Viewing affirmative mentions of gene expression of Il17a (M. musculus) in T cells

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Nakae et al. (2002)Interleukin-17T cellsInterleukin-17 (IL-17) is a proinflammatory cytokine produced by T cells.
Xu et al. (2010)IL-17T cellsThese results imply that C5a affects the crosstalk between DC and gammadelta T cells during sepsis development, and this may result in a large production of inflammatory mediators such as IL-17.
Itoh et al. (2010)IL-17T cellsIntragraft gamma delta (gammadelta) T cells appear to be the predominant source of IL-17 production.
Crispín and Tsokos (2010)Interleukin-17T cellsInterleukin-17-producing T cells in lupus.
Deknuydt et al. (2009)IL-17T cellsModulation of inflammation through IL-17 production by gammadelta T cells: mandatory in the mouse, dispensable in humans?
Peng et al. (2008)IL-17T cellsOur findings in TB patients and healthy human were consistent with other murine investigation that the IL-17-producing gammadelta T cells were main source of IL-17 in mouse model of BCG infection, suggesting that gammadelta T cells might be involved in the formation of tubercular granuloma in pulmonary TB patients, but need further identification.
Braun et al. (2008)IL-17T cellsIL-17 producing gammadelta T cells are required for a controlled inflammatory response after bleomycin-induced lung injury.
Braun et al. (2008)IL-17T cellsCONCLUSION: Mouse gammadelta T cells produce IL-17 in response to lung injury and are required for an organized inflammatory response and epithelial repair.
Van Bezooijen et al. (2002)Interleukin 17T cellsBACKGROUND: Interleukin 17 (IL17) is produced by activated T cells and has been implicated in the development of bone lesions and cartilage degradation in rheumatoid arthritis (RA).
Hellings et al. (2003)IL-17T cellIn summary, our results demonstrate that IL-17 expression in airways is upregulated upon allergen inhalation, and constitutes the link between allergen-induced T cell activation and neutrophilic influx.
Edgerton et al. (2009)IL-17T cellsIL-17 producing CD4+ T cells mediate accelerated ischemia/reperfusion-induced injury in autoimmunity-prone mice.
Edgerton et al. (2009)IL-17T cellsThe tissue-infiltrating T cells were found to produce IL-17.
Sonnenberg et al. (2010)IL-17AT cells+ CD4+ T cells that expressed IL-17A alone, IL-22 alone, or coexpressed IL-17A and IL-22 in the BAL (Fig. 1 E, top; and Fig. 1 F).
Sonnenberg et al. (2010)IL-17AT cells+ CD4+ T cells that expressed IL-17A alone, and a trend toward an increase in the frequency of those that coexpressed IL-17A and IL-22 (Fig. 1 E, bottom).
Leppkes et al. (2009)IL-17AT lymphocytesRESULTS: Adoptive transfer of IL-17A-, IL-17F-, or IL-22-deficient T lymphocytes into RAG1-null mice caused severe colitis that was indistinguishable from that caused by wild-type cells.
Huang et al. (2006)IL-17AT-cellsInterleukin-17A (IL-17A) is a proinflammatory cytokine expressed in activated T-cells.
Lu et al. (2009)IL-17AT cellsPreviously we showed that protection against nasopharyngeal (NP) colonization by intranasal vaccination of mice with killed pneumococci is mediated by T(H)17 cells and correlates with interleukin-17A (IL-17A) expression by T cells in vitro; we have also shown that CWPS and other species-common antigens protect against colonization by a similar mechanism.
Lubberts et al. (2005)Interleukin-17T cellThe role of T cell interleukin-17 in conducting destructive arthritis: lessons from animal models Interleukin-17 (IL-17) is a T cell cytokine spontaneously produced by cultures of rheumatoid arthritis (RA) synovial membranes.
Jensen et al. (2008)IL-17T cellsBut when triggered through the T cell receptor, ligand-naive lymphoid-gammadelta T cells produced IL-17, whereas ligand-experienced cells made IFN-gamma.
Elliott et al. (2008)IL-17T cellA recently identified, strongly proinflammatory limb of the immune response is characterized by T cell IL-17 production.
Chu et al. (2007)IL-17T cellInterleukin-17 (IL-17) is a pivotal T cell cytokine in arthritis, and in vitro studies have indicated that IFNgamma suppresses IL-17 production.
