IL-17 and IL-22: siblings, not twins

Eyerich, Stefanie; Eyerich, Kilian; Cavani, Andrea; Schmidt‐Weber, Carsten B.

doi:10.1016/j.it.2010.06.004

Cited by 206 publications

(228 citation statements)

References 122 publications

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“…The IL-22 receptor (IL-22R) is a heterodimer that consists of IL-22R and the IL-10 receptor β subunit and is expressed by epithelial cells of nonhematopoietic origin mainly in the skin, kidney, liver, gut, and lung. 19 The expression pattern of IL-22R implies that IL-22 exerts its effects exclusively on tissue cells. 20 The engagement of IL-22R was demonstrated to be essential for innate immune defenses in the gut, 15 skin,21 and 22 and airways.…”

Section: Introductionmentioning

confidence: 99%

“…23 IL-22 protects the mucosal surface from extracellular pathogens by inducing the secretion of antimicrobial peptides in epithelial cells.12 , 21 and 23 Furthermore, IL-22 maintains epithelial integrity by preventing injury and accelerating epithelial repair after a variety of lung insults. 19 The inflammatory properties of IL-22 in the lung are conflicting. IL-22 has been shown to induce the recruitment of granulocytes synergistically with IL-17 and thus increases inflammation in mouse models of lung fibrosis and allergic asthma.…”

Section: Introductionmentioning

confidence: 99%

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IL-22 suppresses IFN-γ–mediated lung inflammation in asthmatic patients

Pennino

Bhavsar

Effner³

et al. 2013

Journal of Allergy and Clinical Immunology

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Background IL-22 controls tissue homeostasis by both proinflammatory and anti-inflammatory effects. However, the anti-inflammatory mechanisms of IL-22 remain poorly investigated. ObjectiveWe sought to investigate the anti-inflammatory role for IL-22 in human asthma. MethodsT-cell lines derived from lung biopsy specimens of asthmatic patients were characterized by means of flow cytometry. Human bronchial epithelial cells from healthy and asthmatic subjects were stimulated with IL-22, IFN-γ, or the combination of both cytokines. Effects of cytokine stimulation were investigated by using wholegenome analysis, ELISA, and flow cytometry. The functional consequence of cytokine stimulation was evaluated in an in vitro wound repair model and T cellmediated cytotoxicity experiments. In vivocytokine expression was measured by using immunohistochemistry and Luminex assays in bronchoalveolar lavage fluid of healthy and asthmatic patients. ResultsThe current study identifies a tissue-restricted antagonistic interplay of IL-22 and the proinflammatory cytokine IFN-γ. On the one hand, IFN-γ antagonized IL-22-mediated induction of the antimicrobial peptide S100A7 and epithelial cell migration in bronchial epithelial cells. On the other hand, IL-22 decreased epithelial susceptibility to T cell-mediated cytotoxicity by inhibiting the IFN-γ-induced expression of MHC-I, MHC-II, and CD54/intercellular adhesion molecule 1 molecules. Likewise, IL-22 inhibited IFN-γ-induced secretion of the proinflammatory chemokines CCL5/RANTES and CXCL10/interferon-inducible protein 10in vitro. Consistently, the IL-22 expression in bronchoalveolar lavage fluid of asthmatic patients inversely correlated with the expression of CCL5/RANTES and CXCL10/interferon-inducible protein 10 in vivo. ConclusionsIL-22 might control the extent of IFN-γ-mediated lung inflammation and therefore play a tissue-restricted regulatory role.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

IL-22 suppresses IFN-γ–mediated lung inflammation in asthmatic patients

Pennino

Bhavsar

Effner³

et al. 2013

Journal of Allergy and Clinical Immunology

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“…Exacerbated or uncontrolled activity of IL-22 can cause inflammation, specifically when IL-22 functions in concert with interleukin-17 (IL-17), a pro-inflammatory cytokine produced by Th17 cells (13). We hypothesized that IL-17 levels would be higher in patients with GI GVHD and positively correlated with IL-22 levels.…”

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confidence: 99%

Interleukin-22 levels are increased in gastrointestinal graft-versus-host disease in children

et al. 2018

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“…Natural and induced Th17 (iTh17) cell subsets are distinctly regulated by Akt and mTOR pathways (10,11), but they share similar functional properties because they both can produce IL-17 and IL-22 following TCR cross-linking. It is generally acknowledged that IL-17 and IL-22 can act in concert to resist bacterial infections, even though they exert potentially distinct roles in autoimmune and allergic responses (12). IL-17 is a key cytokine for psoriasis treatment, whereas IL-22 is important for epithelial cell homeostasis, intestinal defense, tissue repair, and wound healing (12)(13)(14)(15).…”

mentioning

confidence: 99%

“…It is generally acknowledged that IL-17 and IL-22 can act in concert to resist bacterial infections, even though they exert potentially distinct roles in autoimmune and allergic responses (12). IL-17 is a key cytokine for psoriasis treatment, whereas IL-22 is important for epithelial cell homeostasis, intestinal defense, tissue repair, and wound healing (12)(13)(14)(15). Thus, the characterization of T cell populations that can produce IL-17 alone or associated with IL-22, as well as the identification of stimuli that promote this production, remain important issues.…”

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confidence: 99%

TLR-Induced Cytokines Promote Effective Proinflammatory Natural Th17 Cell Responses

Massot

Michel

Diem

et al. 2014

The Journal of Immunology

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Naive CD4 lymphocytes undergo a polarization process in the periphery to become induced Th17 (iTh17) cells. Using retinoic acid–related orphan receptor γt (RORγt)-gfp mice, we found that RORγt and the transcription factor promyelocytic leukemia zinc finger (PLZF) are valuable new markers to identify the recently described natural Th17 (nTh17) cell population. nTh17 cells are thymically committed to promptly produce large amounts of IL-17 and IL-22. In this study, we show that, in addition to responding to TCR cross-linking, nTh17 cells secrete IL-17 and IL-22 when stimulated with IL-23 plus IL-1β, either in recombinant form or in supernatants from TLR4-activated dendritic cells. This innate-like ability of RORγt+ nTh17 cells to respond to TLR4-induced cytokines was not shared by iTh17 cells. The other distinct properties of RORγt+ nTh17 cells are their high expression of PLZF and their absence from lamina propria; iTh17 cells are found therein. RORγt+ nTh17 cells are present in the thymus of germ-free RORγt-gfp and IL-6−/− RORγt-gfp mice, indicating that these cells do not require symbiotic microbiota or IL-6 for their generation. Finally, we found that PLZF+RORγt+ nTh17 cells represent one of the primary IL-17–producing innate-like T cell populations in a TLR7 imiquimod model of psoriasis-like disorder, indicating their involvement in this kind of lesion. Collectively, our results reveal RORγt and PLZF as characteristic markers for identifying nTh17 cells and demonstrate one of their novel properties: the ability to respond promptly to TLR-dependent proinflammatory stimuli without TCR engagement, placing them as members of the innate-like T cell family.

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IL-17 and IL-22: siblings, not twins

Cited by 206 publications

References 122 publications

IL-22 suppresses IFN-γ–mediated lung inflammation in asthmatic patients

IL-22 suppresses IFN-γ–mediated lung inflammation in asthmatic patients

Interleukin-22 levels are increased in gastrointestinal graft-versus-host disease in children

TLR-Induced Cytokines Promote Effective Proinflammatory Natural Th17 Cell Responses

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