Of the three groups of innate lymphoid cells, the type 3 innate lymphoid cell(s) (ILC3) include the subgroup of enteric ILC3 that participates in many physiological functions of the organism, such as promoting the repair of damaged mucosa, maintaining the homeostasis of gut symbiotic microorganisms, and presenting specific antigens. ILC3 also includes splenic and decidual ILC3. Like other physiological processes in the organism, enteric ILC3 functions are precisely regulated at the endogenous and exogenous levels. However, there has been no review on the physiological functions and regulatory signals of intestinal ILC3. In this paper, based on the current research on the physiological functions of enteric ILC3 in animals and the human, we summarize the signals that regulate cytokine secretion, antigen presentation and the quantity of ILC3 under normal intestinal conditions. We discuss for the first time the classification of the promoting mechanism of secretagogues of ILC3 into direct and indirect types. We also propose that ILC3 can promote intestinal homeostasis, and intestinal homeostasis can ensure the physiological phenotype of ILC3. If homeostasis is disturbed, ILC3 may participate in intestinal pathological changes. Therefore, regulating ILC3 and maintaining intestinal homeostasis are critical to the body.
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http://dx.doi.org/10.1016/j.lfs.2020.118504 | DOI Listing |
PLoS One
January 2025
Center for Inflammation, Immunity, & Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia, United States of America.
Microbiota-induced production of IL-22 by type 3 innate lymphoid cells (ILC3) plays an important role in maintaining intestinal health. Such IL-22 production is driven, in part, by IL-23 produced by gut myeloid cells that have sensed select microbial-derived mediators. The extent to which ILC3 can directly respond to microbial metabolites via IL-22 production is less clear, in part due to the difficulty of isolating and maintaining sufficient numbers of viable ILC3 ex vivo.
View Article and Find Full Text PDFHepatol Commun
November 2024
Department of Cell Biology, New York University School of Medicine, New York, New York, USA.
Clin Rev Allergy Immunol
December 2024
Division of Allergy and Clinical Immunology, The Johns Hopkins Asthma & Allergy Center, Johns Hopkins University School of Medicine, 5501 Hopkins Bayview Circle, Room 3B.71, Baltimore, MD, 21224, USA.
Asthma is a chronic airway inflammatory disease that affects millions globally. Although glucocorticoids are a mainstay of asthma treatment, a subset of patients show resistance to these therapies, resulting in poor disease control and increased morbidity. The complex mechanisms underlying steroid-resistant asthma (SRA) involve Th1 and Th17 lymphocyte activity, neutrophil recruitment, and NLRP3 inflammasome activation.
View Article and Find Full Text PDFCell Mol Immunol
January 2025
Department of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Group 3 innate lymphoid cells (ILC3s) control tissue homeostasis and orchestrate mucosal inflammation; however, the precise mechanisms governing ILC3 activity are fully understood. Here, we identified the transmembrane protein neuropilin-1 (NRP1) as a positive regulator of interleukin (IL)-17-producing ILC3s in the intestine. NRP1 was markedly upregulated in intestinal mucosal biopsies from patients with inflammatory bowel disease (IBD) compared with healthy controls.
View Article and Find Full Text PDFJ Invest Dermatol
December 2024
Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI) CONICET, ARGENTINA. Electronic address:
Fungal skin infections significantly contribute to the global human disease burden, yet our understanding of cutaneous immunity against dermatophytes remains limited. Previously, we developed a model of epicutaneous infection with Microsporum canis in C57BL/6 mice, which highlighted the critical role of IL-17RA signaling in anti-dermatophyte defenses. Here, we expanded our investigation to the human pathogen Nannizzia gypsea and demonstrated that skin γδTCRint and CD8/CD4 double-negative βTCR+ T cells are the principal producers of IL-17A during dermatophytosis.
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