Relevant bibliographies by topics / Mucosal immunity

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Mucosal immunity'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 March 2023

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Journal articles on the topic "Mucosal immunity"

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Brown, T. A. "Immunity at Mucosal Surfaces." Advances in Dental Research 10, no. 1 (April 1996): 62–65. http://dx.doi.org/10.1177/08959374960100011201.

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The mucosae form a barrier between our bodies and a hostile external environment. Diseases and extrinsic factors which impair mucosal function may lead to serious consequences. The mucosal immune system is the primary mediator of specific immunity at mucosal surfaces. As such, it is responsible for maintaining homeostasis and for defense against both overt and opportunistic pathogens. For this reason, it is also the target of many new vaccine strategies for the induction of mucosal immunity. This brief review will examine the mucosal immune system, its role in maintaining the integrity of the mucosa, and some of the strategies aimed at enhancing specific immunity.
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Mayer, Lloyd. "Mucosal Immunity." Pediatrics 111, Supplement_3 (June 1, 2003): 1595–600. http://dx.doi.org/10.1542/peds.111.s3.1595.

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Food allergy is the manifestation of an abnormal immune response to antigen delivered by the oral route. Normal mucosal immune responses are generally associated with suppression of immunity. A normal mucosal immune response relies heavily on a number of factors: strong physical barriers, luminal digestion of potential antigens, selective antigen sampling sites, and unique T-cell subpopulations that effect suppression. In the newborn, several of these pathways are not matured, allowing for sensitization rather than suppression. With age, the mucosa associated lymphoid tissue matures, and in most individuals this allows for generation of the normal suppressed tone of the mucosa associated lymphoid tissue. As a consequence, food allergies are largely outgrown. This article deals with the normal facets of mucosal immune responses and postulates how the different processes may be defective in food-allergic patients.
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Yasui, Hisako. "Mucosal Immunity/Mucosal Vaccine." Nippon Shokuhin Kagaku Kogaku Kaishi 56, no. 3 (2009): 191. http://dx.doi.org/10.3136/nskkk.56.191.

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van Oss, Carel J. "Mucosal Immunity." Immunological Investigations 14, no. 3 (January 1985): 279. http://dx.doi.org/10.3109/08820138509076154.

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NAGURA, HIROSHI. "Mucosal immunity." Nihon Naika Gakkai Zasshi 84, no. 4 (1995): 632–39. http://dx.doi.org/10.2169/naika.84.632.

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Dwinell, Michael B., and Martin F. Kagnoff. "Mucosal immunity." Current Opinion in Gastroenterology 15, no. 1 (January 1999): 33. http://dx.doi.org/10.1097/00001574-199901000-00007.

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Mayer, Lloyd. "Mucosal immunity." Immunological Reviews 206, no. 1 (August 2005): 5. http://dx.doi.org/10.1111/j.0105-2896.2005.00296.x.

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Petzoldt, Klaus. "Mucosal immunity." Veterinary Immunology and Immunopathology 35 (February 1993): 40–48. http://dx.doi.org/10.1016/0165-2427(93)90134-p.

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Lü, F. X., and R. S. Jacobson. "Oral Mucosal Immunity and HIV/SIV Infection." Journal of Dental Research 86, no. 3 (March 2007): 216–26. http://dx.doi.org/10.1177/154405910708600305.

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Human Immunodeficiency Virus (HIV) transmission through genital and rectal mucosa has led to intensive study of mucosal immune responses to HIV and to the development of a vaccine administered locally. However, HIV transmission through the oral mucosa is a rare event. The oral mucosa represents a physical barrier and contains immunological elements to prevent the invasion of pathogenic organisms. This particular defense differs between micro-compartments represented by the salivary glands, oral mucosa, and palatine tonsils. Secretory immunity of the salivary glands, unique features of cellular structure in the oral mucosa and palatine tonsils, the high rate of oral blood flow, and innate factors in saliva may all contribute to the resistance to HIV/Simian Immunodeficiency Virus (SIV) oral mucosal infection. In the early stage of HIV infection, humoral and cellular immunity and innate immune functions in oral mucosa are maintained. However, these particular immune responses may all be impaired as a result of chronic HIV infection. A better understanding of oral mucosal immune mechanisms should lead to improved prevention of viral and bacterial infections, particularly in immunocompromised persons with Acquired Immune Deficiency Syndrome (AIDS), and to the development of a novel strategy for a mucosal AIDS vaccine, as well as vaccines to combat other oral diseases, such as dental caries and periodontal diseases.
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Nie, Siru, and Yuan Yuan. "The Role of Gastric Mucosal Immunity in Gastric Diseases." Journal of Immunology Research 2020 (July 24, 2020): 1–8. http://dx.doi.org/10.1155/2020/7927054.

