IL-33: A central cytokine in helminth infections.
TL;DR: A review of the literature around this fascinating cytokine, its activity on immune and non-immune cells, the unique (and sometimes counterintuitive) responses it induces, and how it can coordinate the immune response during infections by parasitic helminths is presented in this paper.
About: This article is published in Seminars in Immunology.The article was published on 2021-11-22 and is currently open access. It has received 11 citations till now. The article focuses on the topics: Immune system.
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TL;DR: This review focuses on giving a detailed description of all the presently discovered ILs and their role in various diseases, and discusses the various electrochemical biosensors that can be employed for the detection of ILs in body fluids.
Abstract: Interleukins (ILs) are a major subclass of cytokines acting as molecular messengers playing role in immune system responses via a cascade of signaling pathways. Belonging to the cytokine family, the ILs play a crucial role in the theranostics of various diseases. Their abnormal expression leads to the development of various diseases such as cancer, neurodegenerative diseases, allergies, asthma, autoimmune diseases, and other physiological abnormalities. This paves the path of exploring the ILs for the development of sensitive and efficient biosensors and promoting them for clinical testing in a wide array of diseases. Further, detecting the level of ILs is very important for their early diagnosis and their progression within the body, and simultaneously their possible immunotherapeutic approaches. To achieve this goal, multidisciplinary scientific approaches involving immunology, electrochemistry, nanotechnology, photometry, etc. are already being put into action. The advancements in nanoscience and nanotechnology are aiding the development of highly sensitive biosensors for ILs detection. This review focuses on giving a detailed description of all the presently discovered ILs and their role in various diseases. Simultaneously, it also discusses the various electrochemical biosensors that can be employed for the detection of ILs in body fluids. Moreover, the role of nanomaterials in electrochemical biosensing is also discussed in this review.
21 citations
TL;DR: In this paper , the authors focus on the new discoveries of the cells and cytokines involved in tissue specific immune responses to helminths and how these contribute to host immunity against helminth infection and allow the host to accommodate the presence of parasites when they cannot be eliminated.
10 citations
TL;DR: The concept of the one-airway-one-disease (ONE-AIRWAY-ONE-Disease) is a simplistic approach of the links between upper and lower airway allergic diseases as discussed by the authors .
Abstract: Asthma, rhinitis, and atopic dermatitis (AD) are interrelated clinical phenotypes that partly overlap in the human interactome. The concept of “one‐airway‐one‐disease,” coined over 20 years ago, is a simplistic approach of the links between upper‐ and lower‐airway allergic diseases. With new data, it is time to reassess the concept. This article reviews (i) the clinical observations that led to Allergic Rhinitis and its Impact on Asthma (ARIA), (ii) new insights into polysensitization and multimorbidity, (iii) advances in mHealth for novel phenotype definitions, (iv) confirmation in canonical epidemiologic studies, (v) genomic findings, (vi) treatment approaches, and (vii) novel concepts on the onset of rhinitis and multimorbidity. One recent concept, bringing together upper‐ and lower‐airway allergic diseases with skin, gut, and neuropsychiatric multimorbidities, is the “Epithelial Barrier Hypothesis.” This review determined that the “one‐airway‐one‐disease” concept does not always hold true and that several phenotypes of disease can be defined. These phenotypes include an extreme “allergic” (asthma) phenotype combining asthma, rhinitis, and conjunctivitis. Rhinitis alone and rhinitis and asthma multimorbidity represent two distinct diseases with the following differences: (i) genomic and transcriptomic background (Toll‐Like Receptors and IL‐17 for rhinitis alone as a local disease; IL‐33 and IL‐5 for allergic and non‐allergic multimorbidity as a systemic disease), (ii) allergen sensitization patterns (mono‐ or pauci‐sensitization versus polysensitization), (iii) severity of symptoms, and (iv) treatment response. In conclusion, rhinitis alone (local disease) and rhinitis with asthma multimorbidity (systemic disease) should be considered as two distinct diseases, possibly modulated by the microbiome, and may be a model for understanding the epidemics of chronic and autoimmune diseases.
3 citations
TL;DR: In this article , the collective actions of specialized epithelial cells, stromal niches, stem, muscle and neuroendocrine cells as well as peripheral neurons are highlighted in the detection and elimination of helminths at mucosal sites.
