Mucosal Immunity
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An enteric virus can replace the beneficial function of commensal bacteria : Nature : Nature Publishing Group

Intestinal microbial communities have profound effects on host physiology. Whereas the symbiotic contribution of commensal bacteria is well established, the role of eukaryotic viruses that are present in the gastrointestinal tract under homeostatic conditions is undefined. Here we demonstrate that a common enteric RNA virus can replace the beneficial function of commensal bacteria in the intestine. Murine norovirus (MNV) infection of germ-free or antibiotic-treated mice restored intestinal morphology and lymphocyte function without inducing overt inflammation and disease. The presence of MNV also suppressed an expansion of group 2 innate lymphoid cells observed in the absence of bacteria, and induced transcriptional changes in the intestine associated with immune development and type I interferon (IFN) signalling. Consistent with this observation, the IFN-[agr] receptor was essential for the ability of MNV to compensate for bacterial depletion. Importantly, MNV infection offset the deleterious effect of treatment with antibiotics in models of intestinal injury and pathogenic bacterial infection. These data indicate that eukaryotic viruses have the capacity to support intestinal homeostasis and shape mucosal immunity, similarly to commensal bacteria.

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Mucosal Immunity
The largest immune tissue in the body
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Mucosal Immunity

is the most recent part of Immunology!

It appeared less than 40 years ago, while systemic immunity exploded 60  years ago.

It is still a minor part of Immunology teaching and research, while the mucosal immune system is at the frontline of encounters with germs, antigens... in other words the environment.

major keywords

IgA http://www.scoop.it/t/mucosal-immunity?q=IgA

tolerance http://www.scoop.it/t/mucosal-immunity?q=tolerance

microbiome http://www.scoop.it/t/mucosal-immunity?q=microbiome

 

july 2015: almost 2100 scoops, more than 1700 visitors, more than 3900 views

december 2015, more than 4700 views by more than 2000 visitors of more than 2300 scoops

november 2016, more than 7;2K views more than 2750 scoops

november 2017 >10K views of >3300 scoops

Gilbert C FAURE's insight:

This topic complements the more general Immunology topic.

 http://www.scoop.it/t/immunology

 

It includes also reproductive immunology searchable on

http://www.scoop.it/t/mucosal-immunity?q=reproductive

https://www.scoop.it/t/mucosal-immunity/?&tag=REPRODUCTION


and  also covers lung immunology

http://www.scoop.it/t/mucosal-immunity?q=lung

 

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Critical Role for the Microbiota in Regulation of Intestinal T Cells

Critical Role for the Microbiota in Regulation of Intestinal T Cells | Mucosal Immunity | Scoop.it
Kim et al.'s results identify a cellular mechanism by which the microbiota limits intestinal inflammation and promotes tissue homeostasis.
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Phylogeny-corrected identification of microbial gene families relevant to human gut colonization

Phylogeny-corrected identification of microbial gene families relevant to human gut colonization | Mucosal Immunity | Scoop.it
Author summary Why do certain microbes and not others colonize our gut, and why do they differ between healthy and sick people? One explanation is the genes in their genomes. If we can find microbial genes involved in gut adaptation, we may be able to keep out pathogens and encourage the growth of beneficial microbes. One could look for genes that were present more often in prevalent microbes, and less often in rare ones. However, this ignores that related species are more likely to share an environment and also share many unrelated phenotypes simply because of common ancestry. To solve this problem, we used a method from ecology that accounts for phylogenetic relatedness. We first calculated gut prevalence for thousands of species using a compendium of shotgun sequencing data, then tested for genes associated with prevalence, adjusting for phylogenetic relationships. We found genes that are associated with overall gut prevalence, with a preference for the gut over other body sites, and with the gut in Crohn’s disease versus health. Many of these findings have biological plausibility based on existing literature. We also showed agreement with the results of a previously published high-throughput screen of bacterial gene knockouts in mice. These results, and this type of analysis, may eventually lead to new strategies for maintaining gut health.
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Frontiers | Respiratory Mononuclear Phagocytes in Human Influenza A Virus Infection: Their Role in Immune Protection and As Targets of the Virus | Immunology

