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IL-17 Receptor Signaling Is Required to Control Polymicrobial Sepsis

FREITAS, Andressa; ALVES-FILHO, Jose C.; VICTONI, Tatiana; SECHER, Thomas; LEMOS, Henrique P.; SONEGO, Fabiane; CUNHA, Fernando Q.; RYFFEL, Bernhard
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
56.15%
Sepsis is a systemic inflammatory response resulting from the inability of the host to contain the infection locally. Previously, we demonstrated that during severe sepsis there is a marked failure of neutrophil migration to the infection site, which contributes to dissemination of infection, resulting in high mortality. IL-17 plays an important role in neutrophil recruitment. Herein, we investigated the role of IL-17R signaling in polymicrobial sepsis induced by cecal ligation and puncture (CLP). It was observed that IL-17R-deficient mice, subjected to CLP-induced non-severe sepsis, show reduced neutrophil recruitment into the peritoneal cavity, spread of infection, and increased systemic inflammatory response as compared with C57BL/6 littermates. As a consequence, the mice showed an increased mortality rate. The ability of IL-17 to induce neutrophil migration was demonstrated in vivo and in vitro. Beside its role in neutrophil recruitment to the infection focus, IL-17 enhanced the microbicidal activity of the migrating neutrophils by a mechanism dependent on NO. Therefore, IL-17 plays a critical role in host protection during polymicrobial sepsis. The Journal of Immunology, 2009, 182: 7846-7854.; FAPESP Fundacao de Amparo a Pesquisa do Estado de Sao Paulo; CNPq Conselho Nacional de Pesquisa a Desenvolvimento Tecnologico

IL-17 mediates articular hypernociception in antigen-induced arthritis in mice

PINTO, Larissa G.; CUNHA, Thiago M.; VIEIRA, Silvio M.; LEMOS, Henrique P.; VERRI JR., Waldiceu A.; CUNHA, Fernando Q.; FERREIRA, Sergio H.
Fonte: ELSEVIER SCIENCE BV Publicador: ELSEVIER SCIENCE BV
Tipo: Artigo de Revista Científica
ENG
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IL-17 is an important cytokine in the physiopathology of rheumatoid arthritis (RA). However, its participation in the genesis of nociception during RA remains undetermined. In this study, we evaluated the role of IL-17 in the genesis of articular nociception in a model of antigen (mBSA)-induced arthritis. We found that mBSA challenge in the femur-tibial joint of immunized mice induced a dose-and time-dependent mechanical hypernociception. The local IL-17 concentration within the mBSA-injected joints increased significantly over time. Moreover, co-treatment of mBSA challenged mice with an antibody against IL-17 inhibited hypernociception and neutrophil recruitment. In agreement, intraarticular injection of IL-17 induced hypernociception and neutrophil migration, which were reduced by the pre-treatment with fucoidin, a leukocyte adhesion inhibitor. The hypernociceptive effect of IL-17 was also reduced in TNFR1(-/-) mice and by pre-treatment with infliximab (anti-TNF antibody), a CXCR1/2 antagonist or by an IL-1 receptor antagonist. Consistent with these findings, we found that IL-17 injection into joints increased the production of TNF-alpha, IL-1 beta and CXCL1/KC. Treatment with doxycycline (non-specific MMPs inhibitor), bosentan (ET(A)/ET(B) antagonist)...

Evidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease

CARDOSO, C. R.; GARLET, G. P.; CRIPPA, G. E.; ROSA, A. L.; MARTINS JUNIOR, WALTER; ROSSI, M. A.; SILVA, J. S.
Fonte: WILEY-BLACKWELL PUBLISHING, INC Publicador: WILEY-BLACKWELL PUBLISHING, INC
Tipo: Artigo de Revista Científica
ENG
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Periodontal disease is a chronic inflammation of the attachment structures of the teeth, triggered by potentially hazardous microorganisms and the consequent immune-inflammatory responses. In humans, the T helper type 17 (Th17) lineage, characterized by interleukin-17 (IL-17) production, develops under transforming growth factor-beta (TGF-beta), IL-1 beta, and IL-6 signaling, while its pool is maintained by IL-23. Although this subset of cells has been implicated in various autoimmune, inflammatory, and bone-destructive conditions, the exact role of T lymphocytes in chronic periodontitis is still controversial. Therefore, in this study we investigated the presence of Th17 cells in human periodontal disease. Gingival and alveolar bone samples from healthy patients and patients with chronic periodontitis were collected and used for the subsequent assays. The messenger RNA expression for the cytokines IL-17, TGF-beta, IL-1 beta, IL-6, and IL-23 in gingiva or IL-17 and receptor activator for nuclear factor-kappa B ligand in alveolar bone was evaluated by real-time polymerase chain reaction. The production of IL-17, TGF-beta, IL-1 beta, IL-6, and IL-23 proteins was evaluated by immunohistochemistry and the presence of Th17 cells in the inflamed gingiva was confirmed by immunofluorescence confocal microscopy for CD4 and IL-17 colocalization. Our data demonstrated elevated levels of IL-17...

