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Journal articles on the topic 'Immunité intestinal'

Author: Grafiati

Published: 25 January 2025

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1

Boutherin, Valentine, Florence Piastra-Facon, and Emma Risson. "Le microbiote intestinal, un modulateur clé de la physiologie immunitaire." médecine/sciences 35, no. 6-7 (June 2019): 571–74. http://dx.doi.org/10.1051/medsci/2019111.

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Microbiote et immunité : nouveaux mécanismes, nouveaux acteurs Microbiota and immunity: new mechanisms, new actors Le dossier thématique qui suit a été rédigé par les étudiants de Master 1 de Biologie de l’École normale supérieure (ENS) de Lyon à l’issue de l’UE Microbiologie Moléculaire et Structurale (2018- 19). Le Master de Biologie de l’ENS de Lyon, cohabilité par l’université Claude Bernard Lyon 1, accueille chaque année environ 50 étudiants en M1 et en M2 et propose une formation de haut niveau à la recherche en biosciences. Chaque étudiant y construit son parcours à la carte, en choisissant ses options parmi un large panel de modules, favorisant ainsi une approche pluridisciplinaire des sciences du vivant, et ce en relation étroite avec les laboratoires de recherche du tissu local, national et international. En participant à diverses activités scientifiques connexes aux UE de leur formation, les étudiants préparent également l’obtention du diplôme de l’ENS de Lyon, qui valide leur scolarité à l’ENS. La rédaction du présent dossier, qui vise à transmettre de façon claire les principaux messages issus d’articles scientifiques publiés récemment dans le domaine de la microbiologie, constitue l’une de ces activités connexes proposées aux étudiants. Ces dernières années, des progrès immenses ont été réalisés dans la compréhension des interactions entre le microbiote bactérien, notamment intestinal, et l’immunité (→). (→) Voir le numéro thématique Le microbiote, cet inconnu qui réside en nous, m/s n° 11, novembre 2016, pages 921-1016 En parallèle, de nouvelles avancées techniques ont permis d’identifier et de caractériser les virus présents au sein du microbiote, rendant possible une meilleure appréhension de la diversité du virobiote et de ses impacts fonctionnels. Le présent dossier illustre quelques aspects de ces relations entre microbiote au sens large et immunité.

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2

Shen, Zhaohua, Weiwei Luo, Bei Tan, Kai Nie, Minzi Deng, Shuai Wu, Mengwei Xiao, et al. "Roseburia intestinalis stimulates TLR5-dependent intestinal immunity against Crohn's disease." eBioMedicine 85 (November 2022): 104285. http://dx.doi.org/10.1016/j.ebiom.2022.104285.

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3

Ruemmele, F. "Flore intestinale et immunité." Archives de Pédiatrie 14 (November 2007): 2–4. http://dx.doi.org/10.1016/s0929-693x(07)78703-1.

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4

RMV, Rao. "Immunity in Medically Important Parasitic Infections." Virology & Immunology Journal 5, no. 1 (January 12, 2021): 1–8. http://dx.doi.org/10.23880/vij-16000267.

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Immunity is the rule. It is often incomplete and takes many years to develop and fade away quickly. Human life is a battlefield in which we are like soldiers attacked from all sides by bacteria, viruses, fungi and parasites. Our body is bestowed with a defense mechanism in the form of an immune system It has long been recognized that infections with parasites, such as intestinal worms, are often accompanied by blood eosinophilia, and this is due to an immunological process. Conditions in which blood eosinophilia is common include intestinal infections with Ancylostoma duodenale, Ascaris lumbricoides, Trichuristrichiura, various forms of Wuchereria bancroft, Brugiamalayi, loaloa, Dracunculus medinensis, mite infection of the lungs (including at least some cases of tropical eosinophilia);and hydrated disease is due to Echinococcus granulosus. Eosinophilia, in large numbers invades tissues in which antigen-antibody reaction has taken place. They appear to be attracted by some product of the antigen-antibody reaction and it has been shown that if tissues from sensitized guinea -pigs mixed with antigen in vitro, or tissues from guinea-pigs which have died from anaphylaxis, are transferred to the peritoneal cavity of normal guinea-pigs, the recipient develops very marked eosinophilia within 24 hours. The active agent has not been infected, but it is probably not histamine. The eosinophils of rodents are very actively phagocytic, and ingest cellular debris, mast cell granules, etc, but it is not certain whether this is true of eosinophils from other species, nor it is known what functions the eosinophils serve in these reactions. A multitude of defensive mechanisms are involved in parasitic infection. A humoral response develops when parasites invade blood stream (Malaria, Trypanosoma), whereas cell-mediated immunity is elicited by parasites that grow within the tissues (Eg: Cutaneous leishmaniasis). In protozoal infections, IgG, and IgM are produced. In Addition, IgA also produced in intestinal infection. With helminthic infections, IgG, IgM and IgE antibodies are produced.

