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Namespace Prefixes

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n2:pmcid
PMC0
bibo:doi
10.1084%2Fjem.20041257
n6:contains
_:vb962668 _:vb962661 _:vb962686
Subject Item
_:vb962661
rdf:type
n6:Section
dc:title
materials and methods
n6:contains
_:vb962662 _:vb962663 _:vb962664 _:vb962665 _:vb962666 _:vb962667
Subject Item
_:vb962662
rdf:type
n2:Context
rdf:value
IL-23p19−/− (IL-23–deficient mice) and their WT controls were generated on a mixed B6 × 129 background using approaches described previously (>>1<<).
n2:mentions
n3:12610626
Subject Item
_:vb962663
rdf:type
n2:Context
rdf:value
EAE was induced in female mice at 8–12 wk and clinically assessed as described previously (>>1<<), using 100 μg MOG35-55 per mouse for B6 × 129 and C57BL/6 strains, or 80 μg PLP139-151 (PLP) per mouse for SJL strains and emulsified in CFA.
n2:mentions
n3:12610626
Subject Item
_:vb962664
rdf:type
n2:Context
rdf:value
Where required, brain- and spinal cord–infiltrating cells were isolated from MOG-immunized WT and IL-23p19−/− mice at day 7 (before EAE onset; reference >>1<<), and cultured with 100 μg/ml MOG for 18 h (plus Golgi-Plug for final 4 h) before intracellular cytokine staining.
n2:mentions
n3:12610626
Subject Item
_:vb962665
rdf:type
n2:Context
rdf:value
All samples were activated with 50 ng/ml PMA and 500 ng/ml ionomycin (Sigma-Aldrich) for 4 h before cDNA preparation. mRNA expression was quantitated by real-time PCR as described previously (>>2<<).
n2:mentions
n3:14662908
Subject Item
_:vb962666
rdf:type
n2:Context
rdf:value
Blood was collected and lysed (RBC lysis buffer; Sigma-Aldrich), and mononuclear cells from brains and spinal cord tissue were prepared as described previously (>>1<<) and surface stained with anti–CD4-APC.
n2:mentions
n3:12610626
Subject Item
_:vb962667
rdf:type
n2:Context
rdf:value
cells were sorted from PLP-primed SJL DLN cells cultured with rIL-12 for 10 d, after 3 h stimulation with anti-CD3/anti-CD28, using anti-CD45 anti–IFN-γ bispecific antibody-capture matrix kit (Miltenyi Biotec) as described previously (>>27<<).
n2:mentions
n3:12172546
Subject Item
_:vb962668
rdf:type
n6:Section
dc:title
results
n6:contains
_:vb962676 _:vb962677 _:vb962678 _:vb962679 _:vb962672 _:vb962673 _:vb962674 _:vb962675 _:vb962684 _:vb962685 _:vb962680 _:vb962681 _:vb962682 _:vb962683 _:vb962669 _:vb962670 _:vb962671
Subject Item
_:vb962669
rdf:type
n2:Context
rdf:value
To study the role of IL-23 in autoimmune inflammatory disease pathogenesis, we used a CNS autoimmune model because the target organ is normally free of activated macrophages and CD4+ T cells (>>13<<); therefore, we can monitor the infiltration of inflammatory cells into the CNS during disease development.
n2:mentions
n3:1669702
Subject Item
_:vb962670
rdf:type
n2:Context
rdf:value
TNF production was also markedly reduced in the IL-23p19−/− cells, consistent with a previous paper suggesting that IL-23 is required for TNF production by CNS-infiltrating T cells (>>12<<). Ex vivo analysis of draining LN (DLN) cells from immunized WT and IL-23p19−/− mice reflected the CNS data, with similar IFN-γ levels, but no IL-17 production by the IL-23p19−/− cells (2, 14, 15). These results suggest that IL-23 is not
n2:mentions
n3:12471147
Subject Item
_:vb962671
rdf:type
n2:Context
rdf:value
Ex vivo analysis of draining LN (DLN) cells from immunized WT and IL-23p19−/− mice reflected the CNS data, with similar IFN-γ levels, but no IL-17 production by the IL-23p19−/− cells (>>2<<, 14, 15). These results suggest that IL-23 is not required for Th1 development, but is essential for the development of autoantigen-specific, IL-17–producing CD4+ T cells.
n2:mentions
n3:14662908
Subject Item
_:vb962672
rdf:type
n2:Context
rdf:value
Ex vivo analysis of draining LN (DLN) cells from immunized WT and IL-23p19−/− mice reflected the CNS data, with similar IFN-γ levels, but no IL-17 production by the IL-23p19−/− cells (2, >>14<<, 15). These results suggest that IL-23 is not required for Th1 development, but is essential for the development of autoantigen-specific, IL-17–producing CD4+ T cells.
