value
Other immunosuppressive mechanisms such as the downregulation ICAM-1 and expression of immune inhibitory molecules such as B7-H1 can also dismantle the microglia-T cell combined immune recognition and clearance of gliomas [>>46<<]. Furthermore, gliomas induce upregulation and expression of HLA-G and HLA-E by GAMs in a majority of glioblastomas, thus hindering anti-glioma activity [47]. The anti-glioma functional impairment of GAMs likely occurs relatively late in
n2:mentions
n3:16810329
Subject Item
_:vb24722898
rdf:type
n2:Context
rdf:value
Furthermore, gliomas induce upregulation and expression of HLA-G and HLA-E by GAMs in a majority of glioblastomas, thus hindering anti-glioma activity [>>47<<]. The anti-glioma functional impairment of GAMs likely occurs relatively late in the course of glioblastoma tumor growth, potentially providing a window of opportunity for therapeutic strategies directed towards preventing their
n2:mentions
n3:20167379
Subject Item
_:vb24722899
rdf:type
n2:Context
rdf:value
On the other hand, the lack of positivity of either iNOS or TNF-α in double-labeling experiments indicates that the microglia immunological functions including cytotoxicity, phagocytosis, and antigen presentation are impaired [>>49<<]. Microglia have also been shown to promote invasion and colonization of the brain by breast cancer by serving both as active transporters and guiding rails. This is antagonized by inactivation of microglia as well as by Wnt signaling
n2:mentions
n3:17088948
Subject Item
_:vb24722900
rdf:type
n2:Context
rdf:value
Therefore, microglia were shown to be critical for the successful colonization of the brain by epithelial cancer cells, suggesting that inhibition of microglia could also be a promising anti-metastatic strategy [>>50<<].
n2:mentions
n3:20549749
Subject Item
_:vb24722901
rdf:type
n2:Context
rdf:value
to microglia/macrophages isolated from normal brain; specifically, the former has an impaired capacity to be stimulated by TLR agonist to secrete cytokines, upregulate costimulatory molecules, and activate anti-tumor effector T cells [>>33<<]. Understanding the mechanism of these differences may be critical in the development of novel immunotherapies for malignant gliomas [52].
n2:mentions
n3:16775224
Subject Item
_:vb24722902
rdf:type
n2:Context
rdf:value
Understanding the mechanism of these differences may be critical in the development of novel immunotherapies for malignant gliomas [>>52<<].
n2:mentions
n3:15818597
Subject Item
_:vb24722903
rdf:type
n2:Context
rdf:value
These activated microglia can then induce glioma cell death by blockade of basal autophagic flux inducing secondary apoptosis/necrosis [>>53<<]. Signaling through the JAK-2-STAT-5 pathway was shown to be essential for IL-3-induced activation of microglia [54]. Furthermore, microglia/macrophages depletion increased glioma tumor volume by 33%. This was not believed to be secondary
n2:mentions
n3:19197144
Subject Item
_:vb24722904
rdf:type
n2:Context
rdf:value
Signaling through the JAK-2-STAT-5 pathway was shown to be essential for IL-3-induced activation of microglia [>>54<<]. Furthermore, microglia/macrophages depletion increased glioma tumor volume by 33%. This was not believed to be secondary to the loss of microglia tumoricidal activity because phagocytosis or apoptosis of glioma cells was rarely observed.
n2:mentions
n3:14730712
Subject Item
_:vb24722905
rdf:type
n2:Context
rdf:value
depletion of a subset of CD86+ microglia with M1-like characteristics could present alloantigen and secrete stimulatory cytokines that promoted the expansion of the CD8+ T cells and was likely the etiology for enhanced glioma growth [>>55<<].
n2:mentions
n3:8913775
Subject Item
_:vb24722906
rdf:type
n2:Context
rdf:value
GAMs have been shown to release growth factors such as VEGF, PDGF, and members of the FGF family, and a correlation has been shown between GAM numbers and tumor vascularity in gliomas [>>56<<]. Furthermore, these growth factors sustain malignant cell survival and subsequent tumor growth. Lastly, GAMs are a major source of FasL expression, which likely contributes to the suppression of malignant glioma apoptosis [32].