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Gastric mucosa plays its immune function through innate and adaptive immunity by recruiting immune cells and releasing corresponding cytokines, which have an inseparable relationship with gastric diseases. Whether infective gastric diseases caused by Helicobacter pylori, Epstein-Barr virus or other microbe, noninfective gastric diseases, or gastric cancer, gastric mucosal immunity plays an important role in the occurrence and development of the disease. Understanding the unique immune-related tissue structure of the gastric mucosa and its role in immune responses can help prevent gastric diseases or treat them through immunotherapy. In this review, we summarize the basic feature of gastric mucosal immunity and its relationship with gastric diseases to track the latest progress of gastric mucosal immunity, update relevant knowledge and provide theoretical reference for the prevention and treatment of gastric diseases based on the gastric mucosal immunity.
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Dissertations / Theses on the topic "Mucosal immunity"

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Tjärnlund, Anna. "Mucosal Immunity in Mycobacterial infections." Doctoral thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-6782.

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More than a century after the identification of the tubercle bacillus and the first attempts at vaccination, tuberculosis (TB) still remains one of the world’s most serious infectious diseases. TB, caused by the bacterium Mycobacterium tuberculosis, is typically a disease of the lung, which serves both as port of entry and as the major site of disease manifestation. The currently used vaccine, BCG, is administered parenterally and induces a systemic immune response. However, it fails to protect against pulmonary TB, thereby raising the question whether vaccination targeting the mucosal immunity in the lungs could be favourable.

The respiratory mucosal surfaces represent the first line of defence against a multitude of pathogens. Secretory IgA, in mucosal secretions has an important function by blocking entrance of pathogenic organisms and preventing infections. Additionally, a role for IgA in modulation of immune responses is currently being revealed. In this work, we investigated the relevance of mucosal IgA in protection against mycobacterial infections using mice deficient for IgA and the polymeric Ig receptor, the receptor responsible for mucosal secretions of IgA. Gene-targeted mice were more susceptible to mycobacterial infections in the respiratory tract and displayed reduced production of proinflammatory, and protective, factors such as IFN-γ and TNF-α in the lungs. The mechanisms explaining the defective proinflammatory responses in the lungs of deficient mice might involve impaired signalling through Fcα receptors, or homologous receptors, which could lead to inadequate activation of pulmonary macrophages. This could subsequently result in suboptimal induction and production of cytokines and chemokines important for attraction and migration of immune cells to the site of infection.

Induction of optimal adaptive immune responses to combat mycobacterial infections requires prompt innate immune activation. Toll-like receptors (TLRs) are vital components of the innate branch of the immune system, ensuring early recognition of invading pathogens. Using TLR-deficient mice we demonstrated an important role for TLR2, and partly TLR4, in protection against mycobacterial infection in the respiratory tract. TLR2-deficient mice failed to induce proper proinflammatory responses at the site of infection, and macrophages derived from the knockout mice displayed impaired anti-mycobacterial activity.

Experimental evidence has concluded that the immune response upon an infection can influence the outcome of succeeding infections with other pathogens. Concurrent infections might additionally interfere with responses to vaccinations and have deleterious effects. We developed an in vitro model to study the effect of a malaria infection on a successive M. tuberculosis infection. Our results demonstrate that a malaria blood-stage infection enhances the innate immune response to a subsequent M. tuberculosis infection with a Th1 prone profile. Reduced infectivity of malaria-exposed dendritic cells implies that a malaria infection could impose relative resistance to ensuing M. tuberculosis infection. However, a prolonged Th1 response may interfere with malaria parasite control.

The outcome of this work emphasizes the importance of generating effective immune responses in the local mucosal environment upon respiratory mycobacterial infections. It furthermore puts new light on the immunological interaction between parasites and mycobacteria, which could have implications for future vaccine research.

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Rahman, Muhammad Jubayer. "Mucosal immunity against mycobacterial infection." Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-39170.