Frontiers | Respiratory Mononuclear Phagocytes in Human Influenza A Virus Infection: Their Role in Immune Protection and As Targets of the Virus | Immunology | Mucosal Immunity | Scoop.it
Emerging viruses have become increasingly important with recurrent epidemics. Influenza A virus (IAV), a respiratory virus displaying continuous re-emergence, contributes significantly to global morbidity and mortality, especially in young children, immunocompromised and elderly people. IAV infection is typically confined to the airways and the virus replicates in respiratory epithelial cells but can also infect resident immune cells. Clearance of infection requires virus-specific adaptive immune responses that depend on early and efficient innate immune responses against IAV. Mononuclear phagocytes (MNPs), comprising monocytes, dendritic cells and macrophages, have common but also unique features. In addition to being professional antigen presenting cells, MNPs mediate leukocyte recruitment, sense and phagocytose pathogens, regulate inflammation and shape immune responses. The immune protection mediated by MNPs can be compromised during IAV infection when the cells are also targeted by the virus, leading to impaired cytokine responses and altered interactions with other immune cells. Furthermore, it is becoming increasingly clear that immune cells differ depending on their anatomical location and that it is important to study them where they are expected to exert their function. Defining tissue-resident MNP distribution, phenotype and function during acute and convalescent human IAV infection can offer valuable insights into understanding how MNPs maintain the fin
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Anti-CTLA-4 Induced Inflammatory Bowel Disease: Is There A More Etiological Treatment? Lessons From CTLA-4 Haploinsufficiency|crimson publishers.com

Anti-CTLA-4 Induced Inflammatory Bowel Disease: Is There A More Etiological Treatment? Lessons From CTLA-4 Haploinsufficiency|crimson publishers.com | Mucosal Immunity | Scoop.it
We read with great interest the article by Bamias G et al. [1] entitled “Immunological Characteristics of Colitis Associated with Anti-CTLA-4 Antibody Therapy’’ [1], and we would like to address some issues regarding possible future use of a more etiological treatment for this colitis, namely...

Via Krishan Maggon
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Cytomegalovirus promotes intestinal macrophage-mediated mucosal inflammation through induction of Smad7

Cytomegalovirus promotes intestinal macrophage-mediated mucosal inflammation through induction of Smad7 | Mucosal Immunity | Scoop.it
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Eosinophils can more than kill

Eosinophils can more than kill | Mucosal Immunity | Scoop.it
In this issue of JEM , Arnold et al. (<https://doi.org/10.1084/jem.20172049>;) demonstrate that eosinophils suppress mucosal inflammation by directly interacting with pro-inflammatory Th1 cells. This emphasizes the dual role of eosinophils, which can act both as effector cells that control an...
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CX3CR1+ Macrophages and CD8+ T Cells Control Intestinal IgA Production

CX3CR1+ Macrophages and CD8+ T Cells Control Intestinal IgA Production | Mucosal Immunity | Scoop.it
Secretory IgA is a key host defense mechanism that controls the intestinal microbiota. We investigated the role of CD11c+CX3CR1+CD64+ macrophages in IgA production in the intestine. Intestinal CX3CR1+ macrophages directly induced IgA secretion by B cells.
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Nanotechnology Now: Dental plaque is no match for catalytic nanoparticles: Twice-daily rinses of FDA-approved nanoparticles broke apart oral biofilms and prevented tooth decay in a ...

Nanotechnology Now: Dental plaque is no match for catalytic nanoparticles: Twice-daily rinses of FDA-approved nanoparticles broke apart oral biofilms and prevented tooth decay in a ... | Mucosal Immunity | Scoop.it
Combine a diet high in sugar with poor oral hygiene habits and dental cavities, or caries, will likely result. The sugar triggers the formation of an acidic biofilm, known as plaque, on the teeth, eroding the surface.