B Lymphocyte-Induced Maturation Protein-1 Contributes to Intestinal Mucosa Homeostasis by Limiting the Number of IL-17-Producing CD4(+) T Cells

Salehi, Soofia; Bankoti, Rashmi; Benevides, Luciana; Witten, Jessica; Couse, Michael; Silva, Joao S.; Dhall, Deepti; Meffre, Eric; Targan, Stephan; Martins, Gistaine A.
Fonte: AMER ASSOC IMMUNOLOGISTS; BETHESDA Publicador: AMER ASSOC IMMUNOLOGISTS; BETHESDA
Tipo: Artigo de Revista Científica
ENG
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The transcription factor B lymphocyte induced maturation protein-1 (Blimp-1) plays important roles in embryonic development and immunity. Blimp-1 is required for the differentiation of plasma cells, and mice with T cell specific deletion of Blimp-1 (Blimp-1CKO mice) develop a fatal inflammatory response in the colon. Previous work demonstrated that lack of Blimp-1 in CD4(+) and CD8(+) T cells leads to intrinsic functional defects, but little is known about the functional role of Blimp-1 in regulating differentiation of Th cells in vivo and their contribution to the chronic intestinal inflammation observed in the Blimp1CKO mice. In this study, we show that Blimp-1 is required to restrain the production of the inflammatory cytokine IL-17 by Th cells in vivo. Blimp-1CKO mice have greater numbers of IL-17 producing TCR beta(+)CD4(+)cells in lymphoid organs and in the intestinal mucosa. The increase in IL-17 producing cells was not restored to normal levels in wild-type and Blimp-1CKO mixed bone marrow chimeric mice, suggesting an intrinsic role for Blimp-1 in constraining the production of IL-17 in vivo. The observation that Blimp-1 deficient CD4(+) T cells are more prone to differentiate into IL-17(+)/IFN-gamma(+) cells and cause severe colitis when transferred to Rag1-deficient mice provides further evidence that Blimp-1 represses IL-17 production. Analysis of Blimp-1 expression at the single cell level during Th differentiation reveals that Blimp-1 expression is induced in Th1 and Th2 but repressed by TGF-beta in Th17 cells. Collectively...

Expressão de Foxp3, IL-17 e IL-23 na Leishmaniose Tegumentar Americana causada por Leishmania (Leishmania) amazonensis e Leishmania (Viannia) braziliensis; Expression of Foxp3, IL-17 and IL-23 in American cutaneous leishmaniasis due Leishmania (Leishmania) amazonensis and Leishmania (Viannia) braziliensis

Menezes, Joyce Prieto Bezerra de
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 13/09/2013 PT
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A leishmaniose tegumentar americana (LTA) apresenta um amplo espectro de manifestações clínicas e imunopatológicas resultante da interação entre as diferentes espécies de Leishmania e os mecanismos de resposta imune do hospedeiro. Leishmania (Viannia) braziliensis e Leishmania (Leishmania) amazonensis são as espécies de maior potencial patogênico para o homem e de importância médica no Brasil. As células TCD4, quando ativadas por antígenos via MHC II podem se diferenciar em linhagens de células efetoras como Th1, Th2, Th17 e células T reguladoras (Treg). IL-23 é indispensável para as funções efetoras e manutenção de células Th17. O objetivo deste trabalho foi avaliar a expressão de Foxp3, IL-17 e IL-23 em lesões cutâneas de pacientes com diferentes formas clínicas da LTA. Biópsias parafinadas de 44 pacientes foram submetidas à imunoistoquímica, sendo 6 casos de leishmaniose cutânea anérgica difusa (LCADIDRM-) e leishmaniose cutânea disseminada borderline (LCDBIDRM-), ambas causadas por L.(L) amazonensis e 16 casos de leishmaniose cutânea localizada (LCLIDRM+) também causada por L.(L.) amazonensis; 9 casos de LCLIDRM+, 2 casos de LCDBIDRM- e 5 casos de leishmaniose cutâneo-mucosa (LCMIDRM+), todos causados por L.(V.) braziliensis. A densidade de células Tregs Foxp3+ no espectro clínico da LTA mostrou um aumento progressivo partindo das formas centrais LCL causadas por L.(V.) braziliensis (170mm2) e L.(L) amazonensis (140mm2) para as formas polares...

