Current Opinion in Biotechnology, Год журнала: 2023, Номер 85, С. 103048 - 103048
Опубликована: Дек. 23, 2023
Язык: Английский
Journal of Controlled Release, Год журнала: 2023, Номер 362, С. 425 - 445
Опубликована: Сен. 8, 2023
Язык: Английский
Процитировано
56
Immunity, Год журнала: 2024, Номер 57(6), С. 1260 - 1273.e7
Опубликована: Май 13, 2024
Upon parasitic helminth infection, activated intestinal tuft cells secrete interleukin-25 (IL-25), which initiates a type 2 immune response during lamina propria innate lymphoid (ILC2s) produce IL-13. This causes epithelial remodeling, including cell hyperplasia, the function of is unknown. We identified cholinergic effector cells, are only that expressed choline acetyltransferase (ChAT). During parasite mice with epithelial-specific deletion ChAT had increased worm burden, fitness, and fecal egg counts, even though responses were comparable. Mechanistically, IL-13-amplified release acetylcholine (ACh) into gut lumen. Finally, we demonstrated direct effect ACh on worms, reduced their fecundity via helminth-expressed muscarinic receptors. Thus, sentinels in naive mice, amplification upon infection provides an additional function.
Язык: Английский
Процитировано
22
Cellular and Molecular Immunology, Год журнала: 2025, Номер unknown
Опубликована: Фев. 17, 2025
Язык: Английский
Процитировано
15
Nature, Год журнала: 2025, Номер 637(8045), С. 296 - 303
Опубликована: Янв. 8, 2025
Язык: Английский
Процитировано
3
Immunity, Год журнала: 2023, Номер 56(4), С. 687 - 694
Опубликована: Апрель 1, 2023
Язык: Английский
Процитировано
39
Journal of Allergy and Clinical Immunology, Год журнала: 2023, Номер 153(4), С. 879 - 893
Опубликована: Авг. 25, 2023
Type 2 inflammation is characterized by overexpression and heightened activity of type cytokines, mediators, cells that drive neuroimmune activation sensitization to previously subthreshold stimuli. The consequences altered differ tissue disease; they include skin inflammation, pruritogens, itch amplification in atopic dermatitis prurigo nodularis; airway and/or hyperresponsiveness, loss expiratory volume, airflow obstruction increased mucus production asthma; sense smell chronic rhinosinusitis with nasal polyps; dysphagia eosinophilic esophagitis. We describe the interactions underlie various sensory autonomic pathologies inflammatory diseases present recent advances targeted treatment approaches reduce its associated symptoms these diseases. Further research needed better understand mechanisms chronic, sustained related inflammation. immunity a specialized, evolutionarily conserved arm immune system combats ectoparasitic endoparasitic helminths, expels toxins, promotes repair.1Gandhi N.A. Bennett B.L. Graham N.M.H. Pirozzi G. Stahl N. Yancopoulos G.D. Targeting key proximal drivers disease.Nat Rev Drug Discov. 2016; 15: 35-50Crossref PubMed Scopus (392) Google Scholar, 2Gandhi N.M. Commonality IL-4/IL-13 pathway diseases.Expert Clin Immunol. 2017; 13: 425-437Crossref (276) 3Kopp E.B. Agaronyan K. Licona-Limon I. Nish S.A. Medzhitov R. Modes response initiation.Immunity. 2023; 56: 667-694Abstract Full Text PDF (1) 4Molofsky A.B. Locksley R.M. ins outs innate adaptive immunity.Immunity. 704-722Abstract (0) Scholar When epithelial barrier breached, alarmin cytokines (eg, thymic stromal lymphopoietin [TSLP], IL-25, IL-33) activate tissue-resident (such as mast cells, dendritic group lymphoid [ILC2s]) while simultaneously recruiting granulocytes, including eosinophils basophils. Collectively, orchestrate polarized through histamine, other mediators neutralize expel parasitic helminths toxins repair turnover, remodeling, fibrosis. Although processes are protective intended restore homeostasis, setting allergy continuous stress become pathologic, resulting variety Mechanical reflexes such scratching, constriction, coughing, sneezing, gastrointestinal motility also protect surfaces triggered direct neurons, often concert input target organs. Many manifestations pathologically dysregulation (Fig 1), (but not limited to) (AD), nodularis (PN), asthma, food allergy, polyps (CRSwNP), esophagitis (EoE).1Gandhi Scholar,2Gandhi Scholar,5Hamilton J.D. Harel S. Swanson B.N. Brian W. Chen Z. Rice M.S. et al.Dupilumab suppresses biomarkers across multiple atopic, allergic diseases.Clin Exp Allergy. 