Liu et al. (2005)IL-17T cellsSurprisingly, however, the pattern of regulation of IL-17 is different in mice than in humans, because "costimulation" of T cells through CD28 only mildly enhanced IL-17 expression, whereas levels of IL-2 were dramatically enhanced.
Liu et al. (2005)IL-17T cellsHowever, IL-17 production can occur autonomously in T cells, as neither dendritic cells nor IL-23 were necessary for promoting short-term production of IL-17.
Schwarzenberger et al. (1998)IL-17T cellsSince IL-17 is principally produced by CD4+ T cells, this cytokine could have therapeutic implications in AIDS-related bone marrow failure and opportunistic infections.
Madhur et al. (2010)IL-17T cellsWe found that angiotensin II infusion increased IL-17 production from T cells and IL-17 protein in the aortic media.
Min et al. (2009)IL-17T cellsLy6G+ cells were found to produce IL-17 during the early postoperative period and CD8+ as well as CD4+ T cells were also found to produce IL-17 during alloimmune response.
Min et al. (2009)IL-17T cellsIn conclusion, IL-17 is produced by neutrophils during the early postoperative period and subsequently by T(h)17 and CD8+ T cells during allograft rejection.
Feinen et al. (2010)interleukin-17T-cellsWe found that N. gonorrhoeae induced the production of interleukin-17 (IL-17) in mouse T-cells and Th17-inducing cytokines in mouse and human APCs in vitro.
Wakita et al. (2010)IL-17T cellsIL-17 production by tumor-infiltrating gammadelta T cells was blocked by anti-gammadeltaTCR or anti-NKG2D antibodies, indicating that these ligands, expressed within the tumor microenvironment, are involved in gammadelta T-cell activation.
Wilson et al. (2010)IL-17AT cellsTherefore, by stimulating myofibroblast activation and the production of IL-17A by T cells, TGF-?
Wilson et al. (2010)IL-17AT cells+ T cells providing a brake on the inflammatory response in addition to the early IL-17A production.
Pappu and Dong (2007)IL-17-expressingT cellsGeneration of IL-17-expressing T cells in vitro under defined culture conditions allows investigation of their differentiation regulation.
Komiyama et al. (2006)IL-17T cellsThe major producer of IL-17 upon treatment with myelin digodendrocyte glycopritein was CD4+ T cells rather than CD8+ T cells, and adoptive transfer of IL-17(-/-) CD4+ T cells inefficiently induced EAE in recipient mice.
Komiyama et al. (2006)IL-17T cellsNotably, IL-17-producing T cells were increased in IFN-gamma(-/-) cells, while IFN-gamma-producing cells were increased in IL-17(-/-) cells, suggesting that IL-17 and IFN-gamma mutually regulate IFN-gamma and IL-17 production.
Kleinschnitz et al. (2006)interleukin-17T cellT cell infiltration after chronic constriction injury of mouse sciatic nerve is associated with interleukin-17 expression.
Tan et al. (2006)IL-17AT cellsIn spleen-derived T cells, gamma irradiation induces significant murine IL-17A expression in vivo but not in vitro.
Nagata et al. (2008)IL-17T cellsIn this study, we show that the IL-17F homodimer via IL-17RA is a negative regulator of IL-17 production in T cells and suggest a mechanism whereby IL-17RA on T cells serves as an autocrine/paracrine regulator of IL-17 synthesis in T cells.
Nagata et al. (2008)IL-17T cellsRequirement of IL-17RA in Con A induced hepatitis and negative regulation of IL-17 production in mouse T cells.
Nagata et al. (2008)IL-17AT cellsTh17 cells, a subset of T cells involved in autoimmunity and host defense against extracellular Gram-negative infection, express both IL-17A and IL-17F.
Rutitzky and Stadecker (2006)interleukin-17T cellsCD4 T cells producing pro-inflammatory interleukin-17 mediate high pathology in schistosomiasis.
Staschke et al. (2009)IL-17T cellWe show here that inactivation of IRAK4 kinase in mice (IRAK4 KI) results in significant resistance to experimental autoimmune encephalomyelitis due to a reduction in infiltrating inflammatory cells into the CNS and reduced Ag-specific CD4(+) T cell-mediated IL-17 production.
Van bezooijen et al. (1999)Interleukin-17T cellsInterleukin-17 (IL-17) is a recently cloned cytokine that is exclusively produced by activated T cells, but its receptor has been found on several cells and tissues.