Mecanismos moleculares da ação dos glicocorticóides endógenos e da anexina-A1 sobre o tráfego de neutrófilos: caracterização da ação sobre os  eixos SDF-1α/CXCR4 e IL-17/IL-23/G-CSF; Molecular mechanisms of endogenous glucocorticoid and annexin-a1 actions on neutrophil traffic: characterization of this action on the SDF-1α/CXCR4 e IL-17/IL23/G-CSF axis

Machado, Isabel Daufenback
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 17/12/2013 PT
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O tráfego de leucócitos é um processo complexo, dependente da ação de inúmeras substâncias químicas, além da perfeita interação celular. Desta forma, este estudo teve como objetivo avaliar a ação dos GCe e da ANXA1 sobre o eixo SDF-1α/CXCR4 e IL-17/IL-23/G-CSF e sobre a expressão de moléculas de adesão CD18, CD49d e CD62L. Foram utilizados camundongos machos Balb/C selvagens (WT) ou ANXA1-/-. As avaliações foram realizadas em condições basais, na presença de altas concentrações de GCe e na vigência de processo inflamatório, induzidos pela administração de ACTH (5 µg/animal, i.p.) ou pela injeção de LPS (100 µg/kg, i.p.), respectivamente, ou na ausência da ação dos GCe, pela ação do RU 38486 (RU, 10 mg/kg, i.p.). A participação da ANXA1 e do receptor FPR2 foi avaliada pelo pré-tratamento com Ac2-26 (1 mg/Kg, i.p.) ou com BOC2 (10 µg/animal, i.p.) durante 4 dias, 1 vez ao dia. A quantificação total e diferencial das células foi realizada em câmara de Neubauer e em esfregaços corados por May-Grunwald ou citometria de fluxo. As quantificações de CXCR2, CXCR4, FPR2, CD18, CD49d, CD62L e maturação granulocítica (CD11b/Ly6G) em células da medula e da circulação foram realizadas por citometria de fluxo. A expressão de ANXA1 nos tecidos do estomago e do baço foi realizada por western blotting e nas células da medula óssea e sangue circulante foi realizada por imunofluorescência. As quantificações de IL-17...

Influência da infecção endodôntica associada ou não à diabetes nos níveis da citocina pró-inflamatória IL-17 nos tecidos periapical, hepático e renal de ratos Wistar

Azuma, Mariane Maffei
Fonte: Universidade Estadual Paulista (UNESP) Publicador: Universidade Estadual Paulista (UNESP)
Tipo: Dissertação de Mestrado Formato: 68 f. : il. + 1 CD-ROM
POR
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP); Processo FAPESP: 12/02565-2; Pós-graduação em Ciência Odontólogica - FOA; O objetivo deste trabalho foi avaliar a influência da infecção endodôntica associada ou não à diabetes, nos níveis da citocina pró-inflamatória IL-17, nos tecidos periapical, hepático e renal de ratos Wistar. Foram utilizados 40 ratos machos divididos em quatro grupos contendo 10 animais cada grupo: ratos normoglicêmicos (N); ratos normoglicêmicos com periodontite apical (N-PA); ratos com diabetes experimental (DE); ratos com diabetes experimental e com periodontite apical (DE-PA). A diabetes foi induzida por meio da administração de estreptozotocina via veia peniana. Foi realizada avaliação glicêmica, para confirmar o desenvolvimento da doença, no sexto e no último dia do experimento. A infecção endodôntica foi induzida por meio da exposição pulpar do primeiro molar superior direito ao meio bucal. Após 30 dias, foram coletados o fígado e o rim, para a quantificação da IL-17 pelo método ELISA, bem como a hemi-maxila direita para a quantificação da IL-17 pela técnica imunoistoquímica. Os valores obtidos nos testes paramétricos foram tabulados e analisados...