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This thesis aimed to the identification of immune biomarkers of mycobacterial infection for better diagnosis of tuberculosis (TB) and also focused on new vaccination strategies with a particular emphasis on the immune responses in the respiratory tract using murine models. Since the lung is the natural habitat for the M. tuberculosis, we reasoned that immune responses detected locally in the lungs would be good correlates of infection (Paper I). Likewise, immune responses induced in the respiratory tract following immunization would be more effective against mycobacterial infection. We showed that cytokines (IL-12, TNF, and IFN-γ) and cytokine receptors (sTNFR1 and sTNFR2) together with specific antibodies in the respiratory tract correlated better with the bacterial burden in the organs. In Paper II, we investigated the role of the BCG vaccination as a priming vaccine in a heterologous prime-boost immunization protocol. The results showed that the neonatal BCG vaccination primed the immune system for a relevant antigen and showed a generalized adjuvant effect. Using this immunization protocol, protective immune responses in the lungs were generated independently of the route used for the booster immunization. In Paper III, We showed that exposure to mycobacterial antigens during the gestational period led to antigen transportation from the mother to the fetus and this resulted in an early priming of the fetal immune system. Immunization with the same antigen during the postnatal life increased antigen-specific recall IFN-γ responses and protection against infection. We examined the role of innate immunity for the induction of acquired immune responses upon immunization with mycobacterial antigens using TLR2 deficient mice (Paper IV). Our data indicated that suboptimal innate immune responses in the TLR2-/- mice might compromise the induction of acquired immune responses. Overall, the current findings suggested that a better understanding of the mucosal immunity would be useful for the improvement of diagnostic procedures and the development of efficient vaccines against TB.
At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 4: Manuscript
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Tjärnlund, Anna. "Mucosal Immunity in Mycobacterial infections /." Stockholm : Wenner-Gren Institute for Experimental Biology, Stockholm university, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-6782.

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Bailey, Jennifer Ruth. "Development of mucosal immunity in pigs." Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500402.

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Smerud, Hilde Kloster. "IgA Nephropathy – Mucosal Immunity and Treatment Options." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-168631.

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In the present studies we have explored the link between food hypersensitivity and IgA nephropathy (IgAN) and evaluated treatment options in primary and recurrent disease. Approximately one third of our IgAN patients had a rectal mucosal sensitivity to gluten, as demonstrated by increased local mucosal nitric oxide production and/or myeloperoxidase release after gluten challenge. The gluten sensitivity seemed to be an innate immune reaction unrelated to the pathogenesis of celiac disease. Approximately half of the patients had a rectal mucosal sensitivity to soy or cow’s milk (CM). The levels of IgG antibodies to alfa-lactalbumin, beta-lactoglobulin and casein were significantly higher in CM sensitive as compared with non-sensitive IgAN patients, indicating that an adaptive immune response might be involved in addition to the innate immune reaction observed. With the knowledge of gastrointestinal reactivity enteric treatment was considered as a potential new treatment approach of IgAN. A 6-month prospective trial demonstrated proof-of-concept for the use of enteric budesonide targeted to the ileocaecal region of IgAN patients. We observed a modest, but significant reduction in urine albumin, a minor reduction of serum creatinine and a modest increase of eGFR calculated by the MDRD equation. eGFR calculated from the Cockcroft-Gault formula and cystatin C was not changed. In a retrospective study recurrence of IgAN and graft loss was evaluated in Norwegian and Swedish patients having received a primary renal transplant due to IgAN. Adjusting for relevant covariates, a multiple Cox-regression analysis on time to IgAN recurrence showed that use of statins was associated with reduced risk of recurrence and reduced risk of graft loss. The time lag from diagnosis to first transplantation and female gender were also associated with lower risk of recurrence. Improved graft survival was associated with related donor, low donor age and no or low number of acute rejection episodes.
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Alkazmi, Luay Mahmood M. A. "Mucosal immunity to the hookworm Ancylostoma ceylanicum." Thesis, University of Nottingham, 2004. http://eprints.nottingham.ac.uk/11876/.