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Change of TGF-β1 Gene Expression and TGF-β1 Protein Level in Gingival Crevicular Fluid and Identification of Plaque Bacteria in a Patient with Recurrent Localized Gingival Enlargement before and af...

Change of TGF-β1 Gene Expression and TGF-β1 Protein Level in Gingival Crevicular Fluid and Identification of Plaque Bacteria in a Patient with Recurrent Localized Gingival Enlargement before and af... | Mucosal Immunity | Scoop.it
Case Reports in Dentistry is a peer-reviewed, Open Access journal that publishes case reports and case series in all areas of dentistry, including periodontal diseases, dental implants, oral pathology, as well as oral and maxillofacial surgery.
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Colonic epithelial mTORC1 promotes ulcerative colitis through COX-2-mediated Th17 responses

Colonic epithelial mTORC1 promotes ulcerative colitis through COX-2-mediated Th17 responses | Mucosal Immunity | Scoop.it
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JCI - HIV-1 replicates and persists in vaginal epithelial dendritic cells

JCI - HIV-1 replicates and persists in vaginal epithelial dendritic cells | Mucosal Immunity | Scoop.it
To understand how HIV-1 acquisition could occur when CD4+ T cells are absent from the outermost nonulcerated genital layers, we cleanly separated the epithelium from vaginal lamina propria (Supplemental Figure 1; supplemental material available online with this article; https://doi.org/10.1172/JCI98943DS1). Thus, the subsequent single-cell isolations from the epithelia were not contaminated by contents from the lamina propria. We used previously described discontinuous density gradients (7) and magnetic bead–conjugated antibodies specific for a DC-specific marker (CD1a) to isolate epithelial-based DCs. A significantly lower number of CD1a+ VEDCs as compared with skin LCs was isolated from vaginal tissue as compared with skin (Supplemental Figure 2). Classically, the skin LCs express the C-type lectin receptor langerin, and not the classic DC cell surface marker DC-SIGN (Supplemental Figure 3). A majority of CD1a+ VEDCs also expressed langerin (Figure 1A) and lacked DC-SIGN (Figure 1B), suggesting that these epithelial-based cells are distinct from the subepithelial-based DC-SIGN+ vaginal myeloid DCs (1, 8). A majority of the CD1a+ VEDCs also expressed CD4, CCR5, and CXCR4 (Figure 1, C–E and Supplemental Figure 4). The presence and absence of other markers suggested that the CD1a+ epithelial cell isolations were devoid of tissue macrophages (9) (Supplemental Figure 4) and lymphocytes (Supplemental Figure 5), and the cells were mostly in an inactive state (Supplemental Figure 6). Figure 1 Vaginal CD1a+ cells are a unique DC subset. (A–E) Representative dot plots from a minimum of 3 independent donors show staining for CD1a along with (A) Langerin (CD207) , (B) DC-SIGN (CD209), (C) CD4, (D) CCR5, and (E) CXCR4. Numbers in the quadrants show the percentage of positive cells. Due to limited cell quantities, the CD1a+ VEDCs in these plots are not all from the same tissue. (F and G) Electron micrograph (EM) of the skin with markers denoting epithelium (E), Langerhans cell (LC), and dermis (D). The arrows point at morphological structures consistent with Birbeck granules (BG). (H and I) EM of vaginal tissue demonstrating epithelium (E) and a nucleated cell consistent with an epithelial-based dendritic cell (eDC). (J and K) EM of CD1a+ VEDC pellets with asterisks showing the CD1a beads. (L and M) Two independent Western blots of cell pellets from different vaginal tissue and skin donors. The vaginal epithelial (VE), vaginal CD1a+ cells (V CD1a), skin epithelial (SK), and skin Langerhans cells (SLC) were probed with Lag antibody (Takara), which is deemed specific for BGs. Expected band for BG binding is at 43 kDa, shown by arrow. Bottom blot shows probing for beta-actin. Electron microscopy (EM) of skin cells in situ clearly demonstrated cytoplasmic BGs, a hallmark of all LCs (Figure 1, F and G) (10). In contrast, a minimum of 10 separate fields each in vaginal tissue from 5 different donors revealed no