2021; 51: 915-931Crossref (59) Scholar,6Le Floc'h A. Allinne J. Nagashima Scott Birchard D. Asrat al.Dual blockade IL-4 IL-13 dupilumab, an IL-4Rα antibody, required broadly inhibit inflammation.Allergy. 2020; 75: 1188-1204Crossref (163) extent similarities among pathways regulating mechanical responses remains be fully defined (Table I7Kulka M. Sheen C.H. Tancowny B.P. Grammer L.C. Schleimer R.P. Neuropeptides human cell degranulation chemokine production.Immunology. 2008; 123: 398-410Crossref (340) 8Liang Y. Marcusson J.A. Jacobi H.H. Haak-Frendscho Johansson O. Histamine-containing their relationship NGFr-immunoreactive nerves nodularis: reappraisal.J Cutan Pathol. 1998; 25: 189-198Crossref (49) 9Sonkoly E. Muller Lauerma A.I. Pivarcsi Soto H. Kemeny L. al.IL-31: new link between T pruritus inflammation.J Allergy 2006; 117: 411-417Abstract (759) 10Tominaga Takamori Peripheral dermatitis.Allergol Int. 2022; 71: 265-277Crossref (19) 11Garcovich Maurelli Gisondi P. Peris Yosipovitch Girolomoni Pruritus distinctive feature inflammation.Vaccines (Basel). 9: 303Crossref (50) 12Kim Y.J. Granstein R.D. Roles calcitonin gene-related peptide skin, physiological pathophysiological functions.Brain Behav Immun Health. 18100361PubMed 13Wang F. Trier A.M. Li Kim Chai J.N. al.A basophil-neuronal axis itch.Cell. 184: 422-440.e17Abstract (95) 14Liu B. Tai Achanta Kaelberer M.M. Caceres Shao X. al.IL-33/ST2 signaling excites neurons mediates mouse model poison ivy contact allergy.Proc Natl Acad Sci U S 113: E7572-E7579Crossref (179) 15Wilson S.R. Thé Batia L.M. Beattie Katibah G.E. McClain S.P. al.The cell-derived cytokine TSLP activates induce 2013; 155: 285-295Abstract (676) 16Trier Mack M.R. Fredman Tamari Ver Heul Zhao al.IL-33 promoted dry itch.J 149: 1473-1480Abstract 17Simpson E.L. Parnes J.R. She Crouch Rees Mo al.Tezepelumab, anti–thymic monoclonal moderate severe dermatitis: randomized phase 2a clinical trial.J Am Dermatol. 2019; 80: 1013-1021Abstract 18Oetjen L.K. Feng Whelan T.M. Niu Guo C.J. al.Sensory co-opt classical mediate 171: 217-228.e13Abstract (581) 19Cevikbas Wang Akiyama Kempkes C. Savinko T. Antal neuron-expressed IL-31 receptor helper cell-dependent itch: involvement TRPV1 TRPA1.J 2014; 133: 448-460Abstract (482) 20Blauvelt de Bruin-Weller Gooderham Cather J.C. Weisman Pariser al.Long-term management moderate-to-severe dupilumab concomitant topical corticosteroids (LIBERTY AD CHRONOS): 1-year, randomized, double-blinded, placebo-controlled, 3 trial.Lancet. 389: 2287-2303Abstract (786) 21Silverberg J.I. 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Boguniewicz Sher adolescents uncontrolled trial.JAMA 156: 44-56Crossref (254) 25Paller Wollenberg Arkwright P.D. children 6 11 years old placebo-controlled 83: 1282-1293Abstract (174) 26Paller ages months younger than randomised, double-blind, 400: 908-919Abstract 27Wollenberg Worm Lynde Lacour J.P. al.Tralokinumab for results 52-week, multicentre, (ECZTRA ECZTRA 2).Br 437-449Crossref (214) 28Wollenberg Howell M.D. Silverberg Kell Ranade al.Treatment tralokinumab, anti-IL-13 mAb.J. Clin. 143: 135-141Abstract (252) 29Gutermuth Pink A.E. Soldbro Bjerregård Øland Weidinger Tralokinumab plus inadequate intolerance ciclosporin A: trial 7).Br 186: 440-452Crossref (26) 30Silverberg Toth Alexis A.F. Elewski B.E. trial.Br 450-463Crossref (133) 31Simpson Carsten Flohr Eichenfield L.F. Sofen Taïeb lebrikizumab (an antibody) inadequately controlled corticosteroids: II (TREBLE).J 2018; 78: 863-871.e11Abstract (239) 32Guttman-Yassky Armstrong A.W. Drew lebrikizumab, high-affinity interleukin 13 inhibitor, dermatitis. A 2b 411-420Crossref 33Silverberg Irvine A.D. Stein Gold 388: 1080-1091Crossref (16) 34Silverberg Pinter Pulka Poulin Bouaziz al.Phase 2B study nemolizumab pruritus.J 145: 173-182Abstract (159) 35Kabashima Matsumura Komazaki Kawashima Nemolizumab JP01 JP02 Study Group. agents (AD) provide improvement signs up 68 weeks: III, long-term studies.Br 642-651Crossref 36Ständer Legat F.J. Paul Narbutt al.Trial nodularis.N 382: 706-716Crossref (144) 37Kamata Tada Optimal use Jak inhibitors biologics on basis current evidence.JID Innov. 