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5

Tilg, Herbert. "Diet and Intestinal Immunity." New England Journal of Medicine 366, no. 2 (January 12, 2012): 181–83. http://dx.doi.org/10.1056/nejmcibr1113158.

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6

Cherayil, Bobby J., Shiri Ellenbogen, and Nandakumar N. Shanmugam. "Iron and intestinal immunity." Current Opinion in Gastroenterology 27, no. 6 (November 2011): 523–28. http://dx.doi.org/10.1097/mog.0b013e32834a4cd1.

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7

Klein, JR. "Hormones and intestinal immunity." Biomedicine & Pharmacotherapy 52, no. 1 (January 1998): 44. http://dx.doi.org/10.1016/s0753-3322(97)86241-5.

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8

Schmucker, Douglas L., Karine Thoreux, and Robert L. Owen. "Aging impairs intestinal immunity." Mechanisms of Ageing and Development 122, no. 13 (September 2001): 1397–411. http://dx.doi.org/10.1016/s0047-6374(01)00276-7.

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9

James, Stephen P. "Intestinal immunity and inflammation." Immunology Today 6, no. 3 (March 1985): 66–67. http://dx.doi.org/10.1016/0167-5699(85)90014-3.

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10

Bai, Yajuan, and Mingwei Zhang. "Longan Pulp Polysaccharide Protects Systemic Immunity and Intestinal Immunity in Mice Induced by Cyclophosphamide." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 738. http://dx.doi.org/10.1093/cdn/nzaa052_007.

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Abstract Objectives This study aimed to explore the effect of longan pulp polysaccharide (LP) on the systemic immunity and intestinal mucosal immunity with immunosuppressive mice. The synthesis processing and secretion of intestinal secretory IgA (SIgA) were investigated. Methods Serum IgA, IgG, IgM and intestinal SIgA were detected by ELISA. Genes involved in the synthesis and secretion of SIgA were detected by Q-PCR and western blot. Results LP increased the thymus index, spleen index, and serum IgA level in cyclophosphamide (CTX)-treated mice. SIgA secretion in intestinal lumen was increased by LP as well. The underlying mechanism comes down to the facts as follows: LP increased intestinal cytokines expression and TGFβRII that is associated with pathways of IgA class switch recombination (CSR). By improving protein expression of mucosal address in cell-adhesion molecule-1 (MAdCAM-1) and integrin α4β7, LP was beneficial to gut homing of IgA + plasma cells. LP increased IgA, polymeric immunoglobulin receptor (pIgR), and secretory component (SC) to fortify the SIgA secretion. Conclusions This study suggested that moderate consumption of LP is helpful for improving systemic immunity and intestinal mucosal immunity via promotion of intestinal SIgA to strengthen the mucosal barrier. Funding Sources This work was supported by the National Key Research Project of China (2018YFC1602105, 2019YFD1002304), Guangdong Provincial Science and Technology Project (2018A050506050), President Foundation of Guangdong Academy of Agricultural Sciences (201812B).

