Extracellular regulated mitogen activated kinase activity is required for the regulation of the intestinal epithelial cell barrier function by IL-17

Kinugasa, Tetsushi; Gu, Xuibin; Yang, Huan; Reinecker, Hans–Christian

doi:10.1016/s0016-5085(00)84329-2

Cited by 2 publications

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“…First, IL-17A improves barrier function by strengthening tight junctions after inducing claudin and mucin expression (Kinugasa et al, 2000; Chen et al, 2003). Second, IL-22 improves barrier function by inducing epithelial cell proliferation (Brand et al, 2006) and enhancing goblet cell restoration and mucus production (Sugimoto et al, 2008).…”

Section: A Protective Role For Th17 In the Gutmentioning

confidence: 99%

TH17 Cells in Autoimmunity and Immunodeficiency: Protective or Pathogenic?

et al. 2012

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In 2005 a newly discovered T helper cell subset that secreted interleukin (IL)-17 became the center of attention in immunology. Initial studies painted Th17 cells as the culprit for destruction in many different autoimmune and auto-inflammatory diseases. Subsequently, the discovery of patients with primary immunodeficiencies in the IL-17 pathway taught us that Th17 cells have a critical role in defense against certain fungal and bacterial infections. Moreover, the paradoxical exacerbation of Crohn’s disease in the clinical trials of a Secukinumab (AIN457), a fully human neutralizing antibody to IL-17A, has cast into doubt a universal pro-inflammatory and harmful role for Th17 cells. Evidence now suggests that depending on the environment Th17 cells can alter their differentiation program, ultimately giving rise to either protective or pro-inflammatory cells. In this review we will summarize the evidence from patients with immunodeficiencies, autoimmune, or auto-inflammatory diseases that teaches us how the pro-inflammatory versus protective function of Th17 cells varies within the context of different human diseases.

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Section: A Protective Role For Th17 In the Gutmentioning

confidence: 99%

TH17 Cells in Autoimmunity and Immunodeficiency: Protective or Pathogenic?

et al. 2012

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“…Both IL-17A and IL-17F cause the up-regulation of pro-inflammatory cytokines and chemokines such as IL-6, granulocyte colony-stimulating factor (GCSF), and CXCL1 and CXCL2 (Fossiez et al, 1996 ). In the airways, IL-17A has been shown to cause a release of chemokines that recruit neutrophils and fungicidal peptides (Laan et al, 1999 ; Kinugasa et al, 2000 ; O'Connor et al, 2009 ; Puel et al, 2012 ; Lee et al, 2015 ). Although vital in protecting the host against pathogens, dysregulated inflammation, if sustained, may result in inflammation-associated pathologies such as tissue damage and the disruption of mucosal homeostasis.…”

Section: Introductionmentioning

confidence: 99%

Chronic Rhinosinusitis with Polyps Is Characterized by Increased Mucosal and Blood Th17 Effector Cytokine Producing Cells

et al. 2017

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Background: Recent studies have implied a role for Th17 cells in CRS with nasal polyps (CRSwNP) patients. However, the capacity of these cells to produce Th17 cytokines is still unknown. Here we sought to quantify IL-17A, IL-17F, IL-21, and IL-22 cytokines produced by Th17 cells in mucosal tissue and peripheral blood of CRSwNP, CRS without nasal polyps (CRSsNP) and control patients.Methods: Samples were prospectively collected from CRS patients and non-CRS controls. We used flow cytometry to characterize the Th17 cells and their cytokines in sinonasal tissue and peripheral blood.Results: A total of 36 patients were recruited to the study. CRSwNP patients had significantly more tissue IL-17A (9.53 ± 2.71 vs. 1.11 ± 0.43 vs. 0.77 ± 0.07), IL-17F (4.96 ± 1.48 vs. 0.88 ± 0.31 vs. 0.56 ± 0.04), IL-21 (5.55 ± 2.01 vs. 1.60 ± 0.71 vs. 1.53 ± 0.55) and IL-22 (4.73 ± 1.58 vs. 0.70 ± 0.28 vs. 0.88 ± 0.26) producing Th17 cells compared to CRSsNP and control mucosa per mg of tissue, respectively. Allergic CRSwNP patients had decreased numbers of IL-21 producing Th17 cells compared to non-Allergic CRSwNP. (1.69 ± 0.57 vs. 9.41 ± 3.23) per mg of tissue, respectively (Kruskal-Wallis p < 0.05).Conclusion: In summary our study identified increased numbers of IL-17A, IL-17F, IL-21 and IL-22 positive Th17 cells in CRSwNP patient polyps and peripheral blood suggesting an altered activation state of those cells both locally and systemically. Atopic CRSwNP had decreased amounts of tissue Th17 cell derived IL-21 implying a potential protective role for IL-21 in CRSwNP allergic inflammation.

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Extracellular regulated mitogen activated kinase activity is required for the regulation of the intestinal epithelial cell barrier function by IL-17

Cited by 2 publications

References 0 publications

TH17 Cells in Autoimmunity and Immunodeficiency: Protective or Pathogenic?

TH17 Cells in Autoimmunity and Immunodeficiency: Protective or Pathogenic?

Chronic Rhinosinusitis with Polyps Is Characterized by Increased Mucosal and Blood Th17 Effector Cytokine Producing Cells

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