Lymphoid tissue inducer (LTi)/LTi-like cells are critical for lymphoid organogenesis and regulation of adaptive immunity in various tissues. However, the maintenance and regulation mechanisms of LTi-like cells among different tissues are not clear yet. Here, we find that LTi-like cells from different tissues display heterogeneity. The maintenance of LTi-like cells in the mesenteric lymph node (mLN), but not the gut, requires RANKL signaling from CD4 T cells. LTi-like cells from the mLN, but not the gut, could in turn inhibit the development of T follicular helper cells and subsequent humoral responses during intestinal immunization in an ID2- and PD-L1-dependent manner. Together, our findings implicate that the interaction between LTi-like cells and T cells in the mLN could precisely control the intestinal mucosal adaptive immune response.
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http://dx.doi.org/10.1016/j.celrep.2020.107936 | DOI Listing |
Trends Cell Biol
January 2025
Department of Immunology, Ophthalmology, and ENT, Universidad Complutense de Madrid, Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), Madrid, Spain. Electronic address:
The generation of regulatory T cells (Tregs) through interactions with antigen-presenting cells (APCs) is essential for establishing tolerance to gut commensals. Recent findings highlight the critical role of RORγt-lineage APCs, especially in gut-associated lymphoid tissues, in the induction of microbiota-specific peripheral Tregs and maintaining gut immune homeostasis.
View Article and Find Full Text PDFMucosal Immunol
September 2024
Lydia Becker Institute of Immunology and Inflammation, University of Manchester, M13 9PL, United Kingdom; Centre for Gene Therapy and Regenerative Medicine, School of Basic and Medical Biosciences, Faculty of Life Sciences and Medicine, King's College London, United Kingdom. Electronic address:
Mucosal Immunol
December 2024
Joan and Sanford I. Weill Department of Medicine, Division of Gastroenterology & Hepatology, Weill Cornell Medicine, Cornell University, New York, NY, USA; Department of Microbiology & Immunology, Weill Cornell Medicine, Cornell University, New York, NY, USA; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA. Electronic address:
Group 3 innate lymphoid cells (ILC3s) are abundant in the developing or healthy intestine to critically support tissue homeostasis in response to microbial colonization. However, intestinal ILC3s are reduced during chronic infections, colorectal cancer, or inflammatory bowel disease (IBD), and the mechanisms driving these alterations remain poorly understood. Here we employed RNA sequencing of ILC3s from IBD patients and observed a significant upregulation of RIPK3, the central regulator of necroptosis, during intestinal inflammation.
View Article and Find Full Text PDFCell Rep
November 2023
Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PL, UK; Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, UK. Electronic address:
Innate lymphoid cells (ILCs) are tissue-resident effector cells with roles in tissue homeostasis, protective immunity, and inflammatory disease. Group 3 ILCs (ILC3s) are classically defined by the master transcription factor RORγt. However, ILC3 can be further subdivided into subsets that share type 3 effector modules that exhibit significant ontological, transcriptional, phenotypic, and functional heterogeneity.
View Article and Find Full Text PDFMucosal Immunol
October 2023
Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester, United Kingdom; Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom. Electronic address:
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