Mucosal Immunity
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Associated Lymphoid Tissue in Chickens and Turkeys Andrew Stephen Fix Iowa State University
Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1990 The trs ucture and function of conjunctiva- associated lymphoid tissue in chickens and turkeys Andrew Stephen Fix Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Animal Sciences Commons, and the Veterinary Medicine Commons Recommended Citation Fix, Andrew Stephen, "The trs ucture and function of conjunctiva-associated lymphoid tissue in chickens and turkeys " (1990). Retrospective Theses and Dissertations. 9496. https://lib.dr.iastate.edu/rtd/9496 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. INFORMATION TO USERS The most advanced technology has been used to photograph and reproduce this manuscript from the microfilm master. UMI films the text directly from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may be from any type of computer printer. Hie quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction. In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion. -
The Evolution of Nasal Immune Systems in Vertebrates
Molecular Immunology 69 (2016) 131–138 Contents lists available at ScienceDirect Molecular Immunology j ournal homepage: www.elsevier.com/locate/molimm The evolution of nasal immune systems in vertebrates ∗ Ali Sepahi, Irene Salinas Center for Evolutionary and Theoretical Immunology, Department of Biology, University of New Mexico, Albuquerque, NM, USA a r t i c l e i n f o a b s t r a c t Article history: The olfactory organs of vertebrates are not only extraordinary chemosensory organs but also a powerful Received 15 July 2015 defense system against infection. Nasopharynx-associated lymphoid tissue (NALT) has been traditionally Received in revised form 5 September 2015 considered as the first line of defense against inhaled antigens in birds and mammals. Novel work in Accepted 6 September 2015 early vertebrates such as teleost fish has expanded our view of nasal immune systems, now recognized Available online 19 September 2015 to fight both water-borne and air-borne pathogens reaching the olfactory epithelium. Like other mucosa- associated lymphoid tissues (MALT), NALT of birds and mammals is composed of organized lymphoid Keywords: tissue (O-NALT) (i.e., tonsils) as well as a diffuse network of immune cells, known as diffuse NALT (D- Evolution NALT). In teleosts, only D-NALT is present and shares most of the canonical features of other teleost Nasal immunity NALT MALT. This review focuses on the evolution of NALT in vertebrates with an emphasis on the most recent Mucosal immunity findings in teleosts and lungfish. Whereas teleost are currently the most ancient group where NALT has Vertebrates been found, lungfish appear to be the earliest group to have evolved primitive O-NALT structures. -
Mucosal Immunity Learning Goal
Host Defense 2013 Mucosal Immunity April 16, 2013 Katherine L.Knight, Ph.D. MUCOSAL IMMUNITY LEARNING GOAL You will be able to describe the mucosal immune system. OBJECTIVES To attain the goal for this lecture you will be able to: Describe the components of the mucosal immune system. Draw the structure of secretory IgA. Explain the mechanism of IgA transport across mucosal surfaces. Explain how a response to antigen is generated in the mucosal system. Identify the differences in tolerogenic versus immunogenic responses to mucosal antigen administration. Delineate the functions of the mucosal immune system, including M cells. Describe how the mucosal immune system might be used for immunization. Describe the characteristics of selective IgA deficiency. Describe how intestinal commensal bacteria interact with the host to promote a healthy environment READING ASSIGNMENT Janeway’s Immunobiology 8th Edition (2012), Chapter 12 and Article “Mucosal Immunity and Vaccines” by Robyn Seipp attached at end of lecture notes. LECTURER Katherine L. Knight, Ph.D. Page 1 Host Defense 2013 Mucosal Immunity April 16, 2013 Katherine L.Knight, Ph.D. CONTENT SUMMARY I. INTRODUCTION TO MUCOSAL IMMUNITY II. ORGANIZATION OF THE MUCOSAL IMMUNE SYSTEM A. Components of the Mucosal Immune System B. Induction of a Response C. Features of Mucosal Immunity D. Intraepithelial lymphocytes (IEL) III. IgA SYNTHESIS, STRUCTURE AND TRANSPORT IV. FUNCTIONS OF IgA AT MUCOSAL SURFACES A. Barrier Functions B. Intraepithelial Viral Neutralization C. Excretory Immunity D. Passive Immunity E. IgA Deficiency State V. MUCOSAL IMMUNIZATION VI. MUCOSAL TOLERANCE A. The Induction of Tolerance via Mucosal Sites B. The interaction Between Gut Bacteria and the Intestine I. -
The Role of Intestinal Microbiota and the Immune System