3100195Abstract 38Bieber Kabashima al.Atopic pathomechanisms lessons learned novel systemic therapeutic options.JEADV. 36: 1432-1449Google 39Lee K.P. Plante Korte J.E. Elston D.M. Oral Janus kinase systematic review meta-analysis.Skin Health Dis. 3: e133Crossref 40Rodriguez-Roy Ficheux A.-S. Misery Brenaut Efficacy treatments pruritus: literature meta-analysis.Front 91079323Google 41Huang I.-H. Chung W.-H. Wu P.-C. C.-B. JAK-STAT pathogenesis An updated review.Front 131068260Crossref (12) 42Haas Capellino Phan N.Q. Böhm Luger T.A. Straub R.H. al.Low density sympathetic nerve fibers relative substance P-positive lesional nodularis.J 2010; 58: 193-197Abstract (73) 43Liang Reimert C.M. CGRP-immunoreactive nodularis—an exploration neurogenic 2000; 27: 359-366Crossref (62) 44Williams K.A. Huang A.H. Belzberg Kwatra S.G. Prurigo management.J 1567-1575Abstract 45Molina F.A. Burrows N.P. Jones R.R. Terenghi Polak J.M. Increased neuropeptides nodular prurigo: quantitative immunohistochemical analysis.Br 1992; 127: 344-351Crossref 46Kabata Artis Neuro-immune crosstalk Invest. 129: 1475-1482Crossref (88) 47Teresiak-Mikołajczak Czarnecka-Operacz Jenerowicz Silny Neurogenic markers process relation severity pruritus.Postepy Alergol. 30: 286-292Crossref (33) 48Yang T.B. B.S. 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Zhang Lee Van Dyken al.Pulmonary neuroendocrine amplify asthma 360eaan8546Crossref (228) 64Hara Jha M.K. Mattoo Nash Khan Orengo al.Interleukin 4 directly olfactory induces mice.J 151: AB128Abstract 65Rouyar Classe Gorski Bock Le-Guern Roche al.Type 2/Th2-driven impairs neurogenesis model.Allergy. 74: 549-559Crossref (14) 66Backaert Steelant Hellings P.W. Talavera Gerven TRiP roles transient potential cation channels upper inflammation.Curr Asthma Rep. 21: 20Crossref 67Li Jiang Shen al.Sneezing reflex mediated peptidergic nose brainstem.Cell. 3762-3773Abstract (23) 68Samivel D.W. Son H.R. role CD4+ cell-mediated rhinitis.Oncotarget. 2015; 7: 148-160Crossref 69Yu Chang Yu Capsaicin-sensitive vagal afferent nerve-mediated interoceptive signals esophagus.Molecules. 26: 3929Crossref (3) 70O'Shea K.M. Aceves S.S. Dellon E.S. Pathophysiology esophagitis.Gastroenterology. 154: 333-345Abstract 71Akiho Ihara Motomura Nakamura Cytokine-induced alterations disorders.World Gastrointest Pathophysiol. 2011; 2: 72-81Crossref 72Hu Liu al.Increased acid responsiveness guinea pig esophagitis.Am Physiol Liver 307: G149-G157Crossref (21) 73Zhang Shoda Arva N.C. Chehade Collins M.H. al.Mast cell-pain connection esophagitis.Allergy. 77: 1895-1899Crossref (8) Scholar).Table INeuroimmune affecting AD, PN, CRSwNP, EoEConditionSymptomsNeuroimmune interactionsType profileADPruritus•Colocalization cells7Kulka Scholar,8Liang Scholar•Type OSM promote pruritogen sensitization9Sonkoly Scholar•Neuropeptide proinflammatory basophils)7Kulka Scholar,10Tominaga Scholar•Scratching causes alarmins IL-33), which can act neurons9Sonkoly Scholar,11Garcovich Scholar,14Liu Scholar•Some express receptors IL-13, IL-31, TRPA1, TRPV118Oetjen Scholar,19Cevikbas Scholar•Reducing reduces itch20Blauvelt
Язык: Английский
Процитировано
38
Bioactive Materials, Год журнала: 2024, Номер 36, С. 330 - 357
Опубликована: Март 11, 2024
Nanovaccines have gathered significant attention for their potential to elicit tumor-specific immunological responses. Despite notable progress in tumor immunotherapy, nanovaccines still encounter considerable challenges such as low delivery efficiency, limited targeting ability, and suboptimal efficacy. With an aim of addressing these issues, engineering customized through modification or functionalization has emerged a promising approach. These tailored not only enhance antigen presentation, but also effectively modulate immunosuppression within the microenvironment. Specifically, they are distinguished by diverse sizes, shapes, charges, structures, unique physicochemical properties, along with ligands. features facilitate lymph node accumulation activation/regulation immune cells. This overview bespoke underscores both prophylactic therapeutic applications, offering insights into future development role cancer immunotherapy.