n2:mentions
n3:10353745
Subject Item
_:vb24722907
rdf:type
n2:Context
rdf:value
Lastly, GAMs are a major source of FasL expression, which likely contributes to the suppression of malignant glioma apoptosis [>>32<<].
n2:mentions
n3:11694315
Subject Item
_:vb24722908
rdf:type
n2:Context
rdf:value
Glioma regression has also been correlated with greater numbers of T cells and microglia, suggesting that the combined mobilization of peripheral and CNS endogenous immune cells is required for eradicating large intracranial tumors [>>57<<]. Some soluble factors from reactive microglia are capable of enhancing the expression of ICAM-1 on the brain endothelial cells (ECs).
n2:mentions
n3:16612573
Subject Item
_:vb24722909
rdf:type
n2:Context
rdf:value
As a consequence, large numbers of tumor-primed T lymphocytes can adhere to EC and migrate across the EC monolayer [>>58<<]. Finally, antibody-dependent cell mediated cytotoxicity (ADCC) has also been shown to be involved in microglia anti-tumor activities. Microglia derived from brain cortices of newborn mice were shown to lyse human tumor cell lines
n2:mentions
n3:9521610
Subject Item
_:vb24722910
rdf:type
n2:Context
rdf:value
Microglia derived from brain cortices of newborn mice were shown to lyse human tumor cell lines expressing different levels of epidermal growth factor receptor (EGFR) in the presence of a monoclonal antibody specific to EGFR [>>59<<]. Reconciliation of the cumulative data would indicate that GAMs can be either M1 or M2 or some were in between, but the functional outcome will depend on the relative composition of M1 and M2 cells within the glioma.
n2:mentions
n3:1883522
Subject Item
_:vb24722911
rdf:type
n5:Section
dc:title
interplay between gams and gliomas
n5:contains
_:vb24722928 _:vb24722929 _:vb24722930 _:vb24722931 _:vb24722920 _:vb24722921 _:vb24722922 _:vb24722923 _:vb24722924 _:vb24722925 _:vb24722926 _:vb24722927 _:vb24722912 _:vb24722913 _:vb24722914 _:vb24722915 _:vb24722916 _:vb24722917 _:vb24722918 _:vb24722919
Subject Item
_:vb24722912
rdf:type
n2:Context
rdf:value
The glioma cells simultaneously invade and expand into the dissociated tissue by utilizing the same corridor paved by laminin on astrocytic projection for microglia invasion into the tumors [>>60<<–62]. Glioma secreted factors, by engaging the toll-like receptors and the p38 MAPK pathway, trigger the expression and activity of membrane type 1 metalloprotease (MT1-MMP) on GAMs. The GAM MT1-MMP expression then in turn activates
n2:mentions
n3:18804537 n3:16951167 n3:19617536
Subject Item
_:vb24722913
rdf:type
n2:Context
rdf:value
A deficiency of MyD88, an upstream mediator of MT1-MMP, or microglia depletion, largely attenuates glioma expansion in vivo [>>62<<]. Furthermore, in brain slices inoculated with glioma cells, increased activity of metalloprotease-2 was directly correlated with the abundance of microglia [63]. Another GAM-associated mechanism, the CX3CR1/CX3CL1 interaction, can also
n2:mentions
n3:19617536
Subject Item
_:vb24722914
rdf:type
n2:Context
rdf:value
Furthermore, in brain slices inoculated with glioma cells, increased activity of metalloprotease-2 was directly correlated with the abundance of microglia [>>63<<]. Another GAM-associated mechanism, the CX3CR1/CX3CL1 interaction, can also induce MMPs production resulting in glioma invasion [64]. A recently described factor, STI1 (cochaperone stress inducible factor 1) secreted by microglia was
n2:mentions
n3:16141784
Subject Item
_:vb24722915
rdf:type
n2:Context
rdf:value
Another GAM-associated mechanism, the CX3CR1/CX3CL1 interaction, can also induce MMPs production resulting in glioma invasion [>>64<<]. A recently described factor, STI1 (cochaperone stress inducible factor 1) secreted by microglia was shown to favor tumor growth and invasion through the participation of MMP-9 [65]. Thus, glioma cells stimulate microglia to increase the
n2:mentions
n3:20184883
Subject Item
_:vb24722916
rdf:type
n2:Context
rdf:value
A recently described factor, STI1 (cochaperone stress inducible factor 1) secreted by microglia was shown to favor tumor growth and invasion through the participation of MMP-9 [>>65<<]. Thus, glioma cells stimulate microglia to increase the breakdown of extracellular matrix, thereby, promoting glioma invasion.