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The host-parasite relationship of the hookworm Ancylostoma ceylanicum was explored in a hamster model system, focusing on intestinal mucosal responses to infection. Primary infection induced a rapid reduction in villous height culminating in excess of 75% reduction by day 35. Crypts of Lieberkuhn increased in depth achieving maximum depth by day 35. Mitotic figures in crypts and mast cells increased until day 28. Goblet cells increased continuously from background levels of 50 cell/mm² to exceed 300 cells/mm² by day 42. Paneth cell numbers declined in infected animals. Termination of infection by anthelmintic restored background values of intestinal architecture and goblet cell numbers within 7 days, but mast cells took longer and Paneth cell numbers increased beyond values in naïve controls. Mucosal changes are therefore dependent on the presence of worms, intensity of infection and change dramatically with time. Mucosal changes were studied in hamsters experiencing secondary infections following anthelmintic abbreviation of the immunizing infection, superimposed challenge infection and trickle infections. The kinetics of the responses were compared to animals experiencing primary infections and naive controls. Among the findings were: 1) continuous reduction in villous height and a marked increase in crypt depth from day 10 after challenge in abbreviated primary-challenged hamsters compared to little change in hamsters given superimposed challenge. 2) marked mast, goblet, and Paneth cell and eosinophil responses. 3) less intense mast cell responses in abbreviated primary-challenged compared to superimposed challenge animals 4) after a superimposed challenge poor goblet cell responses because levels were already high at the time of challenge, little change in Paneth cells but intense eosinophil responses 5) slower changes in mucosal architecture and mast cell responses in trickle-infected animals eventually exceeding those in primary infected animals. 6) less marked goblet and Paneth cell responses in trickle-infected groups but more intense, persistent increases in eosinophils Cyclosporin A's (CsA) usefulness as an immunosuppressive therapy for blocking T cell control of immunity was explored. However, CsA turned out to have marked anthelmintic properties and reductions in worm burden confounded the interpretation of mucosal changes.
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Philipson, Casandra Washington. "Systems analysis and characterization of mucosal immunity." Diss., Virginia Tech, 2015. http://hdl.handle.net/10919/74392.

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During acute and chronic infectious diseases hosts develop complex immune responses to cope with bacterial persistence. Depending on a variety of host and microbe factors, outcomes range from peaceful co-existence to detrimental disease. Mechanisms underlying immunity to bacterial stimuli span several spatiotemporal magnitudes and the summation of these hierarchical interactions plays a decisive role in pathogenic versus tolerogenic fate for the host. This dissertation integrates diverse data from immunoinformatics analyses, experimental validation and mathematical modeling to investigate a series of hypotheses driven by computational modeling to study mucosal immunity. Two contrasting microbes, enteroaggregative Escherichia coli and Helicobacter pylori, are used to perturb gut immunity in order to discover host-centric targets for modulating the host immune system. These findings have the potential to be broadly applicable to other infectious and immune-mediated diseases and could assist in the development of antibiotic-free and host-targeted treatments that modulate tolerance to prevent disease.
Ph. D.
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Ye, Lilin. "FcRn mediated mucosal immunity and subunit vaccine delivery." College Park, Md.: University of Maryland, 2009. http://hdl.handle.net/1903/9815.

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Thesis (Ph. D.) -- University of Maryland, College Park, 2009.
Thesis research directed by: Virginia-Maryland Regional College of Veterinary Medicine. Maryland Campus. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Barton, John Roger. "Human gastrointestinal mucosal secretory immunity : investigation and regulation." Thesis, University of Edinburgh, 1992. http://hdl.handle.net/1842/19960.

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Current ideas of human gut immunity are derived heavily from animal studies; the few human studies have mainly addressed cellular aspects, and those on immunoglobulins and antibodies have used serum (or rarely jejunal aspirate) to investigate immune events at the gut level, assuming that these fluids are representative of the gut. The aims of this thesis were to develop, evaluate, and apply protocols for the study of gut secretions in man. Saliva was examined as a secretion in its own right, to investigate the relationship between systemic (serum) and mucosal antibodies, and as a potential mirror of immune events occurring more distally in the gut. Methods for the collection and processing of jejunal fluid, and intestinal fluid obtained via whole gut irrigation were then developed. Enzyme linked immunosorbent assay techniques were used to measure total immunoglobulin concentrations and antibody levels to three representative dietary protein antigens, in saliva, intestinal fluid, jejunal aspirate, and serum. Healthy subjects and groups of patients with a variety of gut diseases likely to have increased immunity were examined. There was great physiological variation in immunoglobulin concentrations and antibody levels in saliva, which were universally decreased by eating. In patients on a gluten-free or elemental diet, salivary antibody levels were maintained despite a lack of antigen stimulation. Neither saliva nor serum reflected immunity in gut lavage fluid, the only regularly observed relationship being a positive correlation between serum and saliva, especially after gut mucosal damage has occurred. Differences between control subjects and patients with coeliac disease were insufficient to allow the use of saliva as a diagnostic or clinical tool. Smoking strikingly influenced immunoglobulin concentrations, with a dose-dependent and reversible decrease in salivry IgA, and an increase in IgM. These alterations were not due to changes in the numbers of immunoglobulin-producing cells in the parotid gland. Smoking may also decrease IgA in lavage fluid.
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Ewing, Patricia A., and n/a. "Developmental profiles of mucosal immunity in pre-school children." University of Canberra. Human & Biomedical Sciences, 2000. http://erl.canberra.edu.au./public/adt-AUC20060707.154930.