Influência da infecção endodôntica e/ou periodontal associadas à diabetes na quantificação sérica da citocina pró-inflamatória IL-17 e na glicemia de ratos Wistar

Samuel, Renata Oliveira
Fonte: Universidade Estadual Paulista (UNESP) Publicador: Universidade Estadual Paulista (UNESP)
Tipo: Dissertação de Mestrado Formato: 62 f : il. + 1 CD-ROM
POR
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq); Pós-graduação em Ciência Odontólogica - FOA; The aim of the study was to evaluate the influence of periapical lesions and/or periodontal disease on the IL-17 serum and dosage glycemic a rat model of diabetes mellitus. Eighty male Wistar rats were divided into eight groups of ten animals each: normal rats (G1), rats with pulpal infection (G2), rats with periodontal disease (G3), rats with pulpal infection and periodontal disease (G4), diabetic rats (G5), diabetic rats with pulpal infection (G6), diabetic rats with periodontal disease (G7), diabetic rats with pulpal infection and periodontal disease (G8). Diabetes was induced using streptozotocin, pulpal infection were induced by dental pulp exposure to the oral environment and the periodontal disease by periodontal ligature. Blood glucose was measured by means of a perforation in the tail of the animal after 0, 6 and 30 days post-operative. The animals were sacrificed after 30 days and the IL-17 levels were measured by ELISA. The total assessed values was tabulated according to each experimental group and statistically analyzed by analysis of variance (ANOVA) followed by Tukey test (p<0.05). Glucose levels were higher in diabetic rats compared to control rats at 6...

Cutting edge : IFN-γ regulates the induction and expansion of IL-17-producing CD4 T cells during mycobacterial infection

Cruz, Andrea; Khader, Shabaana A.; Torrado, Egídio; Fraga, Alexandra G.; Pearl, John E.; Pedrosa, Jorge; Cooper, Andrea M.; Castro, António G.
Fonte: American Association of Immunologists Publicador: American Association of Immunologists
Tipo: Artigo de Revista Científica
Publicado em //2006 ENG
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66.16%
T cell responses are important to the control of infection but are deleterious if not regulated. IFN-γ-deficient mice infected with mycobacteria exhibit enhanced accumulation of activated effector T cells and neutrophils within granulomatous lesions. These cells do not control bacterial growth and compromise the integrity of the infected tissue. We show that IFN-γ-deficient mice have increased numbers of IL-17-producing T cells following infection with Mycobacterium bovis bacille Calmette Gue´rin. Furthermore, exogenous IFN-γ increases IL-12 and decreases IL-23 production by bacille Calmette Gue´rin-infected bone marrow-derived dendritic cells and reduces the frequency of IL-17-producing T cells induced by these bone marrow-derived dendritic cells. These data support the hypothesis that, during mycobacterial infection, both IFN-γ- and IL-17-producing T cells are induced, but that IFN-γ serves to limit the IL-17-producing T cell population. This counterregulation pathway may be an important factor in limiting mycobacterially associated immune- mediated pathology.; Fundacão para a Ciência e Tecnologia (FCT) - grant SFRH/BD/9624/2002

Modulation of IL-17 and Foxp3 expression in the prevention of autoimmune arthritis in mice

Duarte, Joana; Agua-Doce, Ana; Oliveira, Vanessa G.; Fonseca, João Eurico; Graça, Luís
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em /05/2010 ENG
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©2010 Duarte et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.; Background: Rheumatoid Arthritis (RA) is a chronic immune mediated disease associated with deregulation of many cell types. It has been reported that different T cell subsets have opposite effects in disease pathogenesis, in particular Th17 and Treg cells. Methodology and Findings: We investigated whether non-depleting anti-CD4 monoclonal antibodies, which have been reported as pro-tolerogenic, can lead to protection from chronic autoimmune arthritis in SKG mice – a recently described animal model of RA – by influencing the Th17/Treg balance. We found that non-depleting anti-CD4 prevented the onset of chronic autoimmune arthritis in SKG mice. Moreover, treated mice were protected from the induction of arthritis up to 60 days following anti-CD4 treatment, while remaining able to mount CD4-dependent immune responses to unrelated antigens. The antibody treatment also prevented disease progression in arthritic mice, although without leading to remission. Protection from arthritis was associated with an increased ratio of Foxp3...