morphological structure resembling BGs (Figure 1, H and I). EM examination of purified CD1a+ cell pellets showed lobulated nucleus and projecting dendrites, but BGs were not evident (Figure 1, J and K). Western blots demonstrated that vaginal epithelial CD1a+ cells compared with skin LCs had minimal amount of a protein that bound an antibody (Lag) deemed specific for BGs (Figure 1, L and M) (11, 12). In contrast to in vitro studies (11, 13, 14), our observations suggest that langerin expression does not lead to the presence of classic BGs in the CD1a+ VEDCs. Similarly, classic BGs have also not been observed in murine vaginal epithelial presumed LCs (15). Thus, CD1a+ VEDCs are a unique, previously undefined human DC subset because unlike monocyte-derived DCs (MDDCs) or vaginal subepithelial DCs, they express langerin and not DC-SIGN and unlike skin-derived LCs they lack BGs. Previous investigations have suggested that skin LCs internalize HIV-1 using langerin and degrade internalized virus in BGs, although virus challenges initiated at high multiplicity of infection (MOI) can overcome this block (4, 5). Similar to our previous report with other primary strains (16), HIV-1 isolate YU-2, which requires the CCR5 coreceptor for cell entry, did not replicate in skin-derived LCs even when exposed to high MOIs (Figure 2A). In contrast, YU-2 established a low-level spreading infection in CD1a+ VEDCs from different donors (Figure 2, A, B, and F, and Supplemental Figure 7). No infectious virus, however, was observed in the CD1a+ VEDCs exposed to similarly high MOIs of exclusive CXCR4-using viruses NL4-3 and SF2 (Figure 2, B and C). CD1a+ VEDCs also supported replication of a CCR5-dependent infectious molecular clone (IMC) (RHPA) isolated from an individual during the acute phase of infection, termed a transmitted/founder (T/F) variant (Figure 2C) (17). The RHPA–CD1a+ VEDC cultures yielded nearly 3-fold more infectious viruses at day 4 after infection compared with another primary CCR5-using IMC isolated from a heterosexually infected woman during chronic infection (WARO) (Figure 2C) (17). Thus, R5 variants (including a T/F strain) but not X4 viruses replicated in CD1a+ VEDCs and not in skin-derived LCs. Figure 2 R5 and X4 HIV-1 have differential replication in CD1a+ VEDCs. Each graph shows relative light units (RLU) (y axis) generated from TZM-bl cells 48 hours after being exposed to 50 μl of culture supernatant, which was collected days after infection (PI) (x axis). Days PI was defined as either days after virus-exposed cells were washed to remove unbound virus or the start of coculture. Replication of YU-2 (R5; MOI: 15), NL4-3 (X4; MOI: 15), transmitted/founder (RHPA; MOI: 10), chronic infection strain (WARO; MOI: 10), and SF2 (X4; MOI: 8) in (A) CD1a+ VEDCs and skin-derived LCs, (B, C, F) CD1a+ VEDCs, (D and E) vaginal tissue resident lymphocytes, and (F) CD1a+ VEDCs cocultured with autologous vaginal tissue resident lymphocytes. For each graph, the CD1a+ VEDCs were obtained from a different individual’s tissue. Each plotted RLU is the amount above background, and any RLU value below background was assigned a value of 0. RLUs observed at day 2 PI do not reflect residual virus from inocula (see Supplemental Figure 11). As opposed to the differential growth observed in the CD1a+ VEDCs, YU-2, NL4-3, RHPA, and WARO replicated in activated cells from the lamina propria (Figure 2, D and E), which are primarily tissue-resident lymphocytes (TRLs) (Supplemental Figure 8) (18). Furthermore, both NL4-3 and YU-2 replicated in virus-exposed and subsequently washed CD1a+ VEDCs cocultured with autologous activated TRLs (Figure 2F). In aggregate, R5 as compared with X4 variants had differential replication in CD1a+ VEDCs alone but not in activated vaginal TRLs cocultured with or without CD1a+ VEDCs. In contrast to skin LCs, the X4 variants’ poor replication in CD1a+ VEDCs is not due to the absence of the CXCR4 receptor (Figure 1E and Supplemental Figure 4) (3). Indeed, X4 variants fuse with CD1a+ VEDCs at a level similar to that of R5 variants (Figure 3, A–F and Supplemental Figure 9). This phenotype is dramatically different from