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Previous studies of the ontogeny of the mucosal immune system have shown a significant increase in salivary Immunoglobulin A levels occurring at about five years of age. This study has monitored a group of 3 and 4 year old children during one year of attendance at Pre-School to examine whether such an increase could be linked to increased antigenic exposure associated with moving into a school like environment. Saliva samples were collected at regular intervals and analysed for immunoglobulin and total protein levels. Daily health records were maintained for each child, and a detailed social and medical history was collected for each child at the beginning of the study. The elevated mucosal immune response observed in previous studies involving children in day care centres and attending school was not seen in this study. No significant difference was observed between children who had previously attended Pre-School or child care centres and those who were attending for the first time. However, a marked seasonal increase in mean salivary IgA during the winter months was observed and this increase correlated with an increase in respiratory infections. Hence, in studies of developmental aspects of mucosal immune response it is essential that modifiers such as season and infection be recorded.
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Books on the topic "Mucosal immunity"

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I, Gallin John, and Fauci Anthony S. 1940-, eds. Mucosal immunity. New York: Raven Press, 1985.

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Mucosal immunity. San Diego, CA: Academic Press, 2010.

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Warren, Strober, ed. Mucosal immunity and infections at mucosal sufaces. Oxford: Oxford University Press, 1988.

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Warren, Strober, ed. Mucosal immunity and infections at mucosal surfaces. New York: Oxford University Press, 1988.

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Vajdy, Michael, ed. Immunity Against Mucosal Pathogens. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-8412-6.

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1941-, Mestecky Jiri, ed. Mucosal immunology. 3rd ed. Amstedam: Elsevier Academic Press, 2005.

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Belibasakis, Georgios N., George Hajishengallis, Nagihan Bostanci, and Michael A. Curtis, eds. Oral Mucosal Immunity and Microbiome. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28524-1.

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Å, Hanson Lars, and Svanborg-Edén Catharina, eds. Mucosal immunobiology: Cellular-molecular interactions in the mucosal immune system. Basel: Karger, 1988.

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Immunology, Society for Mucosal, ed. Principles of mucosal immunology. London: Taylor & Francis Group, 2013.

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Slayton, Kaetzel Charlotte, ed. Mucosal immune defense: Immunoglobulin A. New York: Springer, 2007.

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Book chapters on the topic "Mucosal immunity"

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Giese, Matthias. "Mucosal Immunity." In Introduction to Molecular Vaccinology, 63–95. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25832-4_3.

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Russell, Michael W. "Mucosal Immunity." In New Bacterial Vaccines, 63–79. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0053-7_5.

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Pascual, David W., Hiroshi Kiyono, and Jerry R. McGhee. "Mucosal Immunity." In Infectious Agents and Pathogenesis, 15–35. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0313-6_2.

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Roux, M. E., M. C. del Lopez, and A. Florin-Christensen. "Mucosal Immunity." In Probiotics 3, 12–28. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-2768-6_1.

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Bishop, Nicolette C., and Michael Gleeson. "Mucosal Immunity." In Encyclopedia of Exercise Medicine in Health and Disease, 596–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_139.

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Simpson, Scott, and Lee M. Wetzler. "Mucosal Immunity." In Immunology, Infection, and Immunity, 399–423. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555816148.ch17.

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Cruse, Julius M., and Robert E. Lewis. "Mucosal Immunity." In Atlas of Immunology, 259–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-11196-3_14.