European Review for Medical and Pharmacological Sciences 2013; 17: 323-333 The role of intestinal microbiota and the immune system F. PURCHIARONI, A. TORTORA, M. GABRIELLI, F. BERTUCCI, G. GIGANTE, G. IANIRO, V. OJETTI, E. SCARPELLINI, A. GASBARRINI Department of Internal Medicine, School of Medicine, Catholic University of the Sacred Heart, Gemelli Hospital, Rome, Italy Abstract. – BACKGROUND: The human gut Introduction is an ecosystem consisting of a great number of commensal bacteria living in symbiosis with the The intestinal microbiota is composed of 1013-14 host. Several data confirm that gut microbiota is engaged in a dynamic interaction with the in- microorganisms (Figure 1), with at least 100 testinal innate and adaptive immune system, af- times as many genes as our genome, the micro- fecting different aspects of its development and biome. Its composition is individual-specific, function. ranges among individuals and also within the AIM: To review the immunological functions same individual during life. Many factors can in- of gut microbiota and improve knowledge of its fluence the gut flora composition, as diet, age, therapeutic implications for several intestinal medications, illness, stress and lifestyle. The gas- and extra-intestinal diseases associated to dys- regulation of the immune system. trointestinal (GI) tract contains both “friendly” METHODS: Significant articles were identified bugs, such as Gram-positive Lactobacilli and Bi- by literature search and selected based on con- fidobacteria dominate (> 85% of total bacteria), tent, including atopic diseases, inflammatory and potential pathogenic bacteria, coexisting in a bowel diseases and treatment of these condi- complex symbiosis. Several evidences show that tions with probiotics. -
Mucosal Immunity
Mucosal Immunity Lloyd Mayer, MD ABSTRACT. Food allergy is the manifestation of an antibody, secretory immunoglobulin A (sIgA), which abnormal immune response to antigen delivered by the is highly suited for the hostile environment of the gut oral route. Normal mucosal immune responses are gen- (Fig 1). All of these in concert eventuate in the im- erally associated with suppression of immunity. A nor- munosuppressed tone of the gastrointestinal (GI) mal mucosal immune response relies heavily on a num- tract. Defects in any individual component may pre- ber of factors: strong physical barriers, luminal digestion dispose to intestinal inflammation or food allergy. of potential antigens, selective antigen sampling sites, and unique T-cell subpopulations that effect suppres- sion. In the newborn, several of these pathways are not MUCOSAL BARRIER matured, allowing for sensitization rather than suppres- The mucosal barrier is a complex structure com- sion. With age, the mucosa associated lymphoid tissue posed of both cellular and noncellular components.5 matures, and in most individuals this allows for genera- Probably the most significant barrier to antigen entry tion of the normal suppressed tone of the mucosa asso- into the mucosa-associated lymphoid tissue (MALT) ciated lymphoid tissue. As a consequence, food allergies are largely outgrown. This article deals with the normal is the presence of enzymes starting in the mouth and facets of mucosal immune responses and postulates how extending down to the stomach, small bowel, and the different processes may be defective in food-allergic colon. Proteolytic enzymes in the stomach (pepsin, patients. Pediatrics 2003;111:1595–1600; gastrointestinal papain) and small bowel (trypsin, chymotrypsin, allergy, food allergy, food hypersensitivity, oral tolerance, pancreatic proteases) perform a function that they mucosal immunology. -
Defective Expression of Gp180, a Novel CD8 Ligand on Intestinal Epithelial Cells, in Inflammatory Bowel Disease
Defective Expression of gp180, a Novel CD8 Ligand on Intestinal Epithelial Cells, in Inflammatory Bowel Disease Lisa S. Toy,*‡ Xian Yang Yio,* Annica Lin,* Shaun Honig,* and Lloyd Mayer* *Division of Clinical Immunology and the ‡Dr. Henry D. Janowitz Division of Gastroenterology, Mount Sinai Medical Center, New York 10029 Abstract active inflammation in an organ where controlled inflamma- tion is the norm. Work from several laboratories has sup- Previous studies support a role for intestinal epithelial cells ported the concept that this active inflammatory process is the (IEC) as antigen-presenting cells in mucosal immune re- result of a dysregulated immune response. More specifically, sponses. T cells activated by IEC are CD8ϩ, suppressor in there is evidence of constitutively activated CD4ϩ T cells function, and dependent upon CD8-associated p56lck acti- within the lamina propria that can leak into the systemic circu- vation. A 180-kD glycoprotein (gp180) recognized by mAbs lation (1, 2). These activated CD4ϩ T cells secrete a panel of B9 and L12 has been identified and shown to be important cytokines that may promote localized cell-mediated granulo- in CD8ϩ T cell activation by IEC. Since IEC derived from matous inflammation (CD) (3–6) or a more diffuse antibody- patients with inflammatory bowel disease (IBD) are incapa- and complement-mediated Arthus-type reaction (UC) (7, 8). ble of activating CD8ϩ T cells, we asked whether this corre- While many pathogenetic mechanisms have been proposed to lated with gp180 expression. While frozen sections of nor- explain these observations, to date no consistent infectious, mal bowel revealed bright gp180 staining on all IEC, both neurohormonal, or immunologic mechanism has been eluci- inflamed and uninflamed ulcerative colitis (UC) specimens dated. -