A Deficiência de vitamina d está associada com níveis aumentados de il-17 e tnfα em pacientes com insuficiência cardíaca crônica

Milovanovic,Milena; Pesic,Gordana; Nikolic,Valentina; Jevtovic-Stoimenov,Tatjana; Vasic,Karin; Jovic,Zorica; Deljanin-Ilic,Marina; Pesic,Srdjan
Fonte: Sociedade Brasileira de Cardiologia - SBC Publicador: Sociedade Brasileira de Cardiologia - SBC
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/03/2012 PT
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FUNDAMENTO: Estudos recentes revelaram uma forte associação entre o estado de vitamina D (VD) e a insuficiência cardíaca crônica (ICC). Hoje, é normalmente aceito que a resposta imune pró-inflamatória é subjacente ao desenvolvimento de ICC. OBJETIVO: Uma vez que a VD possui propriedades anti-inflamatórias, pesquisamos o seu impacto sobre as citocinas envolvidas na ICC, como TNFα e IL-17, em pacientes portadores de ICC. MÉTODOS: Foi extraído sangue de quarenta pacientes com ICC secundária à hipertensão arterial e/ou doença coronariana. Os níveis de VD status, IL-17 e TNFαforam avaliados através de 25-hidroxi VD3 EIA e ELISA de citocinas. Também foram realizadas avaliação clínica e ecocardiograma. RESULTADOS: Pacientes idosos com ICC em Nis (Sudeste da Europa, latitude 43ºN) apresentaram níveis de 25-hidroxi VD3 abaixo do normal. Nossos dados demonstraram que pacientes com ICC secundária à hipertensão arterial têm níveis significativamente menores de 25-hidroxi VD3, e maiores de TNFαe IL-17A, se comparados com os níveis de pacientes com ICC secundária à doença coronariana. CONCLUSÃO: É demonstrado aqui que, mesmo em regiões com muitos dias ensolarados a deficiência de VD é motivo de preocupação. Os dados sugerem que o déficit de VD contribui para os elevados níveis de IL-17 e TNFα e...

Greater expression of the human leukocyte antigen-G (HLA-G) and interleukin-17 (IL-17) in cervical intraepithelial neoplasia: analytical cross-sectional study

Miranda,Lidyane Neves; Reginaldo,Fernanda Priscila Santos; Souza,Daliana Maria Berenice Oliveira; Soares,Christiane Pienna; Silva,Tarsia Giabardo Alves; Rocha,Keyla Borges Ferreira; Jatobá,Carlos André Nunes; Donadi,Eduardo Antonio; Andrade,Joanlise Mar
Fonte: Associação Paulista de Medicina - APM Publicador: Associação Paulista de Medicina - APM
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/01/2014 EN
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CONTEXT AND OBJECTIVE: Impaired local cell immunity seems to contribute towards the pathogenesis and progression of cervical intraepithelial neoplasia (CIN), but the underlying molecular mechanisms promoting its progression remain unclear. Identification of new molecular markers for prognosis and diagnosis of early-stage CIN may aid in decreasing the numbers of CIN cases. Several novel immunoregulatory molecules have been discovered over the past few years, including the human leukocyte antigen G (HLA-G), which through interaction with its receptors exerts important tolerogenic functions. Several lines of evidence suggest that T-helper interleukin-17 (IL-17)-producing cells (Th17 cells) may play a role in antitumor immunity. However, recent reports have implicated Th17 cells and their cytokines in both pro and anti-tumorigenic processes. The aim of the study was to evaluate the roles of HLA-G and Th17 in the immunopathogenesis of CIN I. DESIGN AND SETTING: Analytical cross-sectional study with a control group using 58 cervical specimens from the files of a public university hospital providing tertiary-level care. METHODS: We examined HLA-G and IL-17 expression in the cervical microenvironment by means of immunohistochemistry, and correlated these findings with clinical and pathological features. RESULTS: There was a greater tendency towards HLA-G and IL-17 expression in specimens that showed CIN I...