n2:mentions
n3:22062133
Subject Item
_:vb24722917
rdf:type
n2:Context
rdf:value
Neurodegeneration, neurotoxicity, and neuroinflammation are associated with chronic microglia activation that has been postulated to contribute to gliomagenesis [>>66<<–68]. Cyclooxygenase-1 (COX-1) in microglia/macrophages might represent a key regulatory mechanism in the inflammatory processes associated with neoplasia [69]. COX-1 and COX-2 differential accumulation is observed in microglia/macrophages
n2:mentions
n3:22753228 n3:11426226 n3:20880500
Subject Item
_:vb24722918
rdf:type
n2:Context
rdf:value
Cyclooxygenase-1 (COX-1) in microglia/macrophages might represent a key regulatory mechanism in the inflammatory processes associated with neoplasia [>>69<<]. COX-1 and COX-2 differential accumulation is observed in microglia/macrophages and astrocytes during oligodendroglioma progression in vivo [70]. Furthermore, induction of COX-2 in microglia contributes to the deleterious effects of
n2:mentions
n3:10229132
Subject Item
_:vb24722919
rdf:type
n2:Context
rdf:value
COX-1 and COX-2 differential accumulation is observed in microglia/macrophages and astrocytes during oligodendroglioma progression in vivo [>>70<<]. Furthermore, induction of COX-2 in microglia contributes to the deleterious effects of prostanoids in cerebral edema formation during the progression of oligodendrogliomas [71]. Increased c-Jun-NH2-kinase signaling in
n2:mentions
n3:11121536
Subject Item
_:vb24722920
rdf:type
n2:Context
rdf:value
Furthermore, induction of COX-2 in microglia contributes to the deleterious effects of prostanoids in cerebral edema formation during the progression of oligodendrogliomas [>>71<<]. Increased c-Jun-NH2-kinase signaling in neurofibromatosis-1 heterozygous (Nf1+/−) microglia was shown to promote optic glioma proliferation [72] and glioma growth [73]. Interestingly, IL-4 or IFN-γ-mediated microglia activation
n2:mentions
n3:20052522
Subject Item
_:vb24722921
rdf:type
n2:Context
rdf:value
Increased c-Jun-NH2-kinase signaling in neurofibromatosis-1 heterozygous (Nf1+/−) microglia was shown to promote optic glioma proliferation [>>72<<] and glioma growth [73].
n2:mentions
n3:19074905
Subject Item
_:vb24722922
rdf:type
n2:Context
rdf:value
Increased c-Jun-NH2-kinase signaling in neurofibromatosis-1 heterozygous (Nf1+/−) microglia was shown to promote optic glioma proliferation [72] and glioma growth [>>73<<]. Interestingly, IL-4 or IFN-γ-mediated microglia activation differentially induces oligodendrogenesis and neurogenesis, respectively, from adult stem/progenitor cells. It thus appears that how microglia are activated determines their
n2:mentions
n3:17400655
Subject Item
_:vb24722923
rdf:type
n2:Context
rdf:value
It thus appears that how microglia are activated determines their ability to either support or impair cell renewal and differentiation from adult stem cells [>>74<<].