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Wiedermann, U. "Mucosal Immunity - Mucosal Tolerance." In Chemical Immunology and Allergy, 11–24. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071551.

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Cunliffe, R. N., and Y. R. Mahida. "Intestinal mucosal innate immunity." In Immunological Aspects of Gastroenterology, 1–33. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0790-0_1.

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Brandtzaeg, P., and D. E. Nilssen. "Mucosal Immunity in Immunodeficiency." In Symposium in Immunology III, 119–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78438-5_12.

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Conference papers on the topic "Mucosal immunity"

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Carlier, F., M. Pretolani, B. Detry, N. Heddebaut, T. Planté-Bordeneuve, E. Longchampt, L. Falque, et al. "Altered pIgR/IgA mucosal immunity in bronchiolitis obliterans syndrome." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.4352.

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Zhu, Richard, and Sujata Bhatia. "Optimizing COVID-19 Vaccine Diffusion in Respiratory Mucosa through Stokes-Einstein Modeling." In 2022 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/dmd2022-1065.

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Abstract SARS-COV-2 vaccines, all of which are currently intramuscular shots, have the ability to prevent serious injury. However, the absence of sufficient mucosal immunity is a major concern. To counteract this deficiency that has led to continued transmission from vaccinated individuals and breakthrough cases, reformulating vaccines to be inhalable presents a logical administration route. Predecessor research has reported the inhalable route to be viable as aerosolized vaccine nanoparticles, AAV phage nanoparticles, and PIV-5 viruses were recently identified to elicit immune responses. In this study, the diffusion of vaccine nanoparticles across the mucosa is characterized and modeled, with respect to their observed behavior from previous studies in relation to the Stokes-Einstein equation, to predict the most efficient model of an inhalable COVID-19 vaccine. The Stokes-Einstein equation has been used in several studies to predict diffusion coefficients. These predictions may be modified to fit the specifications of mucosal interactions. It was determined that mucosal interactions play a significant role in vaccine nanoparticle diffusion, as demonstrated by the viral vector and virus-like nanoparticle diffusion, and can be characterized by an equivalent hydrodynamic radius. Moreover, as a counter to mucosal interactions, PEGylation was found to drastically decrease the viscous slowing of the mucus medium.
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Kovach, Melissa A., Fu-Shin Yu, Michael W. Newstead, Xianyng Zeng, Richard Gallo, and Theodore J. Standiford. "Role Of Cathelicidin Related Antimicrobial Peptide In Lung Innate Mucosal Immunity." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5648.

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Kryukova, Nadezda, Natalia Abramova, Ekaterina Khromova, Valeria Zakharova, Svetlana Skhodova, Irina Bisheva, Aleksandra Vinnitskaya, et al. "The mucosal immunity of the respiratory tract in COVID-19 convalescent healthcare professionals." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.oa4307.

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Bozinovski, Steven, Mohib Uddin, Ross Vlahos, Michelle Thompson, Anne-Sophie Merritt, Peter A. Wark, Anastasia Hutchinson, Louis B. Irving, Bruce D. Levy, and Gary P. Anderson. "Serum Amyloid A Augments Mucosal Immunity By Opposing Resolving Lipoxina4 Signaling In Chronic Lung Disease." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2836.

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Constantinides, Michael G., Samira Tamoutounour, Jonathan L. Linehan, Shurjo Sen, Jahangheer Shaik, Sobhan Roy, Erin J. Adams, and Yasmine Belkaid. "Abstract PR16: Mucosal-associated invariant T-cells respond to the cutaneous microbiota and promote skin immunity." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-pr16.

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Krause, Anja, Wendy Wu, Yaqin Xu, Jianping Qiu, Ronald G. Crystal, and Stefan Worgall. "Long-Term Protective Immunity Following Mucosal Immunization With Capsid-Modified AdC7OprF.RGD Expressing The P. Aeruginosa Protein OprF." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3651.

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Yamada, Sirikan, Shunji Kato, Takeshi Matsuhisa, Luksana Makonkawkeyoon, Thiraphat Charkrabandhu, Pawit Sutharat, Nirush Lertprasertsuk, et al. "Abstract 3834: Difference of host immunity and mucosal defense toH. pyloriinfection caused Asian paradox on incidence of gastric cancer: Correlation with mucosal mRNA expression ofIL-8, pepsinogenI/II ratio, andH. pylori cagAgene mutation in Thai and Japanese gastric cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3834.