Current data on IL-17 and Th17 cells and implications for graft versus host disease

Normanton,Marília; Marti,Luciana Cavalheiro
Fonte: Instituto Israelita de Ensino e Pesquisa Albert Einstein Publicador: Instituto Israelita de Ensino e Pesquisa Albert Einstein
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/06/2013 EN
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Human interleukin 17 was first described in 1995 as a new cytokine produced primarily by activated T CD4+ cells that stimulate the secretion of IL-6 and IL-8 by human fibroblasts, besides increasing the expression of ICAM-1. Various authors have reported that IL-17A has a role in the protection of organisms against extracellular bacteria and fungi due to the capacity of IL-17A to recruit neutrophils to the areas of infection, evidencing a pathological role in various models of autoimmune diseases, such as experimental autoimmune encephalitis and arthritis. The participation of IL-17A has also been described in the acute rejection of organ transplants and graft versus host disease. However, the greatest revolution in research with IL-17 happened in 2000, when it was proposed that IL-17 cannot be classified as Th1 or Th2, but rather, simply as a new lineage of IL-17-producing T-cells. These findings modified the previously established Th1/Th2 paradigm, leading to the definition of the CD3+ CD4+ Th17 cellular subtype and establishment of a new model to explain the origin of various immune events, as well as its implication in the graft versus host disease that is discussed in depth in this article.

IL-17 induces the production of IL-16 in rheumatoid arthritis

Cho, Mi-La; Jung, Young Ok; Kim, Kyoung-Woon; Park, Mi-Kyung; Oh, Hye-Joa; Ju, Ji-Hyeon; Cho, Young-Gyu; Min, Jun-Ki; Kim, Sung-Il; Park, Sung-Hwan; Kim, Ho-Youn
Fonte: Korean Society of Medical Biochemistry and Molecular Biology Publicador: Korean Society of Medical Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
EN
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The purpose of this study was to investigate the expression of IL-16 in the rheumatoid synovium and the role of inflammatory cytokines and Toll-like receptor (TLR) ligands in IL-16 production by fibroblastlike synoviocytes (FLS) of rheumatoid arthritis (RA) patients. Immunohistochemical staining was performed with a monoclonal antibody to IL-16 in synovial tissues from patients with RA and likewise in patients with osteoarthritis (OA). FLS were isolated from RA synovial tissues and stimulated with IL-15, IL-1β, IFN-γ, and IL-17. The IL-16 mRNA level was assessed by semiquantitative RT-PCR and real time (RT) PCR and a comparison was made between IL-16 mRNA levels produced by RA-FLS and OA-FLS. Production of IL-16 was identified by a western blot assay, and IL-16 production after stimulation by specific ligands of TLR2 and TLR4 was assessed by RT-PCR. While immunohistochemical staining demonstrated strong expression of IL-16 mRNA in synovial tissues from patients with RA, similar findings were not present in the OA group. Moreover, mRNA expression of IL-16 by RA-FLS increased after treatment with IL-17 but not with IL-15, IL-1β, and IFN-γ. Specifically, IL-17 increased IL-16 mRNA level by RA-FLS and peripheral blood mononuclear cells in a dose-dependent manner. However...

Sequential evolution of IL-17 responses in the early period of allograft rejection

Min, Sang Il; Ha, Jongwon; Park, Chung-Gyu; Won, Jae Kyung; Park, Yang Jin; Min, Seung-Kee; Kim, Sang Joon
Fonte: Korean Society of Medical Biochemistry and Molecular Biology Publicador: Korean Society of Medical Biochemistry and Molecular Biology
Tipo: Artigo de Revista Científica
EN
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In addition to CD4+CD25+Foxp3+ regulatory T (Treg) cells which protect against autoimmune tissue injury, IL-17-producing CD4+ T (Th17) cells have been recently described and shown to play a crucial role in autoimmune injury. It appears that there is a reciprocal developmental pathway between Th17 and Treg cells. Although IL-17 is known to be associated with allograft rejection, the cellular source of IL-17 and the nature of Th17 in the context of allograft rejection remain unknown. In the current study, the dynamics of Treg and IL-17-producing cells after syngeneic and allogeneic transplantation were examined using a wild-type murine cardiac transplantation model. Ly6G+ 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. Graft-infiltrating Ly6G+, CD4+, and even CD8+ cells were found to express IL-17 highly compared to those in spleen. Although the frequencies of Th17 and Treg were found to gradually increase in both syngeneic and allogeneic recipients, Th17/Treg ratios were significantly higher in recipients with allograft rejection than in syngeneic recipients. In conclusion, IL-17 is produced by neutrophils during the early postoperative period and subsequently by Th17 and CD8+ T cells during allograft rejection. Th17/Treg imbalance is associated with the development of allograft rejection. This study would provide basic information on Th17 biology for future investigation in the field of transplantation.