n2:mentions
n3:16297637
Subject Item
_:vb24722924
rdf:type
n2:Context
rdf:value
GSCs are phenotypically similar to normal stem cells, can express CD133, and possess self-renewal potential [>>75<<]. GSCs recapitulate the original polyclonal tumors when xenografted into nude mice and mediate chemo- and radiation resistance, thereby, leading to tumor progression and recurrence. A positive correlation is found between the degree of
n2:mentions
n3:17051156
Subject Item
_:vb24722925
rdf:type
n2:Context
rdf:value
The capacity of GSCs to recruit GAMs was found to be stronger than glioma cell lines indicating that the GSCs play a predominant role in microglia/macrophages tropism to glioma [>>76<<]. In addition, recent mechanistic studies by another group showed that TGFβ1 released by GAMs promoted the expression of MMP-9 by GSCs, and TGFR2 knockdown reduced the invasiveness of these cells in vivo [77].
n2:mentions
n3:21056915
Subject Item
_:vb24722926
rdf:type
n2:Context
rdf:value
the microglia/macrophage to an M2 phenotype, inhibited microglia/macrophage phagocytosis, induced the secretion of the immunosuppressive cytokines IL-10 and TGFβ1 and enhanced the capacity of these cells to inhibit T-cell proliferation [>>44<<]. The inhibition of antigen-presenting capabilities of GAMs by glioma tumor cells has also been demonstrated [25].
n2:mentions
n3:20667896
Subject Item
_:vb24722927
rdf:type
n2:Context
rdf:value
The inhibition of antigen-presenting capabilities of GAMs by glioma tumor cells has also been demonstrated [>>25<<]. Previously, glioma-derived M-CSF was shown to induces markers reflective of the M2 phenotype CD163 and CD204 on monocytes, and in turn these differentiated microglia/macrophage facilitated tumor growth. Both the extent of M-CSF
n2:mentions
n3:11056178
Subject Item
_:vb24722928
rdf:type
n2:Context
rdf:value
Both the extent of M-CSF production and CD163+ and CD204+ expression on microglia were correlated with glioma grade [>>17<<]. A direct correlation has been shown between the immunogenicity of glioma tumor cells and the GAM content and their antigen-presenting function [78, 79]. In addition, the metabolic status of the microglia is altered by the glioma
n2:mentions
n3:18553315
Subject Item
_:vb24722929
rdf:type
n2:Context
rdf:value
A direct correlation has been shown between the immunogenicity of glioma tumor cells and the GAM content and their antigen-presenting function [>>78<<, 79]. In addition, the metabolic status of the microglia is altered by the glioma environment [80]. Abundant amounts of ATP released by the glioma have been suggested to trigger P2X7R signaling, resulting in increase of MIP-1α (macrophage
n2:mentions
n3:217977
Subject Item
_:vb24722930
rdf:type
n2:Context
rdf:value
A direct correlation has been shown between the immunogenicity of glioma tumor cells and the GAM content and their antigen-presenting function [78, >>79<<]. In addition, the metabolic status of the microglia is altered by the glioma environment [80]. Abundant amounts of ATP released by the glioma have been suggested to trigger P2X7R signaling, resulting in increase of MIP-1α (macrophage
n2:mentions
n3:12446006
Subject Item
_:vb24722931
rdf:type
n2:Context
rdf:value
Abundant amounts of ATP released by the glioma have been suggested to trigger P2X7R signaling, resulting in increase of MIP-1α (macrophage inflammatory protein-1α) and MCP-1 (monocyte chemoattractant protein-1) in GAMs [>>81<<]. Cumulatively these data indicate that there is a strong interaction that occurs between the GAM and glioma that ultimately influences the biological behavior of each one.
