Corrigendum: CXCL17 Is a Specific Diagnostic Biomarker for Severe Pandemic Influenza A(H1N1) That Predicts Poor Clinical Outcome

Choreño-Parra, José Alberto; Jiménez-Álvarez, Luis Armando; Ramírez-Martínez, Gustavo; Sandoval-Vega, Montserrat; Salinas-Lara, Citlaltépetl; Sánchez-Garibay, Carlos; Luna-Rivero, César; Hernández-Montiel, Erika Mariana; Fernández-López, Luis Alejandro; Cabrera-Cornejo, María Fernanda; Choreño-Parra, Eduardo M.; Cruz‐Lagunas, Alfredo; Domínguez, Andrea; Márquez-García, Eduardo; Cabello-Gutiérrez, Carlos; Bolaños-Morales, Francina Valezka; Mena-Hernández, Lourdes; Delgado-Zaldivar, Diego; Rebolledo-García, Daniel; Guadarrama-Ortíz, Parménides; Regino-Zamarripa, Nora Elemi; Mendoza-Milla, Criselda; Garcı́a-Latorre, Ethel; Rodríguez‐Reyna, Tatiana Sofía; Cervantes-Rosete, D.; Hernández-Cárdenas, Carmen Margarita; Khader, Shabaana A.; Zlotnik, Albert; Zúñiga, Joaquı́n

doi:10.3389/fimmu.2021.700716

Cited by 3 publications

(3 citation statements)

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“…However, when compared to other endogenous CXCR4 inhibitors, for example, CXCL14 K d ~ 14 nM ( 20 ) or EPI-X4 K i ~ 3 μM ( 22 ), CXCL17 has similar or high affinity for CXCR4. Notably, CXCL17 concentrations can reach up to ~60 ng/ml in vitro, whereas serum CXCL17 concentrations can reach up to ~5 ng/ml during influenza infection ( 10 ). Because CXCL17 expression is highly localized to secretory cells in mucosal tissue ( 37 ) and CXCL17 binds to GAGs and is concentrated in the extracellular matrix in close proximity to the receptor, it is very likely that CXCL17 reaches local concentrations sufficient to inhibit CXCR4 and reduce signaling.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, CXCL17 has antimicrobial properties at high concentrations ( 5 ) and modulates angiogenesis ( 4 , 6 ). CXCL17 has also been implicated in several pathologies including breast ( 7 ) and hepatocellular cancers ( 8 ), as well as inflammatory lung pathologies such as idiopathic pulmonary fibrosis ( 5 ), asthma ( 9 ), influenza ( 10 ), and severe acute respiratory syndrome coronavirus 2 ( 11 ) infection. Despite mediating a wide range of important functional responses, the receptor(s) for CXCL17 are still unknown.…”

Section: Introductionmentioning

confidence: 99%

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CXCL17 is an allosteric inhibitor of CXCR4 through a mechanism of action involving glycosaminoglycans

White,

Platt,

Kilpatrick

et al. 2024

Sci. Signal.

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CXCL17 is a chemokine principally expressed by mucosal tissues, where it facilitates chemotaxis of monocytes, dendritic cells, and macrophages and has antimicrobial properties. CXCL17 is also implicated in the pathology of inflammatory disorders and progression of several cancers, and its expression is increased during viral infections of the lung. However, the exact role of CXCL17 in health and disease requires further investigation, and there is a need for confirmed molecular targets mediating CXCL17 functional responses. Using a range of bioluminescence resonance energy transfer (BRET)–based assays, here we demonstrated that CXCL17 inhibited CXCR4-mediated signaling and ligand binding. Moreover, CXCL17 interacted with neuropillin-1, a VEGFR2 coreceptor. In addition, we found that CXCL17 only inhibited CXCR4 ligand binding in intact cells and demonstrated that this effect was mimicked by known glycosaminoglycan binders, surfen and protamine sulfate. Disruption of putative GAG binding domains in CXCL17 prevented CXCR4 binding. This indicated that CXCL17 inhibited CXCR4 by a mechanism of action that potentially required the presence of a glycosaminoglycan-containing accessory protein. Together, our results revealed that CXCL17 is an endogenous inhibitor of CXCR4 and represents the next step in our understanding of the function of CXCL17 and regulation of CXCR4 signaling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

CXCL17 is an allosteric inhibitor of CXCR4 through a mechanism of action involving glycosaminoglycans

White,

Platt,

Kilpatrick

et al. 2024

Sci. Signal.