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MacBeth, Morgan, Richard Tobin, Robert Van Gulick, Martin D. McCarter, William A. Robinson, and Kasey L. Couts. "Abstract PO048: Loss of intra-tumoral RIG-I immune signaling is a potential microbiome-mediated mechanism underlying poor anti-tumor immunity and immunotherapy resistance in mucosal melanoma." In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-po048.

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SEVBITOV, Andrey, Aleksey DOROFEEV, Sergey MIRONOV, Samer AL-KHOURY, and Anton TIMOSHIN. "PREVENTION OF CANDIDIASIS IN PATIENTS USING REMOVABLE DENTURES." In SOUTHERN BRAZILIAN JOURNAL OF CHEMISTRY 2021 INTERNATIONAL VIRTUAL CONFERENCE. DR. D. SCIENTIFIC CONSULTING, 2022. http://dx.doi.org/10.48141/sbjchem.21scon.04_abstract_sevbitov.pdf.

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Despite innovations in orthopedic dentistry, removable dentures belong to the most popular orthopedic care category. Removable dentures are combined stimuli that affect the mucous membrane and neuro-receptor apparatus. Acrylic plastic prostheses, widely used in prosthetic dentistry, have a negative side mechanical, chemical-toxic, sensitizing, and thermal insulating effect on oral tissue and prosthetic impression area. This is often complicated by a violation of the biocenosis of the oral cavity, the growth of pathogenic microflora that releases toxins, especially an increase in the number of yeast colonies that irritate the oral mucosa and prosthetic stomatitis. It was observed 100 patients with oral candidiasis of various age groups from 45 to 65 years. Of these, 60 patients with removable plate prostheses; 40 patients with partially removable prostheses. Chronic forms of candidiasis were diagnosed in 40 patients and with exacerbation of chronic forms of candidiasis in 60 people. The number of untreated carious cavities and poor hygienic condition of the oral cavity directly affects the severity of candidiasis. Acute forms of candidiasis were observed mainly in patients with high DMF and PMA indices. The severity of candidiasis depends on the degree and duration of wearing dentures and hygienic conditions - the most severe forms of invasive candidiasis were observed in the presence of removable plate prostheses, the complete absence of teeth, and the use of a prosthesis for more than 10-15 years. A combined lesion of the oral mucosa and the red border of the lips was observed mainly in patients older than 60 years. The presence of candidiasis in the oral cavity in patients with removable plate prostheses leads to a statistically significant change in the indicators of local immunity of the oral cavity: an increase in the concentration of serum IgG and IgA and the values of the coefficient of the balance of local immunity factors.
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Reports on the topic "Mucosal immunity"

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Middlebrooks, Bobby L. Investigation of the Role of Immunoglobulin Classes and Subclasses in Humoral and Mucosal Immunity in Cetaceans. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada452454.

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Grueso-Navarro, Elena, Leticia Rodríguez-Alcolado, Ángel Arias, Emilio J. Laserna-Mendieta, and Alfredo J. Lucendo. Influence of HLA-DQA1*05 allele in the response to anti-TNFα drugs in inflammatory bowel diseases. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0076.

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Review question / Objective: Do patients with inflammatory bowel disease and treated with any anti-TNFα drug who had the HLA-DQA1*05 allele (in heterozygosis or homozygosis) have lower response or persistence to those drugs than patients without HLA-DQA1*05 allele? Condition being studied: Inflammatory bowel diseases (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory condition that may affect any part of the digestive tract (CD) or be limited to the colon (UC). While the specific aetiology of IBD remains unknown, it is believed to involve a complex impairment in the immunity of the gut mucosa due to a combination of several genetic and environmental factors, being the microbiota one of the latest that more attraction has received in recent years. Symptoms of IBD (such as abdominal pain, diarrhoea, fever, tiredness or rectal bleeding) may be either constant or alternate between periods of limited disease activity and flares with remarkable presence of symptoms. As IBD is associated with significant morbidity and disability, pharmacological treatment is required in most cases, especially in CD, aimed at reducing the inflammatory response and attenuating the activity of the immune system. In the moderate and severe forms of the disease, therapy is usually based on immunosuppressant and/or biological drugs. Among the latest, anti-TNFα drugs (infliximab or adalimumab) are normally chosen as the initial biological therapy.
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