n2:mentions
n3:21162127
Subject Item
_:vb24722932
rdf:type
n5:Section
dc:title
therapeutic manipulation of the gam
n5:contains
_:vb24722933 _:vb24722934 _:vb24722935 _:vb24722940 _:vb24722941 _:vb24722942 _:vb24722943 _:vb24722936 _:vb24722937 _:vb24722938 _:vb24722939 _:vb24722948 _:vb24722949 _:vb24722950 _:vb24722951 _:vb24722944 _:vb24722945 _:vb24722946 _:vb24722947 _:vb24722952
Subject Item
_:vb24722933
rdf:type
n2:Context
rdf:value
of experimental rat glioma growth by decorin (TGFβ antagonism) gene transfer was associated with decreased microglia infiltration suggesting that the GAMs were participate in the regression of decorin-expressing rat C6 gliomas [>>82<<]. Recent studies have demonstrated that ablation of CD11b+ cells in ganciclovir-treated CD11b-HSVTK mice [83] or in vivo targeting folate receptor β (FRβ)-expressing tumor-associated macrophages, decreases tumor size and improves animal
n2:mentions
n3:10496172
Subject Item
_:vb24722934
rdf:type
n2:Context
rdf:value
Recent studies have demonstrated that ablation of CD11b+ cells in ganciclovir-treated CD11b-HSVTK mice [>>83<<] or in vivo targeting folate receptor β (FRβ)-expressing tumor-associated macrophages, decreases tumor size and improves animal survival [84].
n2:mentions
n3:21264953
Subject Item
_:vb24722935
rdf:type
n2:Context
rdf:value
have demonstrated that ablation of CD11b+ cells in ganciclovir-treated CD11b-HSVTK mice [83] or in vivo targeting folate receptor β (FRβ)-expressing tumor-associated macrophages, decreases tumor size and improves animal survival [>>84<<]. The presence of significant anti-tumor immunity following herpes simplex virus 1 thymidine kinase (HSV-TK) and ganciclovir (GCV) treatments suggests that the immune system plays a critical role in the sustained tumor regressions
n2:mentions
n3:19238383
Subject Item
_:vb24722936
rdf:type
n2:Context
rdf:value
Histologic examination of the brains of the successfully treated animals demonstrated residual tumor cells and inflammatory cells consisting predominantly of macrophages/microglia and T cells [>>85<<]. Another report demonstrates that a reduction of peripheral CD163+ macrophages in vivo and the depletion of CD68+ macrophage/microglia within brain slice ex vivo increase the intratumoral oncolytic viral titer to 5-fold and 10-fold,
n2:mentions
n3:8183911
Subject Item
_:vb24722937
rdf:type
n2:Context
rdf:value
demonstrates that a reduction of peripheral CD163+ macrophages in vivo and the depletion of CD68+ macrophage/microglia within brain slice ex vivo increase the intratumoral oncolytic viral titer to 5-fold and 10-fold, respectively, [>>86<<].