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Gattu, Sureka, Ye-Ji Bang, Mihir Pendse, Chaitanya Dende, Andrew L. Chara, Tamia A. Harris, Yuhao Wang, et al. "Epithelial retinoic acid receptor β regulates serum amyloid A expression and vitamin A-dependent intestinal immunity." Proceedings of the National Academy of Sciences 116, no. 22 (May 16, 2019): 10911–16. http://dx.doi.org/10.1073/pnas.1812069116.

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Vitamin A is a dietary component that is essential for the development of intestinal immunity. Vitamin A is absorbed and converted to its bioactive derivatives retinol and retinoic acid by the intestinal epithelium, yet little is known about how epithelial cells regulate vitamin A-dependent intestinal immunity. Here we show that epithelial cell expression of the transcription factor retinoic acid receptor β (RARβ) is essential for vitamin A-dependent intestinal immunity. Epithelial RARβ activated vitamin A-dependent expression of serum amyloid A (SAA) proteins by binding directly to Saa promoters. In accordance with the known role of SAAs in regulating Th17 cell effector function, epithelial RARβ promoted IL-17 production by intestinal Th17 cells. More broadly, epithelial RARβ was required for the development of key vitamin A-dependent adaptive immune responses, including CD4+ T-cell homing to the intestine and the development of IgA-producing intestinal B cells. Our findings provide insight into how the intestinal epithelium senses dietary vitamin A status to regulate adaptive immunity, and highlight the role of epithelial cells in regulating intestinal immunity in response to diet.

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12

Neil, Jessica A., and Ken Cadwell. "The Intestinal Virome and Immunity." Journal of Immunology 201, no. 6 (September 4, 2018): 1615–24. http://dx.doi.org/10.4049/jimmunol.1800631.

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13

Kernbauer, Elisabeth, and Ken Cadwell. "Autophagy, viruses, and intestinal immunity." Current Opinion in Gastroenterology 30, no. 6 (November 2014): 539–46. http://dx.doi.org/10.1097/mog.0000000000000121.

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Xu, An Tao, Jun Tao Lu, Zhi Hua Ran, and Qing Zheng. "Exosome in intestinal mucosal immunity." Journal of Gastroenterology and Hepatology 31, no. 10 (October 2016): 1694–99. http://dx.doi.org/10.1111/jgh.13413.

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15

Johnson, C. D., and K. A. Kudsk. "Nutrition and intestinal mucosal immunity." Clinical Nutrition 18, no. 6 (December 1999): 337–44. http://dx.doi.org/10.1016/s0261-5614(99)80012-0.

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16

Lee, Sanghyun, and Megan T. Baldridge. "Viruses RIG up intestinal immunity." Nature Immunology 20, no. 12 (October 21, 2019): 1563–64. http://dx.doi.org/10.1038/s41590-019-0530-y.

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17

Veldhoen, Marc, and Verena Brucklacher-Waldert. "Dietary influences on intestinal immunity." Nature Reviews Immunology 12, no. 10 (September 25, 2012): 696–708. http://dx.doi.org/10.1038/nri3299.

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18

Wang, Li, Limeng Zhu, and Song Qin. "Gut Microbiota Modulation on Intestinal Mucosal Adaptive Immunity." Journal of Immunology Research 2019 (October 3, 2019): 1–10. http://dx.doi.org/10.1155/2019/4735040.

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The mammalian intestine harbors a remarkable number of microbes and their components and metabolites, which are fundamental for the instigation and development of the host immune system. The intestinal innate and adaptive immunity coordinate and interact with the symbionts contributing to the intestinal homeostasis through establishment of a mutually beneficial relationship by tolerating to symbiotic microbiota and retaining the ability to exert proinflammatory response towards invasive pathogens. Imbalance between the intestinal immune system and commensal organisms disrupts the intestinal microbiological homeostasis, leading to microbiota dysbiosis, compromised integrity of the intestinal barrier, and proinflammatory immune responses towards symbionts. This, in turn, exacerbates the degree of the imbalance. Intestinal adaptive immunity plays a critical role in maintaining immune tolerance towards symbionts and the integrity of intestinal barrier, while the innate immune system regulates the adaptive immune responses to intestinal commensal bacteria. In this review, we will summarize recent findings on the effects and mechanisms of gut microbiota on intestinal adaptive immunity and the plasticity of several immune cells under diverse microenvironmental settings.

