IL-17 receptor signaling influences virus-induced corneal inflammation

Molesworth-Kenyon, S. J.; Yin, Rong; Oakes, John E.; Lausch, Robert N.

doi:10.1189/jlb.0807571

Cited by 83 publications

(81 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…IL-17 has been shown to be one of the major cytokines involved in the recruitment of neutrophils in several experimental models of inflammation (35,46,47). Our results show that in IL-17R gene-deficient mice marked diminution of neutrophil migration to the infection focus during NS-CLP-induced sepsis and, as a result, had a significantly lower survival rate.…”

Section: Discussionmentioning

confidence: 64%

IL-17 Receptor Signaling Is Required to Control Polymicrobial Sepsis

Freitas

Alves‐Filho

Victoni

et al. 2009

The Journal of Immunology

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 64%

IL-17 Receptor Signaling Is Required to Control Polymicrobial Sepsis

Freitas

Alves‐Filho

Victoni

et al. 2009

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…IL-17 has been detected in the cornea of mice infected with HSV-1 and mice lacking IL-17R had a transient decrease in neutrophil infiltration, but corneal pathology and viral clearance were not significantly different than in wild-type mice [95]. We have recently found that antigenspecific Th17 cells are induced during infection with hepatitis C virus and that these are regulated by innate IL-10 and TGF-b induced in monocytes by the NS4 protein of the virus [34].…”

Section: Role Of Il-17-secreting T Cells In Infectionmentioning

confidence: 90%

Induction, function and regulation of IL‐17‐producing T cells

2008

View full text Add to dashboard Cite

Recent reports have provided convincing evidence that IL-17-producing T cells play a key role in the pathogenesis of organ-specific autoimmune diseases, a function previously attributed exclusively to IFN-c-secreting Th1 cells. Furthermore, it appears that IL-17-producing T cells can also function with Th1 cells to mediate protective immunity to pathogens. Although much of the focus has been on IL-17-secreting CD4 1 T cells, termed The main function of IL-17-secreting T cells is to mediate inflammation, by stimulating production of inflammatory cytokines, such as TNF-a, IL-1b and IL-6, and inflammatory chemokines that promote the recruitment of neutrophils and macrophages.Key words: Autoimmunity . IL-17 . Infection . Inflammation IntroductionMore than 20 years ago Mosmann and Coffman reported that distinct CD4 1 T-cell subtypes, termed Th1 and Th2 cells, could be distinguished on the basis of cytokine secretion and function [1]. The Th1-Th2 model provided a useful but simplistic basis for our understanding of the mechanisms of immunity to infection and also attempted to explain the role of T cells in the pathogenesis of autoimmunity and allergy/asthma. The original hypothesis was that IFN-g-secreting CD4 1 cells mediated protective immunity to intracellular pathogens by promoting macrophage activation and stimulating production of complement fixing and virus neutralizing antibodies, but also promoted inflammatory responses and mediated the pathology in certain autoimmune diseases. In contrast, CD4 1 T cells that secreted IL-4, IL-5, IL-10 and IL-13 were considered to be the main helper T cells providing help for B-cell production of antibody, especially IgG1 in mice, and mediated protective immunity to extracellular pathogens. These Th2 cells were also anti-inflammatory, controlling Th1 responses, but at the same time mediated allergic reactions and had an inflammatory and pathological role in asthma.The identification of additional T-cell subtypes has led to a shift in the Th1-Th2 paradigm and has helped to explain some anomalies in the original model. In the mid 1990s suppressor T cells were re-discovered as Treg cells and were shown to have a major role in controlling immune responses to self-antigens, thereby preventing autoimmunity. Furthermore, these cells rather than the reciprocal Th1 or Th2 populations were shown to be the major regulator of effector T cells, functioning to maintain self-tolerance, prevent autoimmunity and limit collateral damage during immune responses to pathogens [2,3].There were a number of other observations which could not be explained on the basis of the two Th1 and Th2 subtypes. Mini-ReviewDespite the assumption that Th1 cells mediated autoimmunity, mice deficient in IFN-g or IFN-g receptors were found to have increased susceptibility to EAE and collagen-induced arthritis (CIA) [4,5]. Furthermore, EAE was exacerbated in mice deficient in the Th1 polarizing cytokine, 7]. It was then discovered that mice deficient in the novel IL-12 family member, IL-23 were resistant to EAE [6]....

show abstract

“…21,22 Th17 cells are the newly recognized CD4 þ T-cell subset, which mainly produces cytokines, including IL-17A, IL-17F, and IL-22, and is involved in a wide range of autoimmune diseases. [11][12][13] The level of IL-17 was found to be correlated with both activity and severity of various autoimmune diseases. Studies conducted on experimental mice model of DE have found that the level of IL-17 was significantly increased on the ocular surface and in tears.…”

Section: Discussionmentioning

confidence: 99%

“…Both IL-17 and IL-22 are the effective cytokines of Th17 cells, the levels of which, in tears, may represent the immune response of Th17 cells during the pathogenesis of DED. [11][12][13] In this study, we evaluated the levels of IL-17 and IL-22 in tears of patients with Sjögren's or non-Sjögren's syndrome DED. In addition, the correlation between disease severity and IL-17 as well as IL-22 levels in patients was also analyzed.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Th17-associated cytokines in tears of patients with dry eye syndrome

Tan

Sun

Liu³

et al. 2014

Eye

View full text Add to dashboard Cite

Purpose To determine the levels of Th17-associated cytokines, particularly interleukin (IL)-17 and IL-22 in tears of patients with dry eye syndrome. Methods Tear samples were collected from 20 healthy volunteers, 20 dry eye (DE) patients with non-Sjö gren's syndrome (NSSDE) and 20 DE patients with Sjö gren's syndrome (SSDE). Symptom questionnaire was self-administered and multiple dry eye disease (DED)-related clinical tests were performed. The levels of IL-17 and IL-22 in tears were measured by enzyme-linked immunosorbent assay. Results The levels of IL-17 and IL-22 were significantly increased in tears of DE patients compared with those of controls and also higher in SSDE patients compared with those of NSSDE patients (Po0.05). Moreover, the levels of IL-17 and IL-22 were positively correlated with questionnaire score and keratopathy score but negatively correlated with tear film break-up time and Schirmer I test in both NSSDE and SSDE patients (Po0.05). Conclusions The levels of IL-17 and IL-22 in tears were significantly increased in DE patients, which were associated with the disease severity. Therefore, Th17 cellassociated cytokines, particularly IL-17 and IL-22, may have important roles in the immunopathogenesis of the DED.

show abstract

IL-17 receptor signaling influences virus-induced corneal inflammation

Cited by 83 publications

References 34 publications

IL-17 Receptor Signaling Is Required to Control Polymicrobial Sepsis

IL-17 Receptor Signaling Is Required to Control Polymicrobial Sepsis

Induction, function and regulation of IL‐17‐producing T cells

Analysis of Th17-associated cytokines in tears of patients with dry eye syndrome

Contact Info

Product

Resources

About