n2:mentions
n3:17909049
Subject Item
_:vb24722938
rdf:type
n2:Context
rdf:value
STAT-3 blockage by WP1066 stimulates the immune activation of GAMs, as evidenced by their increased expression of costimulatory molecules CD80 and CD86 [>>117<<]. Furthermore, in vivo STAT-3 inhibition in murine GAMs was shown to reduce expression of immunosuppressive cytokines, such as IL-10 and IL-6, while stimulating production of pro-inflammatory TNF-α [118]. Another therapeutic option is
n2:mentions
n3:17942891
Subject Item
_:vb24722939
rdf:type
n2:Context
rdf:value
Furthermore, in vivo STAT-3 inhibition in murine GAMs was shown to reduce expression of immunosuppressive cytokines, such as IL-10 and IL-6, while stimulating production of pro-inflammatory TNF-α [>>118<<]. Another therapeutic option is glycoprotein T11TS, which has been found to upregulate MHC class II, CD2 and CD4 expression in microglia in vivo in a rat glioma model [40]. Because macrophages/microglia express the nicotinic acetylcholine
n2:mentions
n3:19306372
Subject Item
_:vb24722940
rdf:type
n2:Context
rdf:value
Another therapeutic option is glycoprotein T11TS, which has been found to upregulate MHC class II, CD2 and CD4 expression in microglia in vivo in a rat glioma model [>>40<<]. Because macrophages/microglia express the nicotinic acetylcholine receptor (AchR) on their surface, a short AchR-binding peptide derived from the rabies virus glycoprotein (RVG) could also be used for targeted delivery of siRNA to
n2:mentions
n3:19326434
Subject Item
_:vb24722941
rdf:type
n2:Context
rdf:value
This peptide was fused to nona-D-arginine residues (RVG-9dR) to enable siRNA binding [>>124<<]. Recently, GAMs were shown to enhance GSCs' invasion via the TGFβ1 signaling pathway [77]. shRNA against TGFβ1 receptor (TGFβR) on tumor-associated macrophages strongly inhibited glioma invasiveness, indicating that TGFβR is a potential
n2:mentions
n3:20216529
Subject Item
_:vb24722942
rdf:type
n2:Context
rdf:value
shRNA against TGFβ1 receptor (TGFβR) on tumor-associated macrophages strongly inhibited glioma invasiveness, indicating that TGFβR is a potential therapeutic target [>>112<<]. Several small molecules exist with TGFβR inhibitor activity that could be utilized as GAM modulatory agents. Studies of Carpentier et al. [87] revealed that intratumoral injections of oligodeoxynucleotides containing CpG motifs
n2:mentions
n3:17684491
Subject Item
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Studies of Carpentier et al. [>>87<<] revealed that intratumoral injections of oligodeoxynucleotides containing CpG motifs (CpG-ODN) trigger both innate and specific immunities, driving the immune response towards the Th1 phenotype.
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On the other hand, glioma-bearing animals treated with minocycline showed increased survival [>>125<<] and reduced glioma invasion by attenuated microglia MT1-MMP expression [106].
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However, the suppression/inhibition of glioma-derived factors or glioma-mediated immune suppression has been shown to synergize with the efficacy of microglia therapeutic strategies [>>118<<, 126–129], suggesting that there is a therapeutic opportunity.
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However, the suppression/inhibition of glioma-derived factors or glioma-mediated immune suppression has been shown to synergize with the efficacy of microglia therapeutic strategies [118, >>126<<–129], suggesting that there is a therapeutic opportunity.
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GAMs or their precursors could be used to facilitate CNS tumor imaging [>>130<<]. Accurate delineation of tumor margins is vital to the successful surgical resection of brain tumors and the extent of resection impacts survival.
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It could be used to assist intraoperatively in visualizing tumor boundaries because CD11b+ microglia are found at the tumor margin [>>131<<]. Other labeling system include cyclodextrin-based nanoparticles (CDP-NPs) [132] or multiwalled carbon Nanotubes (MWCNTs) [133]. Recently, quantum dots have been shown to be phagocytized by microglia and macrophages that infiltrate
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Other labeling system include cyclodextrin-based nanoparticles (CDP-NPs) [>>132<<] or multiwalled carbon Nanotubes (MWCNTs) [133].
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Other labeling system include cyclodextrin-based nanoparticles (CDP-NPs) [132] or multiwalled carbon Nanotubes (MWCNTs) [>>133<<]. Recently, quantum dots have been shown to be phagocytized by microglia and macrophages that infiltrate experimental gliomas that resulted in improved identification and visualization of tumors, potentially augmenting brain tumor biopsy
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dots have been shown to be phagocytized by microglia and macrophages that infiltrate experimental gliomas that resulted in improved identification and visualization of tumors, potentially augmenting brain tumor biopsy and resection [>>134<<]. Ultimately, these imaging approaches could be exploited as biomarkers to monitor clinical trials targeting the GAM population [135].
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Ultimately, these imaging approaches could be exploited as biomarkers to monitor clinical trials targeting the GAM population [>>135<<].
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