Showing papers in "Mucosal Immunology in 2016"
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TL;DR: It is suggested that RORγt expression in Tregs contributes to an optimal suppressive capacity during gut-specific immune responses, rendering Foxp3+RORγt+ T cells as an important effector Treg subset in the intestinal system.
297 citations
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TL;DR: A first view of the landscape of physiologic oral immunity is provided and shifts in immune cell populations in the common oral inflammatory disease periodontitis are interrogated to serve as a baseline for the characterization of local immunopathology.
198 citations
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TL;DR: It is concluded that M-cell-mediated sampling of commensal bacteria is a required initial step for the efficient induction of intestinal SIgA.
192 citations
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Massachusetts Institute of Technology1, Karolinska University Hospital2, Public Health Agency of Canada3, University of Manitoba4, University of Toronto5, University of Nairobi6, University of Cape Town7, Centre for the AIDS Programme of Research in South Africa8, Columbia University9, National Health Laboratory Service10, University Health Network11
TL;DR: Data reveal strong linkages between mucosal cytokines, barrier function, proteases, and immune cell movement, and propose these as potential mechanisms that increase risk of HIV acquisition.
188 citations
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TL;DR: It is identified that group-2 innate lymphoid cells (ILC2s) produced significant amounts of IL-4 and IL-2 following H. polygyrus infection, highlighting a previously unrecognized and important role for ILC2-derived IL- 4 for TH2 differentiation in a natural TH2-dependent model of human helminthiasis.
172 citations
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TL;DR: It is shown for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of Gram-positive pathogenic and reduction in bile-deconjugating bacterial strains.
163 citations
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TL;DR: Alveolar type II cells are the main source of interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP) generated in response to chitin or migratory helminths, revealing a key interaction between resident lymphoid and structural cells that might underlie similar organizational hierarchies in other organs.
160 citations
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TL;DR: The hypothesis that dysbiosis causes cervicovaginal inflammation and other detrimental changes to the mucosal barrier is supported.
158 citations
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TL;DR: Colonic mDCs in HIV-1-infected subjects had increased CD40 but decreased CD83 expression, and CD40 expression on CD1c+ m DCs positively correlated with mucosal HIV- 1 viral load, with mucosa and systemic cytokine production, and with frequencies of activated colon and blood T cells.
157 citations
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TL;DR: The sMLN and cMLN, and the DCs that migrate to these LNs are anatomically and immunologically separate, which allows immune responses in the SI and colon to be controlled independently.
145 citations
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TL;DR: It is demonstrated that a STAT6-dependent macrophage phenotype promotes mucosal repair in TNBS-treated mice through activation of the Wnt signaling pathway.
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TL;DR: A new and exciting example of cooperation between the epithelial and haematopoietic compartments for the management of enteric parasite infections is presented.
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TL;DR: A large shift in the microbiota of CVID patients characterized by a reduced within-individual bacterial diversity is found without obvious associations to antibiotics use, suggesting a link between immunodeficiency, systemic immune activation, LPS, and altered gut microbiota.
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TL;DR: This review discusses epithelial cell regulatory functions that control reactivity of professional immune cells within the microenvironment of the airways and how these mechanisms are altered in pulmonary diseases.
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TL;DR: It is shown that CD11b-Diphtheria Toxin Receptor (DTR) transgenic mice and three models of IL-13-dependent inflammation, fibrosis, and immunity, show that macrophages are required for the maintenance of type-2 immunity within affected tissues but not secondary lymphoid organs.
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TL;DR: It is shown that Clec9A–diphtheria toxin receptor (DTR) mice after depletion of CD103+CD11b− DCs developed severe, low-dose dextran sodium sulfate (DSS)-induced colitis, whereas the lack of CD 103+CD 11b+ DCs in Clec4a4-DTR mice did not exacerbate intestinal inflammation.
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TL;DR: It is shown that CD161 is also expressed, at intermediate levels, on a prominent subset of polyclonal, polyfunctional tissue-homing CD8+ T-cell populations in humans, including antiviral populations that display a memory phenotype.
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TL;DR: Findings provide evidence that human milk has proresolving actions via comprehensive LM-SPM profiling, describing a potentially novel mechanism in maternal–infant biochemical imprinting.
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TL;DR: This review uses IBD as an archetypal common chronic inflammatory disease to focus on the conceptual and evidential importance of DAMPs in pathogenesis and why DAMPs represent an entirely new class of targets for clinical translation.
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TL;DR: It is found that IL-23 production by CD11c+ MNPs was essential to trigger intestinal immunopathology and MHCII+ monocytes and macrophages as the major source of IL-21, and the pathogenic role of monocytes in dysregulated responses to intestinal bacteria is reinforced.
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TL;DR: It is reported that IL-27, an IL-12 family cytokine known to have both pro- and anti inflammatory roles in T cells, plays a pivotal role in enhancing Treg function to control T cell-induced colitis, a model for inflammatory bowel disease (IBD) in humans.
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TL;DR: It is demonstrated that expression levels of IL-36α are specifically elevated in the colonic mucosa of ulcerative colitis patients, and it is indicated that the IL- 36R pathway may represent a novel target for therapeutic intervention in IBD.
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TL;DR: The fraction of DC and MQ populations expressing aldehyde dehydrogenase activity, reflecting retinoic acid synthesis, in UC colon, both in active disease and remission, were reduced compared to controls and inflamed Crohn’s colon, suggesting that ALDH activity in myeloid cells in the colon of UC patients, regardless of whether the disease is active or in remission, is influenced by the intestinal environment.
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TL;DR: The findings suggest that the compartmentalization between mucosal and systemic PC pools is less strict than previously thought, which may have implications for the development of vaccines as well as for autoantibody-mediated diseases.
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TL;DR: A rapid and sensitive HIV entry assay demonstrated enhanced susceptibility of activated endocervical CD4(+) T cells, and those expressing α(4)β(7) or α( 4) β(1) with HIV envelope, which may relate to increased CCR5 expression by these cell subsets.
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TL;DR: The landscape of effector cells and Fc receptors present within vulnerable tissues is defined and non-ADCC-mediated mechanisms, such as phagocytosis and neutrophil activation, are more likely to play a role in preventative vaccine or reservoir-eliminating therapeutic approaches.
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TL;DR: An internally standardized flow cytometry approach is devised that can identify parallel inflammatory alveolar macrophage phenotypes in both the mouse and human lungs and suggests that heterogeneous innate immune cell phenotypes are an underappreciated component of the human lung disease microenvironment.
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TL;DR: It is suggested that post-migrated PMNs within the intestinal lumen can regulate epithelial homeostasis, thereby identifying ICAM-1 as a potential therapeutic target for promoting mucosal wound healing.
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TL;DR: It is demonstrated that in dendritic cells HIF-1α is necessary for the induction of sufficient numbers of Tregs to control intestinal inflammation, which is associated with dysregulation of the mucosal immune response.
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TL;DR: Findings suggest that the pro-resolving actions of AT-RvD1 during pneumonia represent a novel host-directed therapeutic strategy to complement the current antibiotic-centered approach for combatting infections.