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Transient Receptor Potential Channels and Itch
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Mahar Fatima, Jingyi Liu, Bo Duan
The cytokine thymic stromal lymphopoietin (TSLP) acts as a master switch that triggers both the initiation and maintenance of atopic dermatitis, which is characterized by chronic debilitating itch (67). Keratinocyte-derived TSLP activates sensory neurons directly to evoke itch in an atopic dermatitis mouse model (68). TSLP-sensitive sensory neurons represent a previously unidentified subset of sensory neurons that require both functional TSLP receptors and TRPA1 channels to promote TSLP-evoked itch behaviors (68).
Etiopathogenesis
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Dario Didona, Biagio Didona, Giovanni Paolino, Raffaele Dante Caposiena Caro
Thymic stromal lymphopoietin (TSLP) gene localized at chromosome 5q22.1 encodes thymic stromal lymphopoietin, which produces a cellular signal through a heterodimeric receptor complex composed of the thymic stromal lymphopoietin receptor and the IL-7R alpha chain [2]. This protein leads naive CD4+ T cells to produce Th2 response cytokines (IL-4, IL-5, IL-13, tumor necrosis factor-alpha [TNF-α]) and inhibits production of Th1 response cytokines (IL-10, IFN-γ). As a result, when deficiency of TSLP gene expression occurs, the dominance of Th1 response, which is involved in vitiligo development, is expected [7].
Pathophysiology of asthma
Published in Louis-Philippe Boulet, Applied Respiratory Pathophysiology, 2017
Lung epithelial cells activated by proteases, viruses, or environmental pollutants produce a triad of cytokines including thymic stromal lymphopoietin (TSLP), IL-33, and IL-25, considered as critical initiators of type 2 eosinophilic inflammatory events in lung, gut, and skin. These cytokines are present in increased levels in airways of asthmatics and correlate with disease severity.
Precision medicine in chronic rhinosinusitis – using endotype and endotype-driven therapeutic options
Published in Expert Review of Clinical Immunology, 2023
Yutong Sima, Yan Zhao, Xiangdong Wang, Luo Zhang
ECRS mainly develops in type 2-predominant environments. Eosinophils in CRS are mainly recruited by interleukin-5 (IL-5), eotaxin, regulated upon activation, normal T cell expressed, and secreted RANTES, granulocyte macrophage-colony stimulating factor (GM-CSF), and Staphylococcus aureus. Additionally, IL-5, IL-33, and thymic stromal lymphopoietin (TSLP) can prolong eosinophil survival in tissues. Activated eosinophils secrete proteins and proinflammatory lipids to protect the immune system and can also cause tissue remodeling, tissue damage, mucus secretion, and vascular permeability. Eosinophils can also cause CRS-induced tissue damage by forming eosinophil extracellular traps (EETs), which are composed of DNA and granule proteins. EETs are observed in the subepithelial regions with epithelial barrier defects and are present in mucus, which can increase the viscosity of the latter. Hwang et al. reported that the number of EETs was consistent with the Lund-MacKay score and the number of tissue-infiltrating eosinophils, regardless of the presence of nasal polyps [11].
Novel therapeutic approaches targeting endotypes of severe airway disease
Published in Expert Review of Respiratory Medicine, 2021
Maria De Filippo, Martina Votto, Amelia Licari, Fabio Pagella, Marco Benazzo, Giorgio Ciprandi, Gian Luigi Marseglia
To date, up to 50% of patients with severe non-eosinophilic asthma have limited treatment options. Tezepelumab is the first drug of a new category for severe asthma treatment, targeting thymic stromal lymphopoietin (TSLP), a protein of the cytokine family that is recognized as having an important role in the maturation of T cells. Specifically, tezepelumab is a humanized monoclonal antibody designed to bind specifically to human TSLP, preventing its interaction with its receptor complex. TSLP blockade obtained with tezepelumab prevents the release of pro-inflammatory cytokines by immune system cells ‘marked’ by the presence of TSLP. Due to tezepelumab activity ‘upstream’ of the inflammatory cascade, it could be helpful in a large population of patients with severe uncontrolled asthma, including those whose asthmatic condition is not driven by T2 inflammation [162]. Based on the findings from PATHWAY, tezepelumab was granted a breakthrough.
Thymic stromal lymphopoietin: its role and potential as a therapeutic target in asthma
Published in Expert Opinion on Therapeutic Targets, 2020
Gail M. Gauvreau, Roma Sehmi, Christopher S. Ambrose, Janet M. Griffiths
The immunology of thymic stromal lymphopoietin (TSLP), an epithelial cytokine, provides an opportunity for a novel approach to treat asthma inflammation. A member of a class of epithelial cytokines commonly referred to as alarmins (whose other members are IL-25 and IL-33), TSLP is released by airway epithelial cells in response to various environmental insults, including viruses, bacteria, allergens, chemical irritants and physical injury [16,17]. Functionally, TSLP is a key instigator of the immune response to environmental insults, initiating a range of downstream inflammatory pathways. While TSLP drives a pronounced T2 inflammatory response [18–20], there is emerging evidence of TSLP involvement in non-T2 processes involving interactions with both immune and structural cell types. The considerable scope of effects mediated by TSLP is illustrated by the wide range of cell types that express the TSLP receptor (TSLPR), including hematopoietic progenitor cells, eosinophils, basophils, mast cells, airway smooth muscle cells (ASMCs), group 2 innate lymphoid cells (ILC2s), lymphocytes, dendritic cells and monocytes/macrophages [21,22]. In addition to its actions on specific cell populations, the possibility that TSLP serves as a key mediator between immune cell types and structural cells in the airway milieu is intriguing and is an area of ongoing research.