MDDCs, to which R5 virus fuses at a significantly higher level compared with an X4 variant (Supplemental Figure 10). Both X4 and R5 envelope strains complete reverse transcription and integration in the CD1a+ VEDCs (Figure 3, G–J). In CD1a+ VEDCs an R5 as compared with an X4 envelope virus within an isogenic backbone, however, demonstrated higher reverse transcription (mean fold difference 8.2, range 1.1–22.8, n = 7, P = 0.02) and integration (mean fold difference 10.1, range 0.7–26.7, n = 7, P = 0.30) (Figure 3, H and J). Viral gene transcription was significantly higher in the absence than in the presence of coreceptor blockers in CD1a+ VEDCs for both R5 and X4 pseudoviruses (Figure 3K). Thus, after integration, transcription occurs with both types of viruses. Importantly, luciferase expression (mean fold difference 23.9, range 2.2–104.2, n = 7, P = 0.02) was higher among CD1a+ VEDCs exposed to the R5 as compared with the X4 envelope virus within an isogenic backbone (Figure 3K). Thus, viral envelope host receptor interactions influence the virus postentry life cycle in CD1a+ VEDCs. Figure 3 Limitation in X4 variant replication occurs after entry. (A–F) Fusion observed in CD1a+ VEDCs that were (A) mock infected or exposed to pseudovirions with (B) NL4-3 (X4), (C) YU-2 (R5), (D) VSV-G (positive control), (E) Lai, and (F) Bal envelope. Numbers at the bottom show the percentage of fusion. (G–J) Late reverse transcription products (G and H) and integrated provirus (I and J) in CD1a+ VEDCs among R5 (blue) and X4 (red) envelope viruses in the absence and presence of CCR5 blocker Maraviroc (MVC) (blue outline) and CXCR inhibitor AMD3100 (red outline). Experiments were done with replication-competent infectious molecular clones YU-2 (R5) and NL4-3 (X4) (n = 3 tissues; comparisons used a 2-sided t test) (G and I) or a single-cycle reporter virus pseudotyped with either a CCR5-using (Bal) or CXCR4-using (Lai) envelope (n = 7 tissues; comparisons used a 2-sided Wilcoxon signed rank test with Lai set as the reference) (H and J). (K) Fold difference in luciferase expression in CD1a+ VEDCs (n = 7 tissues) 3 days after exposure to either media alone (set as reference), Lai/Bal (R5), or Lai/Lai (X4) reporter pseudotypes in the presence and absence of entry inhibitors (comparisons used a 2-sided Wilcoxon signed rank test). (L) Fold difference in luciferase expression in CD1a+ VEDCs (n = 4 tissues) 3 days after exposure to either media alone (set as reference) or Lai/Lai (X4) in the presence or absence of entry inhibitor and SIV Vpx (light red shading)(comparison with and without Vpx done with a 2-sided Mann-Whitney U test). (M and N) RLUs generated from TZM-bl cells 48 hours after being exposed to virus supernatants from CD1a+ VEDCs exposed to NL4-3 or NL4-3 in the presence of SIV Vpx. *P < 0.05. Host restriction factor SAMHD1 inhibits HIV-1 reverse transcription and subsequent integration in myeloid cells (19, 20). However, the SIV and HIV-2 accessory protein Vpx can alleviate this block by promoting SAMHD1 degradation (Supplemental Figure 11) (19, 20). CD1a+ VEDCs expressed similar levels of total SAMHD1 and the inactive phosphorylated form of SAMHD1 after exposure to media alone or virus (Supplemental Figure 11). Luciferase expression was higher (mean fold difference 23.2, range 8.3–59.7, n = 4, P = 0.03) in CD1a+ VEDCs in the presence than in the absence of SIV Vpx for an X4 virus (Figure 3L). HIV-1 X4 virus replication was also observed in the presence but not the absence of SIV Vpx in CD1a+ VEDC cultures (Figure 3, M and N). Presence of SIV Vpx did not impact replication in cells from the lamina propria or in CD1a+ VEDCs exposed to YU-2 (Supplemental Figure 11). In aggregate, this demonstrates that SAMHD1 also restricts HIV-1 replication in CD1a+ VEDCs. Contemporaneous vaginal tissue and blood samples were obtained from 2 HIV-1–infected virologically suppressed women to provide evidence that CD1a+ VEDCs are infected in vivo. Averages of 5.0 and 3.7 HIV-1 DNA copies were detected in means of 16,136 (311 copies/106) and 19,523 (191 copies/106) CD1a+ VEDCs from woman I and woman II, respectively (Supplemental Table 