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n2:pmcid
PMC0
bibo:doi
10.1186%2F1471-2407-10-464
n8:contains
_:vb8585367 _:vb8585398 _:vb8585376 _:vb8585378
Subject Item
_:vb8585367
rdf:type
n8:Section
dc:title
results
n8:contains
_:vb8585368 _:vb8585369 _:vb8585370 _:vb8585371 _:vb8585372 _:vb8585373 _:vb8585374 _:vb8585375
Subject Item
_:vb8585368
rdf:type
n2:Context
rdf:value
Similar to the most recent published data, three populations of Gr-1+CD11b+ cells were identified [>>5<<-7]. The Gr-1low MDSC could be further subdivided in two populations based on size and inner complexity of the cells (forward [FSC]/side scatter [SSC]).
n2:mentions
n3:19637228 n3:19941314 n3:19757440
Subject Item
_:vb8585369
rdf:type
n2:Context
rdf:value
Since COX-2 is an essential enzyme for catalyzing the biosynthesis of tumour-derived prostaglandin E2 (PGE2), a molecule that induces MDSC [>>7<<], biopsies were stained for COX-2 expression.
n2:mentions
n3:19757440
Subject Item
_:vb8585370
rdf:type
n2:Context
rdf:value
More recently, it has been shown that macrophages can be derived from MDSC [>>6<<,29]. Therefore this cell population was also analyzed. Macrophages were characterized by FACS based on their FSC/SSC, in combination with the expression of CD11b, F4/80 and MHCII on their membrane. A significant reduction in macrophages
n2:mentions
n3:19941314
Subject Item
_:vb8585371
rdf:type
n2:Context
rdf:value
More recently, it has been shown that macrophages can be derived from MDSC [6,>>29<<]. Therefore this cell population was also analyzed. Macrophages were characterized by FACS based on their FSC/SSC, in combination with the expression of CD11b, F4/80 and MHCII on their membrane. A significant reduction in macrophages was
n2:mentions
n3:18285406
Subject Item
_:vb8585372
rdf:type
n2:Context
rdf:value
It has been shown that MDSC can down regulated the ζ-chain on T cells by ROS production in the lymphoid organs and thereby induce T cell tolerance [>>19<<,30]. We analyzed splenocytes of dietary celecoxib treated and untreated mice for their capability to produce ROS.
n2:mentions
n3:18413722
Subject Item
_:vb8585373
rdf:type
n2:Context
rdf:value
It has been shown that MDSC can down regulated the ζ-chain on T cells by ROS production in the lymphoid organs and thereby induce T cell tolerance [19,>>30<<]. We analyzed splenocytes of dietary celecoxib treated and untreated mice for their capability to produce ROS.
n2:mentions
n3:20142361
Subject Item
_:vb8585374
rdf:type
n2:Context
rdf:value
In our previous study we have shown that DC-based immunotherapy in this murine model leads to the induction of a strong anti-tumour response [>>28<<]. However, the effectiveness of the anti-tumour response was negatively influenced when tumours sizes increased [28].
n2:mentions
n3:15764728
Subject Item
_:vb8585375
rdf:type
n2:Context
rdf:value
However, the effectiveness of the anti-tumour response was negatively influenced when tumours sizes increased [>>28<<]. It has been addressed that one of the main reasons for immunotherapy failure is the induction of T cell tolerance by immune suppressive cells. To determine if treatment with celecoxib also intercepts the induction of T cell tolerance
n2:mentions
n3:15764728
Subject Item
_:vb8585376
rdf:type
n8:Section
dc:title
methods
n8:contains
_:vb8585377
Subject Item
_:vb8585377
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The occurrence of tumour growth, body weight, physical well-being and survival were measured for 2 months, as described previously [>>28<<].