Язык: Английский
Процитировано
15
Frontiers in Immunology, Год журнала: 2024, Номер 15
Опубликована: Апрель 11, 2024
Conventionally, immunity in humans has been classified as innate and adaptive, with the concept that only latter type an immunological memory/recall response against specific antigens or pathogens. Recently, a new of trained (a.k.a. memory response) emerged. According to this concept, immune cells can exhibit enhanced responsiveness subsequent challenges, after initial stimulation antigen/pathogen. Thus, enables respond robustly non-specifically through exposure re-exposure antigens/infections vaccines, providing resistance unrelated pathogens reduced infection severity. For example, individuals vaccinated BCG protect tuberculosis were also protected from malaria SARS-CoV-2 infections. Epigenetic modifications such histone acetylation metabolic reprogramming (e.g. shift towards glycolysis) their inter-linked regulations are key factors underpinning activation cells. The integrated epigenetic rewiring generates sufficient intermediates, which is crucial meet energy demand required produce proinflammatory antimicrobial responses by These determine efficacy durability immunity. Importantly, signaling pathways regulatory molecules be harnessed potential targets for developing novel intervention strategies, better vaccines immunotherapies infectious (e.g., sepsis) non-infectious cancer) diseases. However, aberrant inflammation caused inappropriate onset lead severe autoimmune pathological consequences, systemic sclerosis granulomatosis). In review, we provide overview conventional adaptive summarize various mechanistic associated regulation immunity, focusing on immunologic, metabolic, changes myeloid This review underscores transformative immunology, paving way therapeutic strategies diseases leverage memory.
Язык: Английский
Процитировано
13
Science, Год журнала: 2024, Номер 386(6721)
Опубликована: Окт. 31, 2024
The innate immune system shapes brain development and is implicated in neurodevelopmental diseases. It critical to define the relevant cells signals their impact on circuits. In this work, we found that group 2 lymphoid (ILC2s) cytokine interleukin-13 (IL-13) signaled directly inhibitory interneurons increase synapse density developing mouse brain. ILC2s expanded produced IL-13 meninges. Loss of or signaling decreased inhibitory, but not excitatory, cortical synapses. Conversely, were sufficient pathway led selective impairments social interaction. These data a type neuroimmune circuit early life behavior.
Язык: Английский
Процитировано
12
The Journal of Experimental Medicine, Год журнала: 2024, Номер 221(6)
Опубликована: Апрель 10, 2024
Epithelium-derived cytokines or alarmins, such as interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP), are major players in type 2 immunity asthma. Here, we demonstrate that TNF-like ligand 1A (TL1A) is an epithelial alarmin, constitutively expressed alveolar epithelium at steady state both mice humans, which cooperates with IL-33 for early induction of IL-9high ILC2s during the initiation allergic airway inflammation. Upon synergistic activation by TL1A, lung acquire a transient IL-9highGATA3low “ILC9” phenotype produce prodigious amounts IL-9. A combination large-scale proteomic analyses, intravital microscopy, adoptive transfer ILC9 cells revealed high IL-9 expression distinguishes multicytokine-producing state-of-activated increased capacity to initiate IL-5-dependent Similar TSLP, TL1A basal healthy asthmatic human lungs. Together, these results indicate epithelium-derived cytokine important cofactor airways.
Язык: Английский
Процитировано
10