1). In comparison, provirus copy numbers were around 4- to 8-fold higher in peripheral blood mononuclear cells (PBMCs) (1,261 and 1,561 copies/106 in woman I and woman II, respectively) and in lamina propria cells (2,291 copies/106 in woman II and data not available from woman I). HIV-1 DNA was below 1 copy per 10,000 cells from the CD1a– vaginal epithelial fraction in both individuals. Single genome amplification revealed that full-length envelope sequences from the CD1a+ VEDCs, PBMCs, and cells in the lamina propria were intermingled, suggesting these cells harbored viruses from a similar ancestral stage of infection (Figure 4A). Incorporation of the isolated CD1a+ VEDC and PBMC envelopes into an envelope-deficient NL4-3 backbone yielded both replication-competent R5 and X4 virus stocks (Figure 4, B and C). Thus, CD1a+ VEDCs harbor HIV-1 DNA with functional X4 and R5 envelopes, suggesting they are infected with viruses that use either receptor in vivo. Figure 4 CD1a+ VEDCs are infected in vivo. (A) Maximum likelihood phylogenetic tree of full-length envelope sequences isolated from CD1a+ VEDCs (triangles), peripheral blood mononuclear cells (squares), and the lamina propria (open circles). Sequences from each subject are denoted by different colors. Number of HIV-1 copies estimated per million cells is indicated in the key. The phenotypically determined receptor usage of some of the virus stocks incorporating the isolated envelopes with a HIV-1 NL4-3 backbone is denoted next to a node as either X4 or R5. The Q23-17 (subtype A) outgroup and the NL4-3 (subtype B) nodes are also identified. (B and C) RLUs after 48 hours in TZM-bl cells exposed to virus stocks incorporating the CD1a+ VEDC–isolated envelopes in the presence of no inhibitor (black), TAK779 (red), AMD3100 (blue), and both TAK779 and AMD3100 (white). Bars show mean with SEM of infections done in triplicate. In this study, we isolated vaginal epithelial-based cells that are most likely to encounter virus in the female genital tract. We have shown that the CD1a+ VEDCs are not analogous to classically defined skin LCs as previously presumed (1, 2, 21, 22), and that they are different from other subepithelial and blood-derived DCs. In some respects, our findings agree with mouse models showing that vaginal epithelial-based DCs are phenotypically different from skin-derived LCs (15, 23). In contrast to previous studies, we showed that CD1a+ VEDCs either do not contain or have low levels of BGs, and thus they cannot be characterized as LCs but are rather a unique previously undefined human DC subset. Lack of BGs potentially explains the difference in susceptibility to infection among CD1a+ VEDCs as compared with skin LCs (4, 5). We have also demonstrated that CD1a+ VEDCs support higher replication of R5 compared with X4 HIV-1. This potentially explains the epidemiological observation that the majority of mucosally acquired infecting strains utilize the CCR5 receptor (6). In contrast to other studies (21, 22), our work suggests that the limited replication of X4 viruses occurs from differential replication in the CD1a+ VEDCs and is not due to attenuated replication in or cell-to-cell transfer to activated TRLs. Similar to a previous study, de novo virus production after fusion occurs intermittently, which suggests that after entry there are both receptor-independent blocks, such as SAMHD1, and other potentially novel receptor-dependent barriers (24). Although presence of HIV-1 DNA in CD1a+ VEDCs from infected women confirms in vivo infection, future studies will need to show that the CD1a+ VEDCs that harbor HIV-1 DNA can yield replication-competent virus and that the DNA does not merely represent engulfed infected CD4+ T cells (25). In aggregate, CD1a+ VEDCs are most likely the initial “gatekeeper” that selects viruses that will successfully establish an infection in a naive woman. Furthermore, virus persists in these cells during effective antiretroviral treatment, and thus, CD1a+ VEDCs may be a previously unrecognized latent reservoir.
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Scientists Figured Out Why Our Mouths Heal So Freakishly Fast

