scholarly journals Ragweed pollen induces allergic conjunctivitis immune tolerance in mice via regulation of the NF-κB signal pathway

2021 ◽  
Vol 14 (7) ◽  
pp. 955-964
Author(s):  
Meng-Tian Bai ◽  
◽  
Zhu-Lin Hu ◽  
Keyword(s):  
Immune Tolerance ◽  
Allergic Conjunctivitis ◽  
Interleukin 10 ◽  
Treg Cells ◽  
Signal Pathway ◽  
Ragweed Pollen ◽  
Interleukin 17 ◽  
Inflammatory Factor ◽  
Mice Model ◽  
Total Ige

AIM: To investigate the feasibility and mechanism of immune tolerance in allergic conjunctivitis. METHODS: The allergic conjunctivitis immune tolerance mice model was established by ragweed pollen (RW) and the related cytokines were detected. The mice were divided into 9 groups and the maslinic acid (MA) or PBS were given for different group after modeling. The expression levels of chemokine ligand 5 (CCL5) and P-65 in the conjunctival tissue were analyzed by immunohistochemistry, quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot. The percentage of interleukin-17 (IL-17) and CD4+CD25+ in the splenocyte supernatant was analyzed by flow cytometry. Furthermore, the serum and splenocyte supernatant concentration of total-IgE, interleukin-10 (IL-10), and IL-17 was analyzed by enzyme linked immune response (ELISA). RESULTS: After the model was established, symptoms of conjunctivitis were alleviated, the level of P-65, CCL5, IL-17, and total-IgE was raised, while the expression of IL-10, CD4+CD25+ was decreased. This result fully demonstrated that a typical IL-17/regulatory-T-cells (Treg cells) imbalance and NF-κB activation. When the NF-κB signal pathway was suppressed, it showed that there was a further relief of conjunctivitis in mice. At the same time, the expression of total-IgE, IL-17, and CCL5 was decreased and the expression of anti-inflammatory factor (IL-10, CD4+CD25+) was increased. CONCLUSION: In the state of immune tolerance, symptoms of conjunctivitis in mice are alleviated, the Th-17 cells of allergic conjunctivitis mice are inhibited, and Treg cells activity is enhanced.

scholarly journals Increased Production of Interleukin-17 Over Interleukin-10 by Treg Cells Implicates Inducible Costimulator Molecule in Experimental Spondyloarthritis

2014 ◽  
Vol 66 (9) ◽  
pp. 2412-2422 ◽  
Author(s):  
Luiza M. Araujo ◽  
Ingrid Fert ◽  
Quentin Jouhault ◽  
Karine Labroquère ◽  
Muriel Andrieu ◽  
...  
Keyword(s):  
Interleukin 10 ◽  
Treg Cells ◽  
Interleukin 17 ◽  
Inducible Costimulator

Regulation of IL-17 in chronic inflammation in the human lung

2011 ◽  
Vol 120 (12) ◽  
pp. 515-524 ◽  
Author(s):  
Carol Pridgeon ◽  
Laurence Bugeon ◽  
Louise Donnelly ◽  
Ursula Straschil ◽  
Susan J. Tudhope ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Lung Tissue ◽  
Mononuclear Cells ◽  
Human Lung ◽  
Treg Cells ◽  
Orphan Receptor ◽  
Th2 Cells ◽  
Chronic Obstructive ◽  
Interleukin 17

The regulation of human Th17 cell effector function by Treg cells (regulatory T-cells) is poorly understood. In the present study, we report that human Treg (CD4+CD25+) cells inhibit the proliferative response of Th17 cells but not their capacity to secrete IL (interleukin)-17. However, they could inhibit proliferation and cytokine production by Th1 and Th2 cells as determined by IFN-γ (interferon-γ) and IL-5 biosynthesis. Currently, as there is interest in the role of IL-17-producing cells and Treg cells in chronic inflammatory diseases in humans, we investigated the presence of CD4+CD25+ T-cells and IL-17 in inflammation in the human lung. Transcripts for IL-17 were expressed in mononuclear cells and purified T-cells from lung tissue of patients with chronic pulmonary inflammation and, when activated, these cells secrete soluble protein. The T-cell-specific transcription factors RORCv2 (retinoic acid-related orphan receptor Cv2; for Th17) and FOXP3 (forkhead box P3; for Treg cells) were enriched in the T-cell fraction of lung mononuclear cells. Retrospective stratification of the patient cohort into those with COPD (chronic obstructive pulmonary disease) and non-COPD lung disease revealed no difference in the expression of IL-17 and IL-23 receptor between the groups. We observed that CD4+CD25+ T-cells were present in comparable numbers in COPD and non-COPD lung tissue and with no correlation between the presence of CD4+CD25+ T-cells and IL-17-producing cells. These results suggest that IL-17-expressing cells are present in chronically inflamed lung tissue, but there is no evidence to support this is due to the recruitment or expansion of Treg cells.

scholarly journals CD4+ CD25+ Foxp3+ Regulatory T Cells, Dendritic Cells, and Circulating Cytokines in Uncomplicated Malaria: Do Different Parasite Species Elicit Similar Host Responses?