n2:mentions
n3:14978083
Subject Item
_:vb962673
rdf:type
n2:Context
rdf:value
Ex vivo analysis of draining LN (DLN) cells from immunized WT and IL-23p19−/− mice reflected the CNS data, with similar IFN-γ levels, but no IL-17 production by the IL-23p19−/− cells (2, 14, >>15<<). These results suggest that IL-23 is not required for Th1 development, but is essential for the development of autoantigen-specific, IL-17–producing CD4+ T cells.
n2:mentions
n3:12417590
Subject Item
_:vb962674
rdf:type
n2:Context
rdf:value
These results are consistent with papers suggesting that IL-23 is required for the development and expansion of IL-17–producing CD4+ T cells (>>2<<, 16, 17). Both ThIL-17 and Th1 cells also produced TNF (Fig. S1 A, available at http://www.jem.org/cgi/content/full/jem.20041257/DC1) and were characterized as CD4+ CD62Llo CD44hi, indicative of activated T cells; however, the ThIL-17
n2:mentions
n3:14662908
Subject Item
_:vb962675
rdf:type
n2:Context
rdf:value
These results are consistent with papers suggesting that IL-23 is required for the development and expansion of IL-17–producing CD4+ T cells (2, >>16<<, 17). Both ThIL-17 and Th1 cells also produced TNF (Fig. S1 A, available at http://www.jem.org/cgi/content/full/jem.20041257/DC1) and were characterized as CD4+ CD62Llo CD44hi, indicative of activated T cells; however, the ThIL-17 cells
n2:mentions
n3:9973376
Subject Item
_:vb962676
rdf:type
n2:Context
rdf:value
These results are consistent with papers suggesting that IL-23 is required for the development and expansion of IL-17–producing CD4+ T cells (2, 16, >>17<<). Both ThIL-17 and Th1 cells also produced TNF (Fig. S1 A, available at http://www.jem.org/cgi/content/full/jem.20041257/DC1) and were characterized as CD4+ CD62Llo CD44hi, indicative of activated T cells; however, the ThIL-17 cells
n2:mentions
n3:12707317
Subject Item
_:vb962677
rdf:type
n2:Context
rdf:value
Integrin-α3, which enhances cellular migration within the target organ during inflammation (>>18<<), was also up-regulated in the IL-23–driven cells.
n2:mentions
n3:2458366
Subject Item
_:vb962678
rdf:type
n2:Context
rdf:value
Its capacity to induce IL-17 and other proinflammatory factors appears important for neutrophil recruitment (>>17<<) and granuloma formation (19).
n2:mentions
n3:12707317
Subject Item
_:vb962679
rdf:type
n2:Context
rdf:value
Its capacity to induce IL-17 and other proinflammatory factors appears important for neutrophil recruitment (17) and granuloma formation (>>19<<). However, when dysregulated, it causes inflammatory responses often associated with autoimmunity.
n2:mentions
n3:11739515
Subject Item
_:vb962680
rdf:type
n2:Context
rdf:value
Anti–IL-17 treatment resulted in partial protection from EAE, consistent with a recent paper suggesting that IL-17–deficient mice are resistant to actively induced EAE and CIA (>>20<<), and confirming that the IL-23–IL-17 pathway is important in inflammatory autoimmune diseases.
n2:mentions
n3:14634133
Subject Item
_:vb962681
rdf:type
n2:Context
rdf:value
In addition, IL-17 may also have a role in the initial expansion of the ThIL-17 cells as suggested by a recent paper showing a role for IL-17 during immune priming (>>21<<). It was previously unclear whether the classical Th1-type/IFN-γ–mediated immune response is essential for induction or maintenance of autoimmune disease. Treatments with IFN-γ lead to disease exacerbation in human MS (22), and transgenic
n2:mentions
n3:12721360
Subject Item
_:vb962682
rdf:type
n2:Context
rdf:value
Treatments with IFN-γ lead to disease exacerbation in human MS (>>22<<), and transgenic mice overexpressing IFN-γ in the CNS showed increased oligodendrocyte death leading to demyelinating diseases (23, 24).