Terminology: Nomenclature of Mucosa-Associated Lymphoid Tissue
nature publishing group ARTICLES See COMMENTARY page 8 See REVIEW page 11 Terminology: nomenclature of mucosa-associated lymphoid tissue P B r a n d t z a e g 1 , H K i y o n o 2 , R P a b s t 3 a n d M W R u s s e l l 4 Stimulation of mucosal immunity has great potential in vaccinology and immunotherapy. However, the mucosal immune system is more complex than the systemic counterpart, both in terms of anatomy (inductive and effector tissues) and effectors (cells and molecules). Therefore, immunologists entering this field need a precise terminology as a crucial means of communication. Abbreviations for mucosal immune-function molecules related to the secretory immunoglobulin A system were defined by the Society for Mucosal Immunolgy Nomenclature Committee in 1997, and are briefly recapitulated in this article. In addition, we recommend and justify standard nomenclature and abbreviations for discrete mucosal immune-cell compartments, belonging to, and beyond, mucosa-associated lymphoid tissue. INTRODUCTION for dimers (and larger polymers) of IgA and pentamers of It is instructive to categorize various tissue compartments IgM was proposed in 1974. 3,4 The epithelial glycoprotein involved in mucosal immunity according to their main function. designated secretory component (SC) by WHO in 1972 However, until recently, there was no consensus in the scientific (previously called “ transport piece ” or “ secretory piece ” ) turned community as to how these compartments should be named and out to be responsible for the receptor-mediated transcytosis classified. This lack of standardized terminology has been particu- of J-chain-containing Ig polymers (pIgs) through secretory larly confusing for newcomers to the mucosal immunology field. -
1 Polysaccharide A-Dependent Opposing Effects of Mucosal and Systemic Exposures to Human Gut Commensal Bacteroides Fragilis in T
Page 1 of 44 Diabetes Polysaccharide A-dependent opposing effects of mucosal and systemic exposures to human gut commensal Bacteroides fragilis in type 1 diabetes M. Hanief. Sofi1, Benjamin M. Johnson1, Radhika R. Gudi1, 1, Amy Jolly1, Marie-Claude Gaudreau1, and Chenthamarakshan Vasu1,3 1Microbiology and Immunology, College of Medicine, Medical University of South Carolina, Charleston, SC-29425 3Surgery, College of Medicine, Medical University of South Carolina, Charleston, SC-29425 Running title: Bacteroides fragilis in type 1 diabetes. 5Address Correspondence: Chenthamarakshan Vasu Microbiology and Immunology Medical University of South Carolina 173 Ashley Avenue, BSB208E Charleston, SC-29425 Phone: 843-792-1032, Fax: 843-792-9588 Email: [email protected] 1 Diabetes Publish Ahead of Print, published online July 16, 2019 Diabetes Page 2 of 44 Abstract Bacteroides fragilis (BF) is an integral component of the human colonic commensal microbiota. BF is also the most commonly isolated organism from clinical cases of intra-abdominal abscesses suggesting its potential to induce pro-inflammatory responses, upon accessing the systemic compartment. Hence, we examined the impact of mucosal and systemic exposures to BF on type 1 diabetes (T1D) incidence in non-obese diabetic (NOD) mice. The impact of intestinal exposure to BF under chemically-induced enhanced gut permeability condition, which permits microbial translocation, in T1D was also examined. While oral administration of pre- diabetic mice with heat-killed (HK) BF caused enhanced immune regulation and suppression of autoimmunity resulting in delayed hyperglycemia, mice that received HK BF by i.v. injection showed rapid disease progression. Importantly, polysaccharide-A deficient (ΔPSA) BF failed to produce these opposing effects upon oral and systemic deliveries. -
Lack of Induction of Suppressor T Cells by Intestinal Epithelial Cells from Patients with Inflammatory Bowel Disease
Lack of induction of suppressor T cells by intestinal epithelial cells from patients with inflammatory bowel disease. L Mayer, D Eisenhardt J Clin Invest. 1990;86(4):1255-1260. https://doi.org/10.1172/JCI114832. Research Article The mechanisms underlying the chronic unrelenting inflammatory response seen in inflammatory bowel disease (IBD) are poorly understood. We have recently proposed a novel role for the normal intestinal enterocyte, that of antigen presenting cell. However, in contrast to conventional antigen presenting cells, normal enterocytes appear to selectively activate CD8+ antigen nonspecific suppressor T cells. To determine whether failure of this process may be occurring in inflammatory bowel disease, freshly isolated enterocytes from small and large bowel from normal patients, patients with Crohn's disease, ulcerative colitis, and inflammatory (diverticulitis, ischemic colitis, and gold induced colitis) controls were co-cultured with allogeneic T cells in a modified mixed lymphocyte reaction. In contrast to normal enterocytes, 42/42 Crohn's and 35/38 ulcerative colitis-derived epithelial cells stimulated CD4+ T cells, whereas 65/66 and 9/9 normal and inflammatory control enterocytes, respectively, stimulated CD8+ T cells (as previously described), suggesting that the results seen were not just a reflection of underlying inflammation. Furthermore, IBD enterocytes from both histologically involved and uninvolved tissue were similar in their ability to selectively activate CD4+ T cells, speaking for a more global defect in -