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19

Kim, Myunghoo, Andrea A. Hill, Wan-Jung Wu, and Gretchen E. Diehl. "Intestinal microbes direct CX3CR1+ cells to balance intestinal immunity." Gut Microbes 10, no. 4 (January 6, 2019): 540–46. http://dx.doi.org/10.1080/19490976.2018.1559683.

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20

Pakhomovskaya, N. L., and М. M. Venediktova. "Healthy intestinal colonization in children: strong immunity." Medical Council, no. 17 (October 22, 2018): 199–205. http://dx.doi.org/10.21518/2079-701x-2018-17-199-205.

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The article presents actual data on the composition and functions of the intestinal microbiota, and examines the mechanisms of the microbiota effect on the macroorganism’s health state. The necessity and possibility of correction of microbiota are shown by the analysis of the composition and evaluation of the functions of the intestinal microbiota, and the mechanisms of the symbiotic relationship «microflora macroorganism» and the causes leading to the development of intestinal dysbiosis. The main groups of preparations (probiotics, prebiotics, synbiotics) used for correction of intestinal microbiocenosis are presented by taking into account the modern guidelines.

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21

Kruglov, A. A., and S. A. Nedospasov. "Microbiota, Intestinal Immunity, and Mouse Bustle." Acta Naturae 6, no. 1 (March 15, 2014): 6–8. http://dx.doi.org/10.32607/20758251-2014-6-1-6-8.

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The composition of the intestinal microbiota is regulated by the immune system. This paper discusses the role of cytokines and innate immunity lymphoid cells in the intestinal immune regulation by means of IgA.

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22

Messina, Valeria, Carla Buccione, Giulia Marotta, Giovanna Ziccheddu, Michele Signore, Gianfranco Mattia, Rossella Puglisi, Benedetto Sacchetti, Livia Biancone, and Mauro Valtieri. "Gut Mesenchymal Stromal Cells in Immunity." Stem Cells International 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/8482326.

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Mesenchymal stromal cells (MSCs), first found in bone marrow (BM), are the structural architects of all organs, participating in most biological functions. MSCs possess tissue-specific signatures that allow their discrimination according to their origin and location. Among their multiple functions, MSCs closely interact with immune cells, orchestrating their activity to maintain overall homeostasis. The phenotype of tissue MSCs residing in the bowel overlaps with myofibroblasts, lining the bottom walls of intestinal crypts (pericryptal) or interspersed within intestinal submucosa (intercryptal). In Crohn’s disease, intestinal MSCs are tightly stacked in a chronic inflammatory milieu, which causes their enforced expression of Class II major histocompatibility complex (MHC). The absence of Class II MHC is a hallmark for immune-modulator and tolerogenic properties of normal MSCs and, vice versa, the expression of HLA-DR is peculiar to antigen presenting cells, that is, immune-activator cells. Interferon gamma (IFNγ) is responsible for induction of Class II MHC expression on intestinal MSCs. The reversal of myofibroblasts/MSCs from an immune-modulator to an activator phenotype in Crohn’s disease results in the formation of a fibrotic tube subverting the intestinal structure. Epithelial metaplastic areas in this context can progress to dysplasia and cancer.

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23

Velikova, Tsvetelina, Issa El Kaouri, Konstantina Bakopoulou, Milena Gulinac, Kremena Naydenova, Martin Dimitrov, Milena Peruhova, and Snezhina Lazova. "Mucosal Immunity and Trained Innate Immunity of the Gut." Gastroenterology Insights 15, no. 3 (August 2, 2024): 661–75. http://dx.doi.org/10.3390/gastroent15030048.