2010 ◽  
Vol 78 (11) ◽  
pp. 4763-4772 ◽  
Author(s):  
Raquel M. Gonçalves ◽  
Karina C. Salmazi ◽  
Bianca A. N. Santos ◽  
Melissa S. Bastos ◽  
Sandra C. Rocha ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Parasite Species ◽  
Inflammatory Responses ◽  
Clinical Symptoms ◽  
Clinical Manifestations ◽  
Surface Expression ◽  
Interleukin 10 ◽  
Treg Cells ◽  
Experimental Models ◽  
Necrosis Factor Alpha

ABSTRACT Clearing blood-stage malaria parasites without inducing major host pathology requires a finely tuned balance between pro- and anti-inflammatory responses. The interplay between regulatory T (Treg) cells and dendritic cells (DCs) is one of the key determinants of this balance. Although experimental models have revealed various patterns of Treg cell expansion, DC maturation, and cytokine production according to the infecting malaria parasite species, no studies have compared all of these parameters in human infections with Plasmodium falciparum and P. vivax in the same setting of endemicity. Here we show that during uncomplicated acute malaria, both species induced a significant expansion of CD4+ CD25+ Foxp3+ Treg cells expressing the key immunomodulatory molecule CTLA-4 and a significant increase in the proportion of DCs that were plasmacytoid (CD123+), with a decrease in the myeloid/plasmacytoid DC ratio. These changes were proportional to parasite loads but correlated neither with the intensity of clinical symptoms nor with circulating cytokine levels. One-third of P. vivax-infected patients, but no P. falciparum-infected subjects, showed impaired maturation of circulating DCs, with low surface expression of CD86. Although vivax malaria patients overall had a less inflammatory cytokine response, with a higher interleukin-10 (IL-10)/tumor necrosis factor alpha (TNF-α) ratio, this finding did not translate to milder clinical manifestations than those of falciparum malaria patients. We discuss the potential implications of these findings for species-specific pathogenesis and long-lasting protective immunity to malaria.

scholarly journals Regulatory T Cells Contribute to Resistance against Lyme Arthritis

2020 ◽  
Vol 88 (11) ◽  
Author(s):  
Emily M. Siebers ◽  
Elizabeth S. Liedhegner ◽  
Michael W. Lawlor ◽  
Ronald F. Schell ◽  
Dean T. Nardelli
Keyword(s):  
T Cells ◽  
T Cell ◽  
Lyme Disease ◽  
Regulatory T Cells ◽  
Regulatory T Cell ◽  
Interleukin 10 ◽  
Lyme Arthritis ◽  
Interleukin 17 ◽  
Content Type

ABSTRACT The symptoms of Lyme disease are caused by inflammation induced by species of the Borrelia burgdorferi sensu lato complex. The various presentations of Lyme disease in the population suggest that differences exist in the intensity and regulation of the host response to the spirochete. Previous work has described correlations between the presence of regulatory T cells and recovery from Lyme arthritis. However, the effects of Foxp3-expressing CD4+ T cells existing prior to, and during, B. burgdorferi infection have not been well characterized. Here, we used C57BL/6 “depletion of regulatory T cell” mice to assess the effects these cells have on the arthritis-resistant phenotype characteristic of this mouse strain. We showed that depletion of regulatory T cells prior to infection with B. burgdorferi resulted in sustained swelling, as well as histopathological changes, of the tibiotarsal joints that were not observed in infected control mice. Additionally, in vitro stimulation of splenocytes from these regulatory T cell-depleted mice resulted in increases in gamma interferon and interleukin-17 production and decreases in interleukin-10 production that were not evident among splenocytes of infected mice in which Treg cells were not depleted. Depletion of regulatory T cells at various times after infection also induced rapid joint swelling. Collectively, these findings provide evidence that regulatory T cells existing at the time of, and possibly after, B. burgdorferi infection may play an important role in limiting the development of arthritis.