n2:mentions
n3:15764728
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_:vb8585378
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n8:Section
dc:title
discussion
n8:contains
_:vb8585388 _:vb8585389 _:vb8585390 _:vb8585391 _:vb8585384 _:vb8585385 _:vb8585386 _:vb8585387 _:vb8585380 _:vb8585381 _:vb8585382 _:vb8585383 _:vb8585379 _:vb8585396 _:vb8585397 _:vb8585392 _:vb8585393 _:vb8585394 _:vb8585395
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Subdivision of the heterogeneous group of immature myeloid cells revealed that three types could be identified in tumour-bearing mice, reflecting findings done by others [>>5<<,7]. The PMN-MDSC population was most frequently present in the spleen of tumour-bearing mice. This population was also most capable of ROS production. Previous studies showed that ROS production by MDSC is the main factor for inducing T
n2:mentions
n3:19637228
Subject Item
_:vb8585380
rdf:type
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Subdivision of the heterogeneous group of immature myeloid cells revealed that three types could be identified in tumour-bearing mice, reflecting findings done by others [5,>>7<<]. The PMN-MDSC population was most frequently present in the spleen of tumour-bearing mice. This population was also most capable of ROS production. Previous studies showed that ROS production by MDSC is the main factor for inducing T
n2:mentions
n3:19757440
Subject Item
_:vb8585381
rdf:type
n2:Context
rdf:value
Previous studies showed that ROS production by MDSC is the main factor for inducing T cell tolerance by down regulation of the ζ-chain on activated T cells [>>19<<,30]. Celecoxib-treatment especially influenced this PMN-MDSC population compared to other MDSC subtypes in the spleen of tumour-bearing mice. Greifenberg et. al. recently showed that this population was not capable of NO production and
n2:mentions
n3:18413722
Subject Item
_:vb8585382
rdf:type
n2:Context
rdf:value
Previous studies showed that ROS production by MDSC is the main factor for inducing T cell tolerance by down regulation of the ζ-chain on activated T cells [19,>>30<<]. Celecoxib-treatment especially influenced this PMN-MDSC population compared to other MDSC subtypes in the spleen of tumour-bearing mice. Greifenberg et. al. recently showed that this population was not capable of NO production and
n2:mentions
n3:20142361
Subject Item
_:vb8585383
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recently showed that this population was not capable of NO production and therefore showed no suppressive effect on T cell proliferation in a T cell mixed leukocyte reaction (MLR) [>>5<<]. However, our data provides evidence that PMN-MDSC do play a significant role in tumour-induced immune suppression, since PMN-MDSC are most capable of producing ROS and thereby contribute to the induction of tolerance. Induction of
n2:mentions
n3:19637228
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_:vb8585384
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The decrease in COX-2 enzyme expression has been observed in other studies [>>31<<-33]. The mechanism by which celecoxib perturbs COX-2 protein expression is not known. It has been suggested that PGE2 functions as a feedback on COX-2 protein expression and that celecoxib inhibits this loop [34]. It is also possible that
n2:mentions
n3:14739610 n3:17285134 n3:12164875
Subject Item
_:vb8585385
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It has been suggested that PGE2 functions as a feedback on COX-2 protein expression and that celecoxib inhibits this loop [>>34<<]. It is also possible that the inhibitory effect of celecoxib on the NFκB pathway results in a reduced production of COX-2 proteins [35]. The reduction in COX-2 expression was accompanied by a reduction of PGE2 levels in peritoneal wash
n2:mentions
n3:11423555
Subject Item
_:vb8585386
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It is also possible that the inhibitory effect of celecoxib on the NFκB pathway results in a reduced production of COX-2 proteins [>>35<<]. The reduction in COX-2 expression was accompanied by a reduction of PGE2 levels in peritoneal wash of celecoxib treated mice. Unfortunately no clear division can be made between the MDSC types in tumour tissue. Since Gr-1 (Ly6g) and
n2:mentions
n3:15265936
Subject Item
_:vb8585387
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n2:Context
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Ochoa and colleagues have suggested that prostaglandin E2 produced by tumour cells induced the arginase I expression in MDSC [>>36<<]. For this reason, COX-2 inhibition to reduce MDSC in number and function has been proposed as promising strategy to improve immunotherapy. We have previously shown that upon injection of antigen-loaded DCs an effective immune response
n2:mentions
n3:17255300
Subject Item
_:vb8585388
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We have previously shown that upon injection of antigen-loaded DCs an effective immune response can be induced in a mouse model for mesothelioma depending on the timing of the immunotherapy [>>28<<]. In this study we were able to show that the reduction of MDSC in vivo was associated with an improved anti-tumour response and resulted in prolongation of survival in combination with DC-based immunotherapy. Same results were reported
n2:mentions
n3:15764728
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_:vb8585389
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Same results were reported by others [>>37<<]. We were not able to verify that the improvement of the anti-tumour response in tumour-bearing mice treated with celecoxib was directly caused by the reduction in MDSC.