Haak et al. (2009)IL-17AT cellIn the context of EAE, neither the T cell-driven overexpression of IL-17A nor its complete loss had a major impact on the development of clinical disease.
Haak et al. (2009)IL-17AT cellAlthough ubiquitous overexpression of IL-17A led to skin inflammation and granulocytosis, T cell-specific IL-17A overexpression did not have a perceptible impact on the development and health of the mice.
Haak et al. (2009)IL-17AT cellWe conclude therefore that both IL-17A and IL-17F, while prominently expressed by an encephalitogenic T cell population, may only marginally contribute to the development of autoimmune CNS disease.
Sergejeva and Lindén (2009)IL-17AT cellsWe now know that the IL-17 family includes as a minimum 6 members, of whom at least IL-17A and IL-17F can be produced by T cells.
Kennedy et al. (1996)IL-17 mRNAT cellsMouse IL-17 mRNA is specifically expressed by activated alpha beta TCR + CD4-CD8- T cells, a small subset with a potentially important role in immune regulation.
Miossec (2000)interleukin-17T-cellIndeed, interleukin-17, a T-cell-specific cytokine, is produced by RA synovium and acts as a bone and cartilage destructive factor.
Lochner et al. (2008)IL-17T cellstogether with IL-6 induces CD4+ T cells to produce both IL-17 and IL-10, a population that is not able to induce inflammation in mice (13).
Lochner et al. (2008)IL-17T cellst+ T cells expressing both IL-17 and IL-10, as observed previously (13, 17).
Gao et al. (2010)IL-17T cellAdjuvant treatment suppresses IL-17 production by T cell-independent myeloid sources in nonobese diabetic mice.
Benghiat et al. (2008)IL-17T cellsIL-17 production elicited by allo-major histocompatibility complex class II recognition depends on CD25posCD4pos T cells.
Benghiat et al. (2008)IL-17T cellsRESULTS: Addition of CD25posCD4pos T cells to CD25negCD4pos T cells inhibited IL-2, interferon-[gamma], and IL-13 production but promoted IL-17 synthesis on stimulation by allogenic immature DC.
Benghiat et al. (2008)IL-17T cellsAlloreactive CD25negCD4pos T cells were also induced to produce IL-17 when stimulated by mature DC in the presence of CD25highCD4posFOXP3pos T cells.
Benghiat et al. (2008)IL-17T cellsCONCLUSIONS: We conclude that (1) the cellular source of IL-17 during an antiallo major histocompatibility complex class II response depends on the maturation status of allogenic DC, (2) whereas suppressing Th1 and Th2 cytokine synthesis, naturally occurring regulatory T cells, allow IL-17 production by alloreactive CD4pos T cells.
Ito et al. (2009)IL-17T cellsCONCLUSION: Gamma/delta T cells were antigen independently stimulated by inflammation at affected joints and produced enhanced amounts of IL-17 to exacerbate arthritis in mice with CIA but not in SKG mice with arthritis or patients with RA.
Ito et al. (2009)IL-17T cellsFurthermore, IL-17 production by gamma/delta T cells was induced by IL-1beta plus IL-23 independently of T cell receptor.
Sharp et al. (2008)IL-17T-cellsSplenic T-cells isolated from P2x7 null mice produced greater IFNgamma and IL-17 (from 3 to 12 fold greater levels) than wildtype cells, however cytokine production from P2x7 derived cells was not increased by a selective P2x7 agonist as was cytokine production from wildtype cells.
Paust et al. (2009)IL-17T cellHowever, the functions of the different T cell subsets, particularly the recently identified interleukin-17 (IL-17)-producing T cells (Th17 cells), are incompletely understood in glomerulonephritis.
Dolff et al. (2010)IL-17T cellsIn order to characterise IL-17 producing cells with a suitable marker expressed on the surface we analysed T cells for the expression of CCR6 [20].
Dolff et al. (2010)IL-17T-cellsThe percentages of CD134 and CD80 expressing IL-17 producing T-cells were significantly increased in SLE patients in comparison to healthy controls (CD134: 71.78 ± 14.51% vs. 51.45 ± 16.58%, P = 0.002; CD80: 25.5 ± 14.99% vs. 14.99 ± 5.74%, P = 0.02) (Figure 3a, b).