Scientists Figured Out Why Our Mouths Heal So Freakishly Fast | Mucosal Immunity | Scoop.it
Researchers at the National Institutes of Health think they’ve uncovered just why the mouth heals so easily. Their findings, published Wednesday in Science Translational Medicine, might even help us discover how to make the rest of our body heal quicker, too. And all they had to do was (slightly) hurt some innocent people.
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The hygiene hypothesis: immunological mechanisms of airway tolerance - ScienceDirect

The hygiene hypothesis: immunological mechanisms of airway tolerance - ScienceDirect | Mucosal Immunity | Scoop.it
The hygiene hypothesis was initially proposed as an explanation for the alarming rise in allergy prevalence in the last century. The immunological ide…
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Discovery of new epithelial lung cell type may affect cystic fibrosis therapy

Discovery of new epithelial lung cell type may affect cystic fibrosis therapy | Mucosal Immunity | Scoop.it
Scientists have discovered a new type of cell in the human respiratory tract called the pulmonary ionocyte, and linked it to cystic fibrosis.
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https://www.eurekalert.org/pub_releases/2018-08/hms-nlc080218.php

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Neuroimmunophysiology of the gut: advances and emerging concepts focusing on the epithelium

Neuroimmunophysiology of the gut: advances and emerging concepts focusing on the epithelium | Mucosal Immunity | Scoop.it
In this Review, the authors summarize how various interactions at the gastrointestinal epithelium regulate gut physiology. They also discuss how neuroimmunophysiology has advanced the understanding of gastrointestinal pathophysiology with the potential to reveal novel therapies for disorders such as IBS and IBD.
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Utilizing imaging approaches to study HIV from individual cell infection to mucosal transmission - Veranstaltungskalender der Innsbrucker Universitäten

Utilizing imaging approaches to study HIV from individual cell infection to mucosal transmission - Veranstaltungskalender der Innsbrucker Universitäten | Mucosal Immunity | Scoop.it
Veranstaltungstyp: Gastvortrag;...
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A splenic IgM memory subset with antibacterial specificities is sustained from persistent mucosal responses

A splenic IgM memory subset with antibacterial specificities is sustained from persistent mucosal responses | Mucosal Immunity | Scoop.it
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To what extent immune responses against the gut flora are compartmentalized within mucosal tissues in homeostatic conditions remains a much-debated issue. We describe here, based on an inducible AID fate-mapping mouse model, that systemic memory B cell subsets, including...
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IgA regulates the composition and metabolic function of gut microbiota by promoting symbiosis between bacteria

