Enhanced viral immunoinflammatory lesions in mice lacking IL-23 responses

Kim, Bumseok; Sarangi, Pranita P.; Azkur, Ahmet Kürşat; Kaistha, Shilpa Deshpande; Rouse, Barry T.

doi:10.1016/j.micinf.2007.12.007

Cited by 27 publications

(24 citation statements)

References 30 publications

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“…(b) IL-23 and IL-33 were also markedly increased, especially in severe patients, with large variability exhibited within some patient groups (Table S1). Several studies demonstrate that IL-23 plays a critical role against viral and bacterial infection and in generating airway inflammation [22]–[24]. Moreover, IL-23 stimulates IFN-γ production and enhances cell-mediated immune responses, including CTLs [25]–[27].…”

Section: Discussionmentioning

confidence: 99%

Comparative Study of the Cytokine/Chemokine Response in Children with Differing Disease Severity in Enterovirus 71-Induced Hand, Foot, and Mouth Disease

et al. 2013

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BackgroundEnterovirus 71 (EV71) infection can lead to a rapidly progressing, life-threatening, and severe neurological disease in young children, including the development of human hand, foot, and mouth disease (HFMD). This study aims to further characterize the specific immunological features in EV71–mediated HFMD patients presenting with differing degrees of disease severity.MethodologyComprehensive cytokine and chemokine expression were broadly evaluated by cytokine antibody array in EV71–infected patients hospitalized for HFMD compared to Coxsackievirus A16-infected patients and age-matched healthy controls. More detailed analysis using Luminex-based cytokine bead array was performed in EV71–infected patients stratified into diverse clinic outcomes. Additionally, immune cell frequencies in peripheral blood and EV71–specific antibodies in plasma were also examined.Principal FindingsExpression of several cytokines and chemokines were significantly increased in plasma from EV71–infected patients compared to healthy controls, which further indicated that: (1) GM-CSF, MIP-1β, IL-2, IL-33, and IL-23 secretion was elevated in patients who rapidly developed disease and presented with uncomplicated neurological damage; (2) G-CSF and MCP-1 were distinguishably secreted in EV71 infected very severe patients presenting with acute respiratory failure; (3) IP-10, MCP-1, IL-6, IL-8, and G-CSF levels were much higher in cerebrospinal fluid than in plasma from patients with neurological damage; (4) FACS analysis revealed that the frequency of CD19+HLADR+ mature B cells dynamically changed over time during the course of hospitalization and was accompanied by dramatically increased EV71–specific antibodies. Our data provide a panoramic view of specific immune mediator and cellular immune responses of HFMD and may provide useful immunological profiles for monitoring the progress of EV71–induced fatal neurological symptoms with acute respiratory failure.

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Section: Discussionmentioning

confidence: 99%

Comparative Study of the Cytokine/Chemokine Response in Children with Differing Disease Severity in Enterovirus 71-Induced Hand, Foot, and Mouth Disease

et al. 2013

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“…It is also possible that the γδ T cells recruited to the cornea were promoted to rapidly produce IL-17A, as was shown to occur in vitro when such cells were exposed to cytokines such as IL-1β and IL-23 (41). Both of these activating cytokines have increased expression after HSV ocular infection (50, 51) and their action on γδ T cells could help explain how the infection relates to IL-17A production in the initial stages. In later stages, the virus is no longer present and the γδ T cells are almost absent (31, 52), yet commencing IL-17A neutralization at day 7 pi still resulted in significantly less CV.…”

Section: Discussionmentioning

confidence: 99%

IL-17A Differentially Regulates Corneal Vascular Endothelial Growth Factor (VEGF)-A and Soluble VEGF Receptor 1 Expression and Promotes Corneal Angiogenesis after Herpes Simplex Virus Infection

Suryawanshi

Veiga-Parga

Reddy

et al. 2012

The Journal of Immunology

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Ocular infection with herpes simplex virus (HSV) causes corneal neovascularization (CV), an essential step in the pathogenesis of the blinding immuno-inflammatory lesion, stromal keratitis (SK). The infection results in IL-17A production which contributes to CV in ways that together serve to shift the balance between corneal concentrations of VEGF-A and the soluble receptor molecule sVEGFR-1 which binds to VEGF-A and blocks its function (a so-called VEGF trap). Accordingly, animals lacking responses to IL-17A signaling, either because of IL-17 receptor-A knockout or WT animals that received neutralizing mAb to I L-17A had diminished CV compared to controls. The procedures reduced VEGF-A protein levels, but had no effect on the levels of sVEGFR-1 present. Hence the VEGF trap was strengthened. IL-17A also caused increased CXCL1/KC synthesis, which attracts neutrophils to the inflammatory site. Neutrophils further influenced the extent of CV by acting as an additional source of VEGF-A as well as metalloproteinase (MMP) enzymes that degrade the soluble receptor inhibiting its VEGF blocking activity. Our results indicate that suppressing the expression of IL-17A, or increasing the activity of the VEGF trap, represent useful approaches to inhibit CV and the control of an ocular lesion that is an important cause of human blindness.

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“…Further bacterial peptidoglycans can induce the generation of Th17 cells through nucleotide oligomerization domain 2 (NOD2) receptor signaling in dendritic cells25. Viruses such as Herpes simplex virus 46 and fungus and fungal components such as B–glucans26,47, Cryptococcus 48, Candida albicans 47 and Aspergillus fumigatus 49 can all induce some or all of these polarizing cytokines from dendritic cells and play a role in differentiation of Th17 cells. These studies suggest that relative amounts of the polarizing cytokines induced by the pathogen may define the final outcome of differentiation of naïve T cells to Th1, Th2, Th17 or T regulatory cells during infection.…”

Section: Innate Receptors and Signaling Pathways Involved In Inductiomentioning

confidence: 99%

Th17 cells at the crossroads of innate and adaptive immunity against infectious diseases at the mucosa

2009

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T helper type 17 (Th17) cells are a distinct lineage of T cells that produce the effector molecules IL-17, IL-17F, IL-21 and IL-22. Although the role of Th17 cells in autoimmunity is well documented, there is growing evidence that the Th17 lineage and other IL-17 producing cells are critical for host defense against bacterial, fungal and viral infections at mucosal surfaces. Here we summarize recent progress in our understanding of the function of IL-17 producing cells as a bridge between innate and adaptive immunity against infectious diseases at the mucosa.

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Enhanced viral immunoinflammatory lesions in mice lacking IL-23 responses

Cited by 27 publications

References 30 publications

Comparative Study of the Cytokine/Chemokine Response in Children with Differing Disease Severity in Enterovirus 71-Induced Hand, Foot, and Mouth Disease

Comparative Study of the Cytokine/Chemokine Response in Children with Differing Disease Severity in Enterovirus 71-Induced Hand, Foot, and Mouth Disease

IL-17A Differentially Regulates Corneal Vascular Endothelial Growth Factor (VEGF)-A and Soluble VEGF Receptor 1 Expression and Promotes Corneal Angiogenesis after Herpes Simplex Virus Infection

Th17 cells at the crossroads of innate and adaptive immunity against infectious diseases at the mucosa

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