Dolff et al. (2010)IL17T-cellsExpression of costimulatory markers CD134 and CD80 on IL17-producing T-cells in active and inactive patients and patients with and without lupus nephritis
Dolff et al. (2010)IL-17T-cellsPatients with and without active disease were analysed for CD80 expression on IL-17 producing T-cells.
Dolff et al. (2010)IL-17T cellsThe percentages of CD80 expressing IL-17 producing T cells showed no differences between active and inactive patients (25.02 ± 16.01% vs. 25.97 ± 14.46%, P = 0.87).
Dolff et al. (2010)IL-17T cellsExpression of CD80 on IL-17 producing T cells in active patients tended to be increased as compared to healthy controls (25.02 ± 16.01% vs. 14.99 ± 5.74%, P = 0.07).
Dolff et al. (2010)IL-17T-cellsNo significant difference could be observed comparing the expression of CD80 on IL-17 producing T-cells in patients with class IV and V lupus nephritis (36.25 ± 18.66% vs. 21.93 ± 9.18%, P = 0.63).
Dolff et al. (2010)IL-17T-cellsInterestingly, there was a correlation between CD80 expression on IL-17 producing T-cells and anti-dsDNA titres and decreased C3 levels, respectively (r = 0.6, P = 0.0003 and r = -0.5, P = 0.01).
Dolff et al. (2010)IL-17T cellsExpression of CD134 on IL-17 producing T cells was significantly higher in patients with active disease as compared to healthy controls (74.87 ± 10.64% vs. 51.54 ± 16.58%, P = 0.0009).
Dolff et al. (2010)IL-17T-cellsAlso in patients with inactive disease expression of CD134 on IL-17 producing T-cells was higher as compared to healthy controls (68.69 ± 17.39% vs. 51.45 ± 16.58%, P = 0.0382), but it did not differ from active patients (68.69 ± 17.39% vs. 74.87 ± 10.64%, P = 0.34).
Dolff et al. (2010)IL-17T cellsPatients without lupus nephritis also showed higher levels of CD134 on IL-17 producing T cells in comparison to healthy individuals (70.27 ± 17.18% vs. 51.45 ± 16.58%, P = 0.01).
Dolff et al. (2010)IL-17T-cellsFurther, expression of CD134 on IL-17 producing T-cells showed no significant differences between class IV and V lupus nephritis (69.05 ± 10.97% vs. 78.27 ± 6.51%, P = 0.23).
Ferretti et al. (2003)IL-17T cellsWhen challenged with LPS, despite the absence of T cells, SCID mice also developed a neutrophilic response associated with IL-17 production.
Tanaka et al. (2009)IL-17T cellsNatural occurring IL-17 producing T cells regulate the initial phase of neutrophil mediated airway responses.
Tanaka et al. (2009)IL-17T cellIn this study, we report that the immune system contains a unique set of natural occurring IL-17 producing cell, "natural" Th17 (nTh17), which are a memory-like T cell subset.
Lan et al. (2009)IL-17T cellsCD4(+) T cells are a major source of IL-17, which compose a distinct T helper subset (Th17).
Shibata et al. (2007)IL-17T cellsResident Vdelta1+ gammadelta T cells control early infiltration of neutrophils after Escherichia coli infection via IL-17 production.
Gaffen (2004)IL-17T cellsIL-17 is produced primarily by T cells, particularly those of the memory compartment.
Yang et al. (2008)IL-17T cellsIL-17F is expressed in Th17 cells and other types of IL-17expressing T cells in vivo.
Nakae et al. (2003)IL-17T cellsIL-17 production from activated T cells is required for the spontaneous development of destructive arthritis in mice deficient in IL-1 receptor antagonist.
Nakae et al. (2003)IL-17T cellCross-linking OX40, a cosignaling molecule on CD4(+) T cells that plays an important role in T cell antigen-presenting cell interaction, with anti-OX40 Ab accelerated the production of IL-17 induced by CD3 stimulation.
Park and Lee (2010)IL-17T cellsT cells, and natural killer T cells also produce IL-17 [14,24,25].
Park and Lee (2010)IL-17T cellsA recent study using peripheral blood mononuclear cells and purified CD4+ T cells has demonstrated that treatment of a selective PDE4 inhibitor Zl-n-91 suppresses IL-17 production [103].
Lees et al. (2008)IL-17T cellsHost T cells are the main producers of IL-17 within the central nervous system during initiation of experimental autoimmune encephalomyelitis induced by adoptive transfer of Th1 cell lines.