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Mucosal immunity and trained innate immunity of the gut play a pivotal role in maintaining intestinal homeostasis and defending against microbial pathogens. This review provides an overview of the mechanisms underlying mucosal immunity and the concept of trained innate immunity in the gut. We discuss the interaction between gut microbiota and the host immune system, highlighting the role of epithelial cells, dendritic cells, and innate lymphoid cells, as well as the novel concept of trained innate immunity and its role in perpetuating or attenuating gut inflammation. We also comment on the current models for investigating mucosal immunity, their limitations, and how they can be overcome. Additionally, we explore the potential therapeutic implications of modulating mucosal immunity and trained innate immunity in gastrointestinal diseases. Only by elucidating the mechanisms underlying mucosal immunity and the concept of trained innate immunity, innovative approaches to modulate immune responses and restore intestinal homeostasis in the context of gastrointestinal disorders could be implemented.

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24

Adolph, Timon E., Lisa Mayr, Felix Grabherr, and Herbert Tilg. "Paneth Cells and their Antimicrobials in Intestinal Immunity." Current Pharmaceutical Design 24, no. 10 (May 28, 2018): 1121–29. http://dx.doi.org/10.2174/1381612824666180327161947.

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Since the initial description of granular-rich small-intestinal crypt-based epithelial cells in 1872, today referred to as Paneth cells, a plethora of recent studies underlined their function in intestinal homeostasis. Paneth cells are evolutionary conserved highly secretory cells that produce antimicrobials to control gut microbial communities. Moreover, Paneth cells emerged as stem cell regulators that translate environmental cues into intestinal epithelial responses. Paneth cell disturbances may instigate intestinal inflammation and provide susceptibility to infection. Altered Paneth cell functions have been associated with a variety of inflammatory disease models and were linked to human intestinal disease processes including inflammatory bowel diseases such as Crohn´s disease and ulcerative colitis. This review summarizes our current understanding of Paneth cells and their antimicrobials in health and disease.

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25

Bo, Yan, Ren Sha, and Haodong Yu. "Interaction Between Neuroimmune Activation Mechanisms in Epilepsy: the S100b Signaling Network and Brain-gut-bio-axis." Theoretical and Natural Science 3, no. 1 (April 28, 2023): 505–12. http://dx.doi.org/10.54254/2753-8818/3/20220334.

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Epilepsy is a syndrome characterized by abnormal firing in the brain, with numerous risk factors. Autoimmune central nervous system diseases are currently being widely explored; however, the neuroimmune processes involved in epilepsy have not been fully elucidated. This disorder is associated with the rise in the blood protein S100b concentration; hence, S100b levels are considered damage markers. From a recent review, we discovered the interaction of epilepsy with neural immunity and intestinal immunity. Neural immunity in epilepsy is associated with S100b generation and consumption. Therefore, we expect that S100b can be used as immune activation material to amplify immune responses in epilepsy simultaneously with intestinal immune suppression. The symbiotic relationship with intestinal biological immune upregulates the intestinal immune function, alleviating adverse outcomes of neural immunity in local brain regions.

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Zeng, Tian, Saleem Jaffar, Yijuan Xu, and Yixiang Qi. "The Intestinal Immune Defense System in Insects." International Journal of Molecular Sciences 23, no. 23 (December 1, 2022): 15132. http://dx.doi.org/10.3390/ijms232315132.

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Over a long period of evolution, insects have developed unique intestinal defenses against invasion by foreign microorganisms, including physical defenses and immune responses. The physical defenses of the insect gut consist mainly of the peritrophic matrix (PM) and mucus layer, which are the first barriers to pathogens. Gut microbes also prevent the colonization of pathogens. Importantly, the immune-deficiency (Imd) pathways produce antimicrobial peptides to eliminate pathogens; mechanisms related to reactive oxygen species are another important pathway for insect intestinal immunity. The janus kinase/STAT signaling pathway is involved in intestinal immunity by producing bactericidal substances and regulating tissue repair. Melanization can produce many bactericidal active substances into the intestine; meanwhile, there are multiple responses in the intestine to fight against viral and parasitic infections. Furthermore, intestinal stem cells (ISCs) are also indispensable in intestinal immunity. Only the coordinated combination of the intestinal immune defense system and intestinal tissue renewal can effectively defend against pathogenic microorganisms.