IgA regulates the composition and metabolic function of gut microbiota by promoting symbiosis between bacteria | Mucosal Immunity | Scoop.it
![Figure][1]</img>



Immunoglobulin A (IgA) promotes health by regulating the composition and function of gut microbiota, but the molecular requirements for such homeostatic IgA function remain unknown.
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Pulmonary alveolar proteinosis in adults: pathophysiology and clinical approach

Pulmonary alveolar proteinosis in adults: pathophysiology and clinical approach | Mucosal Immunity | Scoop.it
Pulmonary alveolar proteinosis (PAP) is a diffuse lung disease that results from the
accumulation of lipoproteinaceous material in the alveoli and alveolar macrophages
due to abnormal surfactant homoeostasis.
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Defective IgA response to atypical intestinal commensals in IL-21 receptor deficiency reshapes immune cell homeostasis and mucosal immunity

Defective IgA response to atypical intestinal commensals in IL-21 receptor deficiency reshapes immune cell homeostasis and mucosal immunity | Mucosal Immunity | Scoop.it
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IgA—about the unexpected

IgA—about the unexpected | Mucosal Immunity | Scoop.it
In this issue of JEM , Nakajima et al. (<https://doi.org/10.1084/jem.20180427>) demonstrate that glycan-dependent, epitope-independent IgA coating of intestinal bacteria alters bacterial gene expression and metabolism. This conferred coated bacteria with fitness within the mucus niche and contributed to intestinal homeostasis through cross-phylum interactions.
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Current Paediatric Coeliac Disease Screening Strategies and Relevance of Questionnaire Survey - FullText - International Archives of Allergy and Immunology - Karger Publishers

Current Paediatric Coeliac Disease Screening Strategies and Relevance of Questionnaire Survey - FullText - International Archives of Allergy and Immunology - Karger Publishers | Mucosal Immunity | Scoop.it
Coeliac disease (CD) is an autoimmune enteropathy triggered by the ingestion of gluten-containing grains in genetically predisposed individuals.Identification of CD in clinical practice is often diff...
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Frontiers | Insights Into Mucosal-Associated Invariant T Cell Biology From Studies of Invariant Natural Killer T Cells | Immunology

Frontiers | Insights Into Mucosal-Associated Invariant T Cell Biology From Studies of Invariant Natural Killer T Cells | Immunology | Mucosal Immunity | Scoop.it
Mucosal-associated invariant T (MAIT) cells and invariant natural killer T (iNKT) cells are innate-like T cells that function at the interface between innate and adaptive immunity. They express semi-invariant T cell receptors (TCR) and recognise unconventional non-peptide ligands bound to the MHC Class I-like molecules MR1 and CD1d, respectively. MAIT cells and iNKT cells exhibit an effector-memory phenotype and are enriched within the liver and at mucosal sites. In humans, MAIT cell frequencies dwarf those of iNKT cells, while in laboratory mouse strains the opposite is true. Upon activation via TCR- or cytokine-dependent pathways, MAIT cells and iNKT cells rapidly produce cytokines and show direct cytotoxic activity. Consequently, they are essential for effective immunity, and alterations in their frequency and function are associated with numerous infectious, inflammatory, and malignant diseases. Due to their abundance in mice and the earlier development of reagents, iNKT cells have been more extensively studied than MAIT cells. This has led to the routine use of iNKT cells as a reference population for the study of MAIT cells, and such an approach has proven very fruitful. However, MAIT cells and iNKT cells show important phenotypic, functional, and developmental differences that are often overlooked. With the recent availability of new tools, most importantly MR1 tetramers, it is now possible to directly study MAIT cells to understand their biology.
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Researchers find connection between viruses and inflammatory bowel disease

Researchers find connection between viruses and inflammatory bowel disease | Mucosal Immunity | Scoop.it
A study led by a researcher at the University of Colorado Anschutz Medical Campus reveals a key connection between viruses and inflammatory bowel diseases like ulcerative colitis and Crohn's disease.
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