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Mucosal vaccine strategies
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Nils Lycke, Jan Holmgren, Harry B. Greenberg
In the early days of mucosal immunology, it was assumed that immune responses initiated at one mucosal site would be disseminated widely to multiple mucosal tissues. Had this common mucosal immune system existed, it could have meant that immunization by any mucosal route, such as oral immunization, could be used for inducing effective immune responses, not only in the gastrointestinal tract, but also in the airways and the urogenital tract. However, further work showed that mucosal immune responses are generally compartmentalized, not only between separate mucosal organs but also between regions from the same mucosal organ, such as the gut proximal duodenum and rectum. Irrespective of sampling mechanism, antigens taken up at the mucosal surface are transported to draining lymph nodes by DCs or are directly captured by FAE and delivered to professional APCs in the PPs and presented to CD4+ and CD8+ αβ T cells. Also, it appears that certain antigens may be processed and presented directly by epithelial cells to T cells located close to mucosal membranes, although the significance of this induction pathway is poorly understood.
Inflammation resolution and specialized pro-resolving lipid mediators in chronic rhinosinusitis
Published in Expert Review of Clinical Immunology, 2023
Peyton Z. Robinson, Daniel N. Frank, Vijay R. Ramakrishnan
A relatively simple approach to understanding CRS has proliferated in the field from early insights into disease physiology, wherein an imbalance pro-inflammatory and anti-inflammatory mechanisms is the primary problem resulting in disease, whether the factors involved are exogenous (e.g. aeroallergen) or endogenous (e.g., immune hyperresponsiveness). We must remember that inflammation is not always problematic; in fact, it is key to the maintenance of tissue homeostasis. As most CRS develops in adulthood, and can result from any number or combination of stimuli, the transition from acute inflammation to sustained chronic inflammation is really the critical problem for disease development. A key concept that has been recently developed in mucosal immunology is recognition and understanding of the active endogenous process of inflammatory resolution. Incorporating this additional pillar of resolution into a temporal understanding of inflammation in mucosal homeostasis represents a new opportunity to comprehend and treat CRS. A common dictum in CRS is that it is a chronic disease that requires long-term maintenance therapy to keep under control. Interestingly, however, some patients do achieve disease resolution and return to tissue homeostasis.
Mapping Resident Immune Cells in the Murine Ocular Surface and Lacrimal Gland by Flow Cytometry
Published in Ocular Immunology and Inflammation, 2023
Baikai Ma, Yifan Zhou, Yuzhe Hu, Hongyu Duan, Zhengze Sun, Pingzhang Wang, Wei Li, Wenling Han, Hong Qi
ILCs, which do not express the type of diversified antigen receptors of T cells and B cells, are largely tissue-resident and are regarded as innate counterparts of T cells. ILCs have been given considerable attention in mucosal immunology,23 yet the composition and functions of ILCs in ocular surface was still unknown. To disclose the composition of ILCs in the conjunctiva, Lineage− immune cells were clustered into 7 subpopulations after tSNE dimensionality reduction and FlowSOM clustering based on the expression of NK1.1, CD127, IFN-γ, IL-5, RORγt, and IL-17A: IL-17A+ILC3 (4.22%), IL-17A−ILC3 (2.06%), IFN-γ+Lin− cells (3.05%), IFN-γ+ NK cells (3.86%), IFN-γ− NK cells (13.82%), ILC2 (26.21%), and undefined cells (46.77%) (Figure 3F-H). ILC1 were not found in the conjunctiva (Supplementary Fig. 7 G). Considering targeting antigens in the lineage cocktail antibodies included CD3e, Gr-1, CD11b, CD45R and TER-119, the undefined Lin− cells might contain CD11c+ cells, mast cells, and others.
Innate lymphoid cells link gut microbes with mucosal T cell immunity
Published in Gut Microbes, 2020
Jim G. Castellanos, Randy S. Longman
Intestinal mononuclear phagocytes (MNPs) act as sentinels for the intestinal immune system. CX3CR1+ MNPs can form transepithelial dendrites and sample the intestinal microbiota in an active process regulated by the microbiota .4 In the setting of dysbiosis, these largely tissue-resident MNPs can upregulate CCR7 and migrate to lymphatics carrying antigens from non-invasive luminal microbes .5 During inflammation, however, these MNPs expand and co-localize with ILC3s in the tissue .6–8 Following infection with Citrobacter rodentium, CX3CR1+ MNPs are required for mucosal protection via ILC3 production of IL-22 .7,8 Although genetic deletion models in mice revealed that CD103+ dendritic cells (DCs) were dispensable, 9 a coordinated response with conventional DCs may be required for protective ILC3 immunity .10 Thus, the MNP-ILC3 interface creates a functional unit linking microbial signals with ILC3 effector functions, but the mechanisms regulating their interactions are not clearly defined. In our recent paper, we defined a key role for MNP-derived TL1A in regulating ILC3 mucosal immunity. This addendum aims to contextualize the key mechanistic findings of this study in their contribution to inflammatory bowel disease (IBD) and mucosal immunology.