The Future of Mucosal Immunology: Studying an Integrated System-Wide Organ
cOmmEntARY The future of mucosal immunology: studying an integrated system-wide organ Navkiran Gill, Marta Wlodarska & B Brett Finlay Over the next 10 years, it will be important to shift the focus of mucosal immunology research to make further advances. Examination of the mucosal immune system as a global organ, rather than as a group of individual components, will identify and characterize relationships between mucosal sites. he term ‘common mucosal immunological Tsystem’ was coined by John Bienenstock a nearly 40 years ago. He suggested the con- cept when the bronchus-associated lymphoid tissues his group described were found to be Oral Airway epithelium Antigen epithelium similar to those in the gastrointestinal tract. Fibroblasts Ironically, appreciation of the importance of Smooth muscle T 2T this term is only now truly beginning. Since H reg Treg DC then, the mucosal immune system has received MHC B B Mast cell a great deal of attention and is described as an integrated network of tissues, cells and effector Cervical AMPs Lumen molecules that protect the host from infection Virus epithelium b Intestinal and environmental insult at mucous membrane epithelium Health Disease surfaces. Mucosal surfaces are immunologically Goblet cell Signals Microbial unique, as they act as the primary interface TH2 T 1 H B cell community between the host and the physical environ- T cell T 17 © 2010 Nature America, Inc. All rights reserved. All rights Inc. America, Nature © 2010 H ment yet also have key barrier functions. It Treg has become increasingly evident that mucosal surfaces are also the main sites of interaction IEC- Mucins between the host and its associated commen- Tolerance Inflammation associated microbial Lamina sal microbial community. -
Vaccines for Mucosal Immunity to Combat Emerging Infectious Diseases
Synopses Vaccines for Mucosal Immunity to Combat Emerging Infectious Diseases Frederik W. van Ginkel, Huan H. Nguyen, and Jerry R. McGhee The University of Alabama at Birmingham, Birmingham, Alabama, USA The mucosal immune system consists of molecules, cells, and organized lymphoid structures intended to provide immunity to pathogens that impinge upon mucosal surfaces. Mucosal infection by intracellular pathogens results in the induction of cell- mediated immunity, as manifested by CD4-positive (CD4+) T helper-type 1 cells, as well as CD8+ cytotoxic T-lymphocytes. These responses are normally accompanied by the synthesis of secretory immunoglobulin A (S-IgA) antibodies, which provide an important first line of defense against invasion of deeper tissues by these pathogens. New- generation live, attenuated viral vaccines, such as the cold-adapted, recombinant nasal influenza and oral rotavirus vaccines, optimize this form of mucosal immune protection. Despite these advances, new and reemerging infectious diseases are tipping the balance in favor of the parasite; continued mucosal vaccine development will be needed to effectively combat these new threats. Behavioral changes in the human host may would most likely be prevalent under current be contributing to the emergence of new diseases. conditions. Pathogens in this category include Perhaps emerging pathogens become resistant to respiratory viruses, for example, influenza virus. antibiotics or (through genetic recombination) Another group includes sexually transmitted become more resistant to host defenses. disease (STD) pathogens, for example, HIV. The Recombination events or lack of exposure can fact that a) pneumonia and influenza virus and b) result in loss of immunity of the population to the HIV infection were listed as the leading causes of pathogen, as has been well documented with death (ranked number 6 and 8, respectively) by influenza virus. -
The Henry Kunkel Society Annual Meeting: Infectious Disease Susceptibility and the Expanding Universe of Primary Immunodeficiency
The Henry Kunkel Society Annual Meeting: Infectious Disease Susceptibility and the Expanding Universe of Primary Immunodeficiency The Rockefeller University New York, NY April 17–20, 2013 Henry George Kunkel 1916–1983 enry Kunkel received his B.S. degree from Princeton and his M.D. degree from Johns Hopkins University. He arrived at The Rockefeller Institute (now University) in 1945 where he spent his entire scientific career H until his death in 1983. His contributions to the field of basic and clinical immunology are legendary. He made numerous seminal observations in liver disease, rheumatic diseases and other allied disorders. He was perhaps best known for his pioneering and extensive studies on the immunoglobulins. His