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27

Bai, Xiao-Dong. "Intestinal colonization withCandida albicansand mucosal immunity." World Journal of Gastroenterology 10, no. 14 (2004): 2124. http://dx.doi.org/10.3748/wjg.v10.i14.2124.

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28

Chandra, Ranjit Kumar, and Manju Wadhwa. "Nutritional modulation of Intestinal mucosal Immunity." Immunological Investigations 18, no. 1-4 (January 1989): 119–26. http://dx.doi.org/10.3109/08820138909112232.

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29

Mowat, Allan McI, and Joanne L. Viney. "The anatomical basis of intestinal immunity." Immunological Reviews 156, no. 1 (April 1997): 145–66. http://dx.doi.org/10.1111/j.1600-065x.1997.tb00966.x.

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30

Willinger, T. "Oxysterols in intestinal immunity and inflammation." Journal of Internal Medicine 285, no. 4 (November 26, 2018): 367–80. http://dx.doi.org/10.1111/joim.12855.

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31

Hogan, Simon P., Amanda Waddell, and Patricia C. Fulkerson. "Eosinophils in infection and intestinal immunity." Current Opinion in Gastroenterology 29, no. 1 (January 2013): 7–14. http://dx.doi.org/10.1097/mog.0b013e32835ab29a.

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32

Yuan, Shuai. "Th17 cells and intestinal mucosal immunity." World Chinese Journal of Digestology 23, no. 19 (2015): 3094. http://dx.doi.org/10.11569/wcjd.v23.i19.3094.

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33

Denning, Timothy L., and Shanthi V. Sitaraman. "Segmented Filamentous Bacteria Shape Intestinal Immunity." Gastroenterology 139, no. 1 (July 2010): 351–53. http://dx.doi.org/10.1053/j.gastro.2010.05.032.

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34

Wang, Penghua, Shu Zhu, Long Yang, Shuang Cui, Wen Pan, Ruaidhri Jackson, Yunjiang Zheng, et al. "Nlrp6 regulates intestinal antiviral innate immunity." Science 350, no. 6262 (October 22, 2015): 826–30. http://dx.doi.org/10.1126/science.aab3145.

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35

Lamas, Bruno, Jane M. Natividad, and Harry Sokol. "Aryl hydrocarbon receptor and intestinal immunity." Mucosal Immunology 11, no. 4 (April 7, 2018): 1024–38. http://dx.doi.org/10.1038/s41385-018-0019-2.

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WAKELIN, D., S. E. FARIAS, and J. E. BRADLEY. "Variation and immunity to intestinal worms." Parasitology 125, no. 7 (October 2002): S39—S50. http://dx.doi.org/10.1017/s0031182002001440.

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Genetically determined variation in host capacity to express resistance to a given parasite plays a major role in determining the outcome of infection. It can be assumed that the same is true of variation in parasites, but very much less is known of its influence on the host–parasite relationship. Phenotypic and genotypic variation within species of intestinal worms is now well documented, detailed studies having been made of parasites such asAscarisin humans and trichostrongyles in domestic animals. However, the extent to which this variation affects the course of infection or the host immune response in these hosts is limited. Of the nematodes used as experimental models in laboratory rodents, detailed data on phenotypic or genotypic variation are limited toStrongyloidesandTrichinella. Parasite variation is known to be subject to host-mediated selection, the emergence of anthelmintic resistance being a good example. Repeated passage has been used to select lines of parasite that survive in abnormal hosts or which show adaptation to host immunity. Experimental studies withTrichinellagenotypes in mice have demonstrated the extent to which parasite variation influences the nature and degree of the host's immune and inflammatory responses, the complex interplay between immunogenicity and pathogenicity influencing both partners in the relationship. Recent studies with isolates ofTrichuris murishave shown how parasite variation influences the capacity of mice to express the T helper cell responses necessary for resistance. Molecular differences betweenT. murisisolates have been shown in their excreted/secreted products as well as at the level of their DNA. Knowledge of the functional consequences of parasite variation will add to our understanding of host-parasite evolution as well as providing a rational basis for predicting the outcome of controls strategies that rest on the improvement of host resistance through vaccination or selective breeding.