n2:mentions
n3:14633712
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For example MDSC are critically depending on IFN-γ production by T cells [>>2<<]. To determine that the abolishment of suppression in celecoxib treatment mice was most likely caused by the reduction of MDSC number and function, we screened splenocytes of all mice for other cell-types.
n2:mentions
n3:19197294
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Significant correlations between the levels of COX-2 expression and survival were observed in many human cancers [>>38<<-40], including malignant pleural mesothelioma.
n2:mentions
n3:19088039 n3:19039588 n3:18797196
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For this reason COX-2 inhibition has been proposed as potential therapeutic target for mesothelioma [>>10<<,11]. Also PGE2 contributes to proliferation, survival, angiogenesis, migration and invasion of tumour cells [41].
n2:mentions
n3:12060628
Subject Item
_:vb8585393
rdf:type
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For this reason COX-2 inhibition has been proposed as potential therapeutic target for mesothelioma [10,>>11<<]. Also PGE2 contributes to proliferation, survival, angiogenesis, migration and invasion of tumour cells [41].
n2:mentions
n3:15115874
Subject Item
_:vb8585394
rdf:type
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Also PGE2 contributes to proliferation, survival, angiogenesis, migration and invasion of tumour cells [>>41<<].
n2:mentions
n3:19136477
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Although it is generally accepted that MDSC are part of the tumour microenvironment [>>19<<], their numbers or function may differ in various tumour cell-lines or other tumour model.
n2:mentions
n3:18413722
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_:vb8585396
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This is caused by differences in the cytokine, chemokine and growth factor production of tumour cells that determines the specific microenvironments [>>42<<,43]. To determine which patients may benefit from celecoxib treatment alone or in combination with immunotherapy, more research is needed.
n2:mentions
n3:17511773
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_:vb8585397
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This is caused by differences in the cytokine, chemokine and growth factor production of tumour cells that determines the specific microenvironments [42,>>43<<]. To determine which patients may benefit from celecoxib treatment alone or in combination with immunotherapy, more research is needed.
n2:mentions
n3:19124500
Subject Item
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n8:Section
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_:vb8585404 _:vb8585405 _:vb8585406 _:vb8585407 _:vb8585400 _:vb8585401 _:vb8585402 _:vb8585403 _:vb8585399 _:vb8585412 _:vb8585408 _:vb8585409 _:vb8585410 _:vb8585411
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These cells can inhibit anti-tumour responses in an antigen-specific and in a non-specific way [>>1<<,2]. Antigen-specific suppression takes place in lymphoid organs and depends on reactive oxygen species (ROS) production, leading to T cell tolerance. Antigen-non-specific suppression takes place at the tumour site and is mainly dependent
n2:mentions
n3:19307988
Subject Item
_:vb8585400
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n2:Context
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These cells can inhibit anti-tumour responses in an antigen-specific and in a non-specific way [1,>>2<<]. Antigen-specific suppression takes place in lymphoid organs and depends on reactive oxygen species (ROS) production, leading to T cell tolerance. Antigen-non-specific suppression takes place at the tumour site and is mainly dependent on
n2:mentions
n3:19197294
Subject Item
_:vb8585401
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Antigen-non-specific suppression takes place at the tumour site and is mainly dependent on nitric oxide (NO) secretion, causing T cell specific apoptosis [>>2<<-4]. More recently, it has been shown that the heterogeneous group of MDSC can be subdivided into three major groups. Polymorph nuclei MDSC (PMN-MDSC), mononuclear MDSC (MO-MDSC) and Gr-1low MDSC [5-7]. Greifenberg et. al. showed that the
n2:mentions
n3:19197294 n3:12111117 n3:16056256
Subject Item
_:vb8585402
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Polymorph nuclei MDSC (PMN-MDSC), mononuclear MDSC (MO-MDSC) and Gr-1low MDSC [>>5<<-7]. Greifenberg et. al. showed that the MO-MDSC and a subpopulation of Gr-1low MDSC can inhibit T cell proliferation by the production of NO, in contrast to the PMN-MDSC that did not show this suppressive capacity [5]. However, the exact
n2:mentions
n3:19637228 n3:19941314 n3:19757440
Subject Item
_:vb8585403
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showed that the MO-MDSC and a subpopulation of Gr-1low MDSC can inhibit T cell proliferation by the production of NO, in contrast to the PMN-MDSC that did not show this suppressive capacity [>>5<<]. However, the exact mechanisms that play a role in the induction of T cell tolerance by MDSC subtypes need to be further explored. As ROS production by MDSC also contributes to the induction of tolerance we determined the ROS producing
n2:mentions
n3:19637228
Subject Item
_:vb8585404
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The production of ROS by MDSC is highly depending upon cyclooxygenase-2 (COX-2) enzyme activity [>>8<<,9]. The inducible COX-2 enzyme is essential in the biosynthesis of prostaglandins.
