The IL-17F/IL-17RC Axis Promotes Respiratory Allergy in the Proximal Airways

Luca, Antonella De; Pariano, Marilena; Cellini, Barbara; Costantini, Claudio; Villella, Valeria Rachela; Jose, Shyam Sushama; Palmieri, Massimiliano; Borghi, Monica; Galosi, Claudia; Paolicelli, Giuseppe; Maiuri, Luigi; Frič, Jan; Zelante, Teresa

doi:10.1016/j.celrep.2017.07.063

Cited by 44 publications

(43 citation statements)

References 54 publications

(58 reference statements)

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“…Interleukin‐17A is required for full eosinophil recruitment at the peak of inflammation, underscoring the potential for non‐Type 2 cytokines in driving ‘allergic’ responses following fungal exposure. Recent work has shown that signalling via IL‐17RA and IL‐17RC may drive divergent allergic outcomes, with the IL‐17F–IL‐17RC axis favouring respiratory allergy in the proximal airways. Collectively, these studies demonstrate the potentially varied functions of T‐cell responses to fungal challenge, and how repeated exposure to fungi and their products can drive development of allergic airway disease.…”

Section: Type 17 Responses To Pulmonary Mycosesmentioning

confidence: 99%

Helper T‐cell responses and pulmonary fungal infections

McDermott

Klein

2018

Immunology

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The mucosal surface of the respiratory tract encounters microbes, such as fungal particles, with every inhaled breath. When pathogenic fungi breach the physical barrier and innate immune system within the lung to establish an infection, adaptive immunity is engaged, often in the form of helper CD4 T-cell responses. Type 1 responses, characterized by interferon-γ production from CD4 cells, promote clearance of Histoplasma capsulatum and Cryptococcus neoformans infection. Likewise, interleukin-17A (IL-17A) production from Th17 cells promotes immunity to Blastomyces dermatitidis and Coccidioides species infection by recruiting neutrophils. In contrast the development of T helper type 2 responses, characterized by IL-5 production from T cells and eosinophil influx into the lungs, drives allergic bronchopulmonary aspergillosis and poor outcomes during C. neoformans infection. Experimental vaccines against several endemic mycoses, including Histoplasma capsulatum, Coccidioides, Cryptococcus and Blastomyces dermatitidis, induce protective T-cell responses and foreshadow the development of vaccines against pulmonary fungal infections for use in humans. Additionally, recent work using antifungal T cells as immunotherapy to protect immune-compromised patients from opportunist fungal infections also shows great promise. This review covers the role of T-cell responses in driving protection and pathology in response to pulmonary fungal infections, and highlights promising therapeutic applications of antifungal T cells.

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Section: Type 17 Responses To Pulmonary Mycosesmentioning

confidence: 99%

Helper T‐cell responses and pulmonary fungal infections

McDermott

Klein

2018

Immunology

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“…Epithelial cell-derived cytokines such as thymic stromal lymphoprotein (TSLP), IL-25, and IL-33 promote eosinophilia by inducing IL-5 production ( 81 ). Additionally, dysregulation of the IL-17F/IL-17RC axis has been shown to predispose allergic inflammation in murine models of fungal allergic asthma ( 82 ). Besides murine models of fungal allergic asthma, mouse models using the house dust mite (HDM) also feature similarities to human allergic asthma, including eosinophilic lung inflammation and cytokines primarily associated with Th2-type inflammation ( 83 ).…”

Section: Respiratory Inflammation and Spn Infectiomentioning

confidence: 99%

Role of Inflammatory Risk Factors in the Pathogenesis of Streptococcus pneumoniae

et al. 2018

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Streptococcus pneumoniae (Spn) is a colonizer of the human nasopharynx (NP), causing a variety of infections in humans including otitis media, pneumonia, sepsis, and meningitis. The NP is an immune permissive site which allows for the persistence of commensal bacteria. Acute or chronic respiratory airway inflammation constitutes a significant risk factor for the manifestation of Spn infections. The inflammatory conditions caused by an upper respiratory viral infection or respiratory conditions such as allergic asthma and chronic obstructive pulmonary disorders (COPDs) are implicated in the dysregulation of airway inflammation and tissue damage, which compromise the respiratory barrier integrity. These immune events promote bacterial outgrowth leading to Spn dissemination and invasion into the bloodstream. Therefore, suppression of inflammation and restoration of respiratory barrier integrity could contain Spn infections manifesting in the backdrop of an inflammatory disease condition. The gained knowledge could be harnessed in the design of novel therapeutic interventions to circumvent Spn bacterial infections.

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“…To investigate a potential activation of the liver non-parenchymal cells by IL-17A in proliferative process of liver regeneration, we analyzed in WT and in IL-17RA −/− livers the expression of C/ebpβ and A20 genes specifically activated by IL-17A pathway [44]. Notably, comparing the expression of C/ebpβ (Figure 4(b)) and A20 (Figure 4(c)) in WT and in IL-17RA −/− mice liver, we found a great difference in expression between the two populations.…”

Section: Involvement Of Non-parenchymal Cellsmentioning

confidence: 99%

Role of IL-17RA in the proliferative priming of hepatocytes in liver regeneration

et al. 2018

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A tight link has been established between inflammation and cancer. Liver regeneration is a widely used model to study the correlation between inflammation and proliferation. IL-6 is essentially involved in liver regeneration and in cancer. Recently, IL-17A has been shown to regulate not only inflammation, but also cell proliferation. Here, we analyze the role played by IL-17A signaling in liver regeneration by comparing cell proliferation in Wild Type and IL-17RA −/− mice. Partial hepatectomy experiments performed in IL-17RA −/− mice showed a delay in expression of earlygenes to prime the residual hepatocyte to proliferate, with subsequent delay in G 1 /S-phase transition. We demonstrated that IL-17RA regulates, by recruitment of non-parenchymal cell, the expression of IL-6, which in turn triggers the proliferation of residual hepatocytes. Our data indicate an important role played by IL-17RA in liver proliferation via IL-6. ARTICLE HISTORY

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The IL-17F/IL-17RC Axis Promotes Respiratory Allergy in the Proximal Airways

Cited by 44 publications

References 54 publications

Helper T‐cell responses and pulmonary fungal infections

Helper T‐cell responses and pulmonary fungal infections

Role of Inflammatory Risk Factors in the Pathogenesis of Streptococcus pneumoniae

Role of IL-17RA in the proliferative priming of hepatocytes in liver regeneration

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