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37

Elson, Charles O., Martin F. Kagnoff, Claudio Fiocchi, A. Dean Befus, and Stephan Targan. "Intestinal immunity and inflammation: Recent progress." Gastroenterology 91, no. 3 (September 1986): 746–68. http://dx.doi.org/10.1016/0016-5085(86)90649-9.

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38

Didierlaurent, A., M. Simonet, and J. C. Sirard. "Intestinal epithelial barrier and mucosal immunity." Cellular and Molecular Life Sciences 62, no. 12 (June 2005): 1285–87. http://dx.doi.org/10.1007/s00018-005-5032-4.

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39

Rumbo, M., and E. J. Schiffrin. "Intestinal epithelial barrier and mucosal immunity." Cellular and Molecular Life Sciences 62, no. 12 (June 2005): 1288–96. http://dx.doi.org/10.1007/s00018-005-5033-3.

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Müller, C. A., I. B. Autenrieth, and A. Peschel. "Intestinal epithelial barrier and mucosal immunity." Cellular and Molecular Life Sciences 62, no. 12 (June 2005): 1297–307. http://dx.doi.org/10.1007/s00018-005-5034-2.

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Dubois, B., A. Goubier, G. Joubert, and D. Kaiserlian. "Intestinal epithelial barrier and mucosal immunity." Cellular and Molecular Life Sciences 62, no. 12 (June 2005): 1322–32. http://dx.doi.org/10.1007/s00018-005-5036-0.

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Sato, A., and A. Iwasaki. "Intestinal epithelial barrier and mucosal immunity." Cellular and Molecular Life Sciences 62, no. 12 (June 2005): 1333–38. http://dx.doi.org/10.1007/s00018-005-5037-z.

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Collier-Hyams, L. S., and A. S. Neish. "Intestinal epithelial barrier and mucosal immunity." Cellular and Molecular Life Sciences 62, no. 12 (June 2005): 1339–48. http://dx.doi.org/10.1007/s00018-005-5038-y.

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44

Alexopoulou, L., and D. Kontoyiannis. "Intestinal epithelial barrier and mucosal immunity." Cellular and Molecular Life Sciences 62, no. 12 (June 2005): 1349–58. http://dx.doi.org/10.1007/s00018-005-5039-x.

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Dezfuli, B. S., G. Bosi, J. A. DePasquale, M. Manera, and L. Giari. "Fish innate immunity against intestinal helminths." Fish & Shellfish Immunology 50 (March 2016): 274–87. http://dx.doi.org/10.1016/j.fsi.2016.02.002.

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46

Vaarala, Outi. "Intestinal Immunity and Type 1 Diabetes." Journal of Pediatric Gastroenterology and Nutrition 39, Supplement 3 (June 2004): S732—S733. http://dx.doi.org/10.1097/00005176-200406003-00008.

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Kulkarni, Devesha H., and Rodney D. Newberry. "Intestinal Macromolecular Transport Supporting Adaptive Immunity." Cellular and Molecular Gastroenterology and Hepatology 7, no. 4 (2019): 729–37. http://dx.doi.org/10.1016/j.jcmgh.2019.01.003.

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48

Brave, Martina, Dana J. Lukin, and Sridhar Mani. "Microbial control of intestinal innate immunity." Oncotarget 6, no. 24 (July 3, 2015): 19962–63. http://dx.doi.org/10.18632/oncotarget.4780.

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Perez-Lopez, Araceli, Judith Behnsen, Sean-Paul Nuccio, and Manuela Raffatellu. "Mucosal immunity to pathogenic intestinal bacteria." Nature Reviews Immunology 16, no. 3 (February 22, 2016): 135–48. http://dx.doi.org/10.1038/nri.2015.17.

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Tong, Yiqing, and Jianguo Tang. "Candida albicans infection and intestinal immunity." Microbiological Research 198 (May 2017): 27–35. http://dx.doi.org/10.1016/j.micres.2017.02.002.

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