n2:mentions
n3:17483367
Subject Item
_:vb8585405
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The production of ROS by MDSC is highly depending upon cyclooxygenase-2 (COX-2) enzyme activity [8,>>9<<]. The inducible COX-2 enzyme is essential in the biosynthesis of prostaglandins.
n2:mentions
n3:16186186
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_:vb8585406
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Therefore, high expression of COX-2 has been correlated with poor prognosis in cancer [>>10<<-12]. In addition, several studies showed the relevance of COX-2 inhibition in cancer progression [13-15]. Although the relation between COX-2 over-expression and prostaglandin E2 (PGE2) synthesis in cancer has been studied extensively,
n2:mentions
n3:12060628 n3:15115874 n3:15261433
Subject Item
_:vb8585407
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In addition, several studies showed the relevance of COX-2 inhibition in cancer progression [>>13<<-15]. Although the relation between COX-2 over-expression and prostaglandin E2 (PGE2) synthesis in cancer has been studied extensively, the impact on the tumour microenvironment is still under investigation [16-18].
n2:mentions
n3:18281656 n3:16943401 n3:16151811
Subject Item
_:vb8585408
rdf:type
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Although the relation between COX-2 over-expression and prostaglandin E2 (PGE2) synthesis in cancer has been studied extensively, the impact on the tumour microenvironment is still under investigation [>>16<<-18].
n2:mentions
n3:15374627 n3:12472107
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Increased evidence indicates that immune suppressive cells, recruited by tumour-derived factors, are the main cause of failure of novel anti-cancer therapies, including immunotherapy [>>4<<,19-24]. We investigated dendritic cell (DC)-based immunotherapy in a murine model of mesothelioma.
n2:mentions
n3:16056256
Subject Item
_:vb8585410
rdf:type
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Increased evidence indicates that immune suppressive cells, recruited by tumour-derived factors, are the main cause of failure of novel anti-cancer therapies, including immunotherapy [4,>>19<<-24]. We investigated dendritic cell (DC)-based immunotherapy in a murine model of mesothelioma.
n2:mentions
n3:18364001 n3:16967326 n3:11722621 n3:18650914 n3:18413722 n3:17695721
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It was found that the efficacy of this treatment is hampered by the highly immunosuppressive environment in mesothelioma [>>25<<]. Adjacent to this, it was found that COX-2 over-expression in mesothelioma correlates with poor prognosis [26]. Combining the current knowledge on MDSC, COX-2 over-expression and immune suppression, we aimed to determine the effect of
n2:mentions
n3:16540497
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_:vb8585412
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Adjacent to this, it was found that COX-2 over-expression in mesothelioma correlates with poor prognosis [>>26<<]. Combining the current knowledge on MDSC, COX-2 over-expression and immune suppression, we aimed to determine the effect of selective COX-2 inhibition on MDSC populations in the optimization of DC-based immunotherapy. We studied the
n2:mentions
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