View full text Add to dashboard Cite

show abstract

“…An investigation reported that CXCL17 attenuated imiquimod‐induced psoriasis‐like skin inflammation via recruitment of myeloid‐derived suppressor cells (MDSCs) and regulatory T cells (Tregs) (Oka et al 2017). In infectious diseases such as influenza A(H1N1) pdm09, study on peripheral blood monocyte‐derived macrophages and human alveolar A549 cells showed that levels of CXCL17 significantly elevated and this chemokine can be used as a potential specific diagnostic biomarker for influenza A (H1N1) infections (Choreño‐Parra et al 2021). In asthma, CXCL17 overexpressed following decreasing in the levels of miR221‐3p in epithelial and sputum, inhibiting airway eosinophilic inflammation in a protective fashion (Zhang et al 2018).…”

Section: Role Of Cxcl17 In the Immune System And Related Phenomenamentioning

confidence: 99%

The cryptic role of CXCL17/CXCR8 axis in the pathogenesis of cancers: a review of the latest evidence

Hashemi

Khorramdelazad

2022

J. Cell Commun. Signal.

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Chemokines are immune system mediators that mediate various activities and play a role in the pathogenesis of several cancers. Among these chemokines, C‐X‐C motif chemokine 17 (CXCL‐17) is a relatively novel molecule produced along the airway epithelium in physiological and pathological conditions, and evidence shows that it plays a homeostatic role in most cases. CXCL17 has a protective role in some cancers and a pathological role in others, such as liver and lung cancer. This chemokine, along with its possible receptor termed G protein‐coupled receptor 35 (GPR35) or CXCR8, are involved in recruiting myeloid cells, regulating angiogenesis, defending against pathogenic microorganisms, and numerous other mechanisms. Considering the few studies that have been performed on the dual role of CXCL17 in human malignancies, this review has investigated the possible pro‐tumor and anti‐tumor roles of this chemokine, as well as future treatment options in cancer therapy.

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The Chemokine System as a Key Regulator of Pulmonary Fibrosis: Converging Pathways in Human Idiopathic Pulmonary Fibrosis (IPF) and the Bleomycin-Induced Lung Fibrosis Model in Mice

Russo,

Ryffel

2024

Cells

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Idiopathic pulmonary fibrosis (IPF) is a chronic and lethal interstitial lung disease (ILD) of unknown origin, characterized by limited treatment efficacy and a fibroproliferative nature. It is marked by excessive extracellular matrix deposition in the pulmonary parenchyma, leading to progressive lung volume decline and impaired gas exchange. The chemokine system, a network of proteins involved in cellular communication with diverse biological functions, plays a crucial role in various respiratory diseases. Chemokine receptors trigger the activation, proliferation, and migration of lung-resident cells, including pneumocytes, endothelial cells, alveolar macrophages, and fibroblasts. Around 50 chemokines can potentially interact with 20 receptors, expressed by both leukocytes and non-leukocytes such as tissue parenchyma cells, contributing to processes such as leukocyte mobilization from the bone marrow, recirculation through lymphoid organs, and tissue influx during inflammation or immune response. This narrative review explores the complexity of the chemokine system in the context of IPF and the bleomycin-induced lung fibrosis mouse model. The goal is to identify specific chemokines and receptors as potential therapeutic targets. Recent progress in understanding the role of the chemokine system during IPF, using experimental models and molecular diagnosis, underscores the complex nature of this system in the context of the disease. Despite advances in experimental models and molecular diagnostics, discovering an effective therapy for IPF remains a significant challenge in both medicine and pharmacology. This work delves into microarray results from lung samples of IPF patients and murine samples at different stages of bleomycin-induced pulmonary fibrosis. By discussing common pathways identified in both IPF and the experimental model, we aim to shed light on potential targets for therapeutic intervention. Dysregulation caused by abnormal chemokine levels observed in IPF lungs may activate multiple targets, suggesting that chemokine signaling plays a central role in maintaining or perpetuating lung fibrogenesis. The highlighted chemokine axes (CCL8-CCR2, CCL19/CCL21-CCR7, CXCL9-CXCR3, CCL3/CCL4/CCL5-CCR5, and CCL20-CCR6) present promising opportunities for advancing IPF treatment research and uncovering new pharmacological targets within the chemokine system.

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Corrigendum: CXCL17 Is a Specific Diagnostic Biomarker for Severe Pandemic Influenza A(H1N1) That Predicts Poor Clinical Outcome

Cited by 3 publications

References 0 publications

CXCL17 is an allosteric inhibitor of CXCR4 through a mechanism of action involving glycosaminoglycans

CXCL17 is an allosteric inhibitor of CXCR4 through a mechanism of action involving glycosaminoglycans

The cryptic role of CXCL17/CXCR8 axis in the pathogenesis of cancers: a review of the latest evidence

The Chemokine System as a Key Regulator of Pulmonary Fibrosis: Converging Pathways in Human Idiopathic Pulmonary Fibrosis (IPF) and the Bleomycin-Induced Lung Fibrosis Model in Mice

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