Acetyl salicylic acid inhibits Th17 airway inflammation via blockade of IL-6 and IL-17 positive feedback

Moon, Hyung-Geun; Kang, Chil Sung; Choi, Jun-Pyo; Choi, Dong Sic; Choi, Hyun Il; Choi, Yong Wook; Jeon, Seong Gyu; Yoo, Joo-Yeon; Jang, Myoung Ho; Gho, Yong Song; Kim, Yoon-Keun
Fonte: Nature Publishing Group Publicador: Nature Publishing Group
Tipo: Artigo de Revista Científica
EN
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T-helper (Th)17 cell responses are important for the development of neutrophilic inflammatory disease. Recently, we found that acetyl salicylic acid (ASA) inhibited Th17 airway inflammation in an asthma mouse model induced by sensitization with lipopolysaccharide (LPS)-containing allergens. To investigate the mechanism(s) of the inhibitory effect of ASA on the development of Th17 airway inflammation, a neutrophilic asthma mouse model was generated by intranasal sensitization with LPS plus ovalbumin (OVA) and then challenged with OVA alone. Immunologic parameters and airway inflammation were evaluated 6 and 48 h after the last OVA challenge. ASA inhibited the production of interleukin (IL)-17 from lung T cells as well as in vitro Th17 polarization induced by IL-6. Additionally, ASA, but not salicylic acid, suppressed Th17 airway inflammation, which was associated with decreased expression of acetyl-STAT3 (downstream signaling of IL-6) in the lung. Moreover, the production of IL-6 from inflammatory cells, induced by IL-17, was abolished by treatment with ASA, whereas that induced by LPS was not. Altogether, ASA, likely via its acetyl moiety, inhibits Th17 airway inflammation by blockade of IL-6 and IL-17 positive feedback.

IL-17 producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity

Kim, Hye Young; Lee, Hyun Jun; Chang, Ya-Jen; Pichavant, Muriel; Shore, Stephanie A.; Fitzgerald, Katherine A.; Iwakura, Yoichiro; Israel, Elliot; Bolger, Kenneth; Faul, John; DeKruyff, Rosemarie H.; Umetsu, Dale T.
Fonte: Harvard University Publicador: Harvard University
Tipo: Artigo de Revista Científica
EN_US
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Obesity is associated with the development of asthma and considerable asthma-related healthcare utilization. To understand the immunological pathways that lead to obesity-associated asthma, we fed mice a high fat diet for 12 weeks, which resulted in obesity and the development of airway hyperreactivity (AHR), a cardinal feature of asthma. This AHR depended on innate immunity, since it occurred in obese Rag−/− mice, and on IL-17A and the NLRP3 inflammasome, since it did not develop in obese Il17−/− or Nlrp3−/− mice. The AHR was also associated with the presence in the lungs of CCR6+ innate lymphoid cells producing IL-17A (ILC3 cells), which could by themselves mediate AHR when adoptively transferred into Rag2−/− Il2rγ−/− mice. IL-1β played an important role by expanding the ILC3 cells, and treatment to block the function of IL-1β abolished obesity-induced AHR. Since we found ILC3-like cells in the bronchoalveolar lavage fluid of human patients with asthma, we suggest that obesity-associated asthma is facilitated by inflammation mediated by NLRP3, IL-1β and ILC3 cells.

Imunoexpressão da IL-17 e RORγt em carcinomas de células escamosas de lábio e língua

Bezerra, Thâmara Manoela Marinho
Fonte: Universidade Federal do Rio Grande do Norte; BR; UFRN; Programa de Pós-Graduação em Patologia Oral; Odontologia Publicador: Universidade Federal do Rio Grande do Norte; BR; UFRN; Programa de Pós-Graduação em Patologia Oral; Odontologia
Tipo: Dissertação Formato: application/pdf
POR
Relevância na Pesquisa
56.23%
Th17 cells have been strongly associated to the pathogenesis of inflammatory and autoimmune diseases, although their influence on the carcinogenesis is still little known, there are reports of anti-tumor and protumoral actions. The objective of this study is to research the presence of Th17 lineage in lip and tongue SCC, using the analysis of the immunoexpression of IL-17 and RORγt, relating this immunoexpression with clinical and morphological findings in the attempt to better comprehend the role of these cells on the tumoral immunity of OSCCs. The results were submitted to non-parametric statistical tests with significance level of 5%. On the histomorphological analysis, it was observed the predominance of low level lesions on lip and high level lesions on tongue (p=0,024). It was not observed statistical significance between clinical stage and histological gradation of malignancy (p=0,644). For the immunohistochemical study, 5 random fields with greater immunoreactivity of the peritumoral inflammatory infiltrate were photomicrographed on the 400x magnification. It was done the count of lymphocytes which showed cytoplasmic and pericytoplasmic staining for the IL-17 cytokine as well as nuclear and cytoplasmic staining for RORγt. It was observed statistical significance difference on the quantity of immunopositive lymphocytes to IL-17 between the groups of SCC of lip and tongue (p=0...