3 citations
TL;DR: In this article , the authors explore the recent literature to highlight the main immune alterations and mechanisms that affect the control of viral coinfection, which are valuable in the understanding of clinical observations in helminth-prevalent areas.
1 citations
References
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TL;DR: A member of theIL-1 family, IL-33, which mediates its biological effects via IL-1 receptor ST 2, activates NF-kappaB and MAP kinases, and drives production of T(H)2-associated cytokines from in vitro polarized T( H)2 cells is reported.
3,306 citations
University of Amsterdam1, University of Pennsylvania2, Washington University in St. Louis3, University of Freiburg4, Pasteur Institute5, University of California, San Francisco6, Laboratory of Molecular Biology7, VU University Amsterdam8, John Radcliffe Hospital9, Centre national de la recherche scientifique10, French Institute of Health and Medical Research11
TL;DR: It is proposed that ILCs should be categorized into three groups based on the cytokines that they can produce and the transcription factors that regulate their development and function.
Abstract: Innate lymphoid cells (ILCs) are a family of developmentally related cells that are involved in immunity and in tissue development and remodelling. Recent research has identified several distinct members of this family. Confusingly, many different names have been used to characterize these newly identified ILC subsets. Here, we propose that ILCs should be categorized into three groups based on the cytokines that they can produce and the transcription factors that regulate their development and function.
2,039 citations
TL;DR: The identification and functional characterization of a new innate type-2 immune effector leukocyte that is named the nuocyte is presented, which represents a critically important innate effector cell in type- 2 immunity.
Abstract: Innate immunity provides the first line of defence against invading pathogens and provides important cues for the development of adaptive immunity. Type-2 immunity-responsible for protective immune responses to helminth parasites and the underlying cause of the pathogenesis of allergic asthma-consists of responses dominated by the cardinal type-2 cytokines interleukin (IL)4, IL5 and IL13 (ref. 5). T cells are an important source of these cytokines in adaptive immune responses, but the innate cell sources remain to be comprehensively determined. Here, through the use of novel Il13-eGFP reporter mice, we present the identification and functional characterization of a new innate type-2 immune effector leukocyte that we have named the nuocyte. Nuocytes expand in vivo in response to the type-2-inducing cytokines IL25 and IL33, and represent the predominant early source of IL13 during helminth infection with Nippostrongylus brasiliensis. In the combined absence of IL25 and IL33 signalling, nuocytes fail to expand, resulting in a severe defect in worm expulsion that is rescued by the adoptive transfer of in vitro cultured wild-type, but not IL13-deficient, nuocytes. Thus, nuocytes represent a critically important innate effector cell in type-2 immunity.
1,896 citations
TL;DR: A critical role for lung ILCs in restoring airway epithelial integrity and tissue homeostasis after infection with influenza virus is demonstrated.
Abstract: Innate lymphoid cells (ILCs), a heterogeneous cell population, are critical in orchestrating immunity and inflammation in the intestine, but whether ILCs influence immune responses or tissue homeostasis at other mucosal sites remains poorly characterized. Here we identify a population of lung-resident ILCs in mice and humans that expressed the alloantigen Thy-1 (CD90), interleukin 2 (IL-2) receptor a-chain (CD25), IL-7 receptor a-chain (CD127) and the IL-33 receptor subunit T1-ST2. Notably, mouse ILCs accumulated in the lung after infection with influenza virus, and depletion of ILCs resulted in loss of airway epithelial integrity, diminished lung function and impaired airway remodeling. These defects were restored by administration of the lung ILC product amphiregulin. Collectively, our results demonstrate a critical role for lung ILCs in restoring airway epithelial integrity and tissue homeostasis after infection with influenza virus.
1,270 citations
TL;DR: It is revealed that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation in order to increase population density, and expansion of innate cells necessary for pathogen control or wound repair can occur without recruitment of potentially tissue-destructive inflammatory cells.
Abstract: A defining feature of inflammation is the accumulation of innate immune cells in the tissue that are thought to be recruited from the blood. We reveal that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation in order to increase population density. This inflammatory mechanism occurred during T helper 2 (T(H)2)-related pathologies under the control of the archetypal T(H)2 cytokine interleukin-4 (IL-4) and was a fundamental component of T(H)2 inflammation because exogenous IL-4 was sufficient to drive accumulation of tissue macrophages through self-renewal. Thus, expansion of innate cells necessary for pathogen control or wound repair can occur without recruitment of potentially tissue-destructive inflammatory cells.
1,270 citations