n2:mentions
n3:2882294
Subject Item
_:vb962683
rdf:type
n2:Context
rdf:value
Treatments with IFN-γ lead to disease exacerbation in human MS (22), and transgenic mice overexpressing IFN-γ in the CNS showed increased oligodendrocyte death leading to demyelinating diseases (>>23<<, 24). However, despite the potential toxic effects of IFN-γ in the CNS, mice that lack critical components of the Th1–IFN-γ pathway are highly susceptible to EAE (8–12). Consistent with this, treatment of PLP-immunized mice with
n2:mentions
n3:9888990
Subject Item
_:vb962684
rdf:type
n2:Context
rdf:value
Treatments with IFN-γ lead to disease exacerbation in human MS (22), and transgenic mice overexpressing IFN-γ in the CNS showed increased oligodendrocyte death leading to demyelinating diseases (23, >>24<<). However, despite the potential toxic effects of IFN-γ in the CNS, mice that lack critical components of the Th1–IFN-γ pathway are highly susceptible to EAE (8–12). Consistent with this, treatment of PLP-immunized mice with neutralizing
n2:mentions
n3:8612196
Subject Item
_:vb962685
rdf:type
n2:Context
rdf:value
However, despite the potential toxic effects of IFN-γ in the CNS, mice that lack critical components of the Th1–IFN-γ pathway are highly susceptible to EAE (>>8<<–12). Consistent with this, treatment of PLP-immunized mice with neutralizing antibodies against IFN-γ demonstrated intensified disease leading to >75% mortality (Fig. 6 B), indicating that loss of IFN-γ results in disease exacerbation.
n2:mentions
n3:12189243 n3:12574388 n3:12471147 n3:8598493 n3:8871615
Subject Item
_:vb962686
rdf:type
n6:Section
dc:title
discussion
n6:contains
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In key published EAE passive transfer papers (>>25<<, 26), PLP-primed DLN cells were cultured with rIL-12 for 4 d before transfer of 20–30 × 106 cells into recipient mice.
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In key published EAE passive transfer papers (25, >>26<<), PLP-primed DLN cells were cultured with rIL-12 for 4 d before transfer of 20–30 × 106 cells into recipient mice.
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A recent paper demonstrated that antigen-primed IFN-γ+ versus IFN-γ− cells have differential in vivo survival potentials (>>27<<). The IFN-γ+ cells were short-lived and performed immediate effector functions, whereas the IFN-γ− cells had increased durability and possessed long-term memory function.
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In addition, some but not all IFN-γ− cells could produce IFN-γ at a later stage after strong antigenic stimulation in the presence of IL-12 (>>27<<), suggesting a shared a precursor lineage.
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3, A and B, and reference >>3<<). In vitro activation of naive T cells in the presence of IL-23 could induce the generation of a small population of IL-17–producing T cells; however, during this short-term culture, IL-23 was unable to affect residual IFN-γ production.
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For example, naive T cells from autoimmune-prone DBA-1 mice can be driven to produce IL-17 when alternatively stimulated via ICOS (>>28<<).
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IL-17–deficient mice are resistant to CIA and EAE (>>20<<), and therapeutic treatment with an IL-17 antagonist antibody can reverse ongoing CIA (29), consistent with the notion that IL-17 functions during the effector phase of an inflammatory response.
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IL-17–deficient mice are resistant to CIA and EAE (20), and therapeutic treatment with an IL-17 antagonist antibody can reverse ongoing CIA (>>29<<), consistent with the notion that IL-17 functions during the effector phase of an inflammatory response.
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In addition, IL-17 has been found in many human autoimmune diseases, including multiple sclerosis (>>30<<), rheumatoid arthritis (31), and psoriasis (32).
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In addition, IL-17 has been found in many human autoimmune diseases, including multiple sclerosis (30), rheumatoid arthritis (>>31<<), and psoriasis (32).
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In addition, IL-17 has been found in many human autoimmune diseases, including multiple sclerosis (30), rheumatoid arthritis (31), and psoriasis (>>32<<). IL-17–producing T cells have also been identified in the synovial fluid of patients with Lyme arthritis (33), suggesting involvement of IL-17 in infection-induced immunopathology. IL-17 receptors that bind both IL-17 and IL-17F are
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IL-17–producing T cells have also been identified in the synovial fluid of patients with Lyme arthritis (>>33<<), suggesting involvement of IL-17 in infection-induced immunopathology.
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Engagement of IL-17 and/or IL-17F on these cell types promotes expression of IL-1, IL-6, IL-8, TNF, and ICAM-1, which are all critical factors that drive inflammation (>>34<<).
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IL-6 produced by LPS-activated dendritic cells can turn off regulatory T cell (T reg cell) function, allowing effector T cell activation (>>35<<). It is tempting to speculate that in the absence of microbe-activated dendritic cells, the IL-6–producing ThIL-17 cells may have the potential to directly inhibit the action of T reg cell function within the target organ during
n2:mentions
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The role of TNF in chronic inflammatory diseases is well recognized (>>36<<). Interestingly, TNF is produced by both Th1 and ThIL-17 cells after in vitro stimulation, suggesting that TNF may play a role in both IL-12 and IL-23 linked immune responses.
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