ZBTB7B (Th-POK) regulates the development of IL-17 -producing-CD1d-restricted mouse NKT cells

Enders, Anselm; Stankovic, Sanda; Teh, Charis; Uldrich, Adam P; Yabas, Mehmet; Juelich, Torsten; Altin, John A.; Frankenreiter, Sandra; Bergmann, Hannes; Roots, Carla M.; Kyparissoudis, Konstantinos; Goodnow, Chris C.; Godfrey, Dale I.
Fonte: American Association of Immunologists Publicador: American Association of Immunologists
Tipo: Artigo de Revista Científica Formato: 10 + 5 pages
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66.04%
CD1d-dependent NKT cells represent a heterogeneous family of effector T cells including CD4+CD8- and CD4-CD8- subsets that respond to glycolipid Ags with rapid and potent cytokine production. NKT cell development is regulated by a unique combination of factors, however very little is known about factors that control the development of NKT subsets. In this study, we analyze a novel mouse strain (helpless) with a mis-sense mutation in the BTB-POZ domain of ZBTB7B and demonstrate that this mutation has dramatic, intrinsic effects on development of NKT cell subsets. Although NKT cell numbers are similar in Zbtb7b mutant mice, these cells are hyperproliferative and most lack CD4 and instead express CD8. Moreover, the majority of ZBTB7B mutant NKT cells in the thymus are retinoic acid-related orphan receptor γt positive, and a high frequency produce IL-17 while very few produce IFN-γ or other cytokines, sharply contrasting the profile of normal NKT cells. Mice heterozygous for the helpless mutation also have reduced numbers of CD4+ NKT cells and increased production of IL-17 without an increase in CD8+ cells, suggesting that ZBTB7B acts at multiple stages of NKT cell development. These results reveal ZBTB7B as a critical factor genetically predetermining the balance of effector subsets within the NKT cell population.; NHMRC (National Health and Medical Research Council of Australia)

Lipopolysaccharide-Mediated Regulation of IL-17 Receptor Levels in Human Monocytes

ZHANG, Xiubo
Fonte: Quens University Publicador: Quens University
Tipo: Tese de Doutorado
EN; EN
Relevância na Pesquisa
56.24%
IL-17 promotes inflammation through the recruitment of monocytes and induction of various chemokines and inflammatory cytokines. Monocytes respond to IL-17 through the heteromeric IL-17 receptor (IL-17R) composed of subunits IL-17RA and IL-17RC. Together, monocytes and IL-17 amplify inflammation. Controlling the cellular response to IL-17 is crucial to prevent hyperactivation of inflammatory responses, which could lead to chronic inflammatory diseases. The cellular response to increased IL-17 levels may be limited by controlling the receptor levels. Before we understand how monocytes respond to IL-17 during infection, we must first characterize the expression of IL-17R in these cells in response to LPS, a well-characterized pro-inflammatory signal. The aim of this study is to understand the mechanisms which regulate IL-17R levels in human monocytes. IL-17R mRNA and protein levels were measured in response to LPS by RT-PCR and Western blot analysis in primary human monocytes, peripheral blood mononuclear cells (PBMC), and the human monocytic cell line, THP-1. LPS enhanced IL-17RA and RC transcript levels in monocytes and PBMC. In contrast, IL-17RA protein levels decreased with LPS treatment in these cells. Investigation into mechanisms regulating IL-17RA protein levels lead to the observation that IL-17RA undergoes receptor degradation in response to LPS. This work identifies for the first time that 1) LPS enhances transcript levels of IL-17R and 2) after LPS treatment...