Serum interleukin 17, interleukin 23, and interleukin 10 values in children with atopic eczema/dermatitis syndrome (AEDS): Association with clinical severity and phenotype

2015 ◽  
Vol 36 (1) ◽  
pp. 74-81 ◽  
Author(s):  
Salvatore Leonardi ◽  
Caterina Cuppari ◽  
Sara Manti ◽  
Martina Filippelli ◽  
Giuseppe Fabio Parisi ◽  
...  
Keyword(s):  
Atopic Eczema ◽  
Interleukin 10 ◽  
Clinical Severity ◽  
Interleukin 17 ◽  
Interleukin 23

scholarly journals Microglial M2 Polarization Mediated the Neuroprotective Effect of Morroniside in Transient MCAO-Induced Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Hao Liu ◽  
Mei-Xian Ou ◽  
Qiao-Qiao Han
Keyword(s):  
Neuroprotective Effect ◽  
Interleukin 10 ◽  
Artery Occlusion ◽  
Inflammatory Factor ◽  
Cornus Officinalis ◽  
M2 Polarization ◽  
Mitogen Activated Protein ◽  
Enhanced Expression ◽  
Glucagon Like Peptide 1 ◽  
Cerebral Artery Occlusion

Morroniside, a secoiridoid glycoside from Cornus officinalis, is a class of small molecule non-peptide glucagon-like peptide-1 receptor (GLP-1R) agonists and possess many important biomedical functions. Our previous studies reported that GLP-1R agonist exenatide promoted M2 polarization and the expression of cell-specific anti-inflammatory factor interleukin-10 in neuropathological pain model. In this study, we proved that morroniside not only induced M2 polarization and stimulated interleukin-10 expression specifically in cortical primary microglia by p38β mitogen-activated protein kinases pathway but also protected nerve cells against H2O2-induced cell oxidative damage and prohibited ischemic injury by reducing infarct size, which is at least in part mediated by enhanced expression of microglial interleukin-10. In the cortical penumbra area in middle cerebral artery occlusion (MCAO) mice. In general, our results indicated that GLP-1R agonist morroniside might play a neuroprotective effect by inducing M2 polarization, and cyclic-AMP/protein kinase A/p38β pathway might mediate morroniside-induced expression of interleukin-10 protein in M2 microglia.

Abstract 459: Differential Responses of Bone Marrow-Derived Macrophages to Lipopolysaccharide in the Treml1 Null Mouse

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Amanda I Pacheco ◽  
Anthony V Washington ◽  
Marieli Gonzalez
Keyword(s):  
Bone Marrow ◽  
Vessel Wall ◽  
Interleukin 10 ◽  
Chronic Inflammatory Disease ◽  
Macrophage Infiltration ◽  
Null Mouse ◽  
Mice Model ◽  
Monocyte Chemoattractant Protein 1 ◽  
Platelet Receptor

Atherosclerosis, the hardening and narrowing of the arteries, is a chronic inflammatory disease driven by a crosstalk of signaling molecules between circulating immune cells and the vessel wall. In the classic view of this cardiovascular disease, hyperlipidemia initiates an inflammatory cascade that promotes macrophage infiltration into the vessel wall leading to a feedback mechanism which exacerbates lesion growth and ultimately, atherothrombosis. Our laboratory has characterized a novel atherosclerotic mice model, in which deletion of the platelet receptor Triggering Receptor Expressed on Myeloid Cells (TREM)-Like Transcript-1 (TLT-1) on a apolipoprotein E ( apoe -/- /treml1 -/- ) background dampens early macrophage infiltration into the vessel wall. This leads to decreased lesion size, instability, and calcification of atherosclerotic lesions. We have demonstrated that one of the mechanisms for dampened lesion progression is decreased platelet activation and we hypothesize that the macrophage infiltration differences may also be due to fundamental differences in macrophage phenotypic functions. In order to further define the mechanism by which TLT-1 modulates macrophage infiltration, we analyzed macrophage function in vitro . Analysis of bone marrow-derived macrophages (BMDM) from apoe -/- /treml1 -/- and apoe -/- /treml1 -/+ mice revealed no significant differences in the phagocytic function of long chain fatty acids. However, analysis of basal levels of monocyte chemoattractant protein-1 (MCP1), a key chemokine regulating monocyte infiltration, were significantly decreased in the apoe -/- /treml1 -/- BMDM supernatants. Accordingly, levels of Interleukin 6 (IL6) and Interleukin 10 (IL10) were significantly decreased in the apoe -/- /treml1 -/- BMDM supernatants after two hours of lipopolysaccharide (LPS) stimulation (p<0.05; n=5-8). These findings define an underlying difference in the BMDM secretory phenotype of the apoe -/- /treml1 -/- mice. However, it also opens the possibility of treml1 expression in macrophages, which may account for these differences. We will now investigate if an alternate isoform of treml1 is expressed in macrophages or at some period of their differentiation.

Abstract 16582: Costimulation Blockade With Anti Cd80 and Cd86 Monoclonal Antibodies Prolonged Graft Survival in Allogeneic Ips Cell-Derived Cardiomyocyte Patch Transplantation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Masaro Nakae ◽  
Shigeru Miyagawa ◽  
Takuji Kawamura ◽  
Koichiro Uchida ◽  
Ko Okumura ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
Graft Survival ◽  
Immune Tolerance ◽  
Immune Rejection ◽  
Mice Model ◽  
Ips Cell ◽  
T Cell Anergy ◽  
Cell Anergy ◽  
Costimulatory Pathway

Introduction: How to avoid immune rejection after transplantation should be elucidated for confirmed efficacy in clinical application of allogenic induced pluripotent stem cell derived cardiomyocyte patch. The blockade of CD28-CD80/86 costimulation is known to induce T cell anergy and immune tolerance by the recruitment of regulatory T cells (T reg) and prolong graft survival in organ transplantation. Hypothesis: We hypothesized that the blockade of CD28-CD80/CD86 costimulatory pathway by anti-CD80/CD86 monoclonal antibodies (mAbs) induces T cell anergy in vivo and suppresses immune rejection in allogeneic iPSC-CMs subcutaneous transplantation mice model. Methods: T cell anergy was induced in vitro by co-culture of Balb/c and 25Gy irradiated C57BL/6 splenocytes with anti-CD80/86 mAbs for 5 days. The inhibitory effect of anergic cells was evaluated by mixed lymphocyte reaction (MLR) in C57BL/6 and Balb/c splenocytes with anergic cells. IFN-g in MLR supernatants was measured by ELISAs to assess immune response. C57BL/6 iPSC-CMs expressing luciferase were subcutaneously transplanted into Balb/c. Anti-CD80/CD86 mAbs were injected intraperitoneally 250μg/dose on day 0, 1, and 2 (treated mice, n=6). In control mice (n=6), equivalent volume of saline was injected. To evaluate iPSC-CMs graft survival, photon counts of iPSC-CMs were measured by bioluminescence imaging system (BLI). Cells of harvested grafts were analyzed by immunofluorescence staining (IF). Results: On ELISAs, IFN-g in MLR supernatants co-cultured with anergic cells was significantly lower as compared with those without anergic cells (12.3±14.4 vs. 251±80.2 pg/ml, p=0.007). The ability to suppress the alloresponses was dose-dependent. BLI showed that photon counts on day 14 in treated mice were significantly higher than in control mice (7397±2651 vs. 2703±1271, p=0.003). IF showed a siginificantly higher ratio of CD4 and Foxp3 double positive cells to CD4-postive cells in the grafts on day 7 in treated mice as compared with in control mice (23±3% vs. 9±3%, p=0.009) Conclusions: The blockade of CD28-CD80/CD86 costimulatory pathway might suppress immune rejection in allogeneic iPSC-CMs transplantation mice model and T reg might involve this immune tolerance.

scholarly journals Ascidian Tunicate Extracts Attenuate Rheumatoid Arthritis in a Collagen-induced Murine Model

2014 ◽  
Vol 9 (6) ◽  
pp. 1934578X1400900
Author(s):  
Seong-Ho Hong ◽  
Jung-Taek Kwon ◽  
Jae-Ho Lee ◽  
Somin Lee ◽  
Ah Young Lee ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Interleukin 10 ◽  
Treated Group ◽  
Pcr Analysis ◽  
Prostaglandin E ◽  
Therapeutic Effects ◽  
Paw Edema ◽  
Mice Model ◽  
The Matrix ◽  
Inflammatory Proteins

Murine rheumatoid arthritis models are often used to investigate the potential therapeutic effects of candidate drugs. The present study has been conducted in order to investigate the therapeutic efficacy of ascidian tunicate extracts in a collagen-induced arthritis DBA1/J mice model. Four types of formulas, ascidian tunicate extracts (ATE), crude ascidian tunicate glycans (ATEC), ascidian tunicate extracts with licorice extracts (ATEL), and crude ascidian tunicate glycans with licorice extracts (ATECL) were orally administered into DBA/1J mice for 3 weeks and paw edema and thickness were evaluated. Changes in inflammatory proteins and cytokines levels were monitored in hind leg tissues by Western blot and quantitative PCR analysis. The oral administration of ascidian tunicate extracts alleviated paw edema and improved the histological hind leg cartilage status. The extracts also reduced the matrix metalloproteinase-9 (MMP-9) protein and prostaglandin E synthase (PGES) levels. In addition, the extracts-treated groups showed increased interleukin-10 (IL-10) levels compared with the non-treated group. These findings suggest that orally administered ascidian tunicate extracts might have potential therapeutic effects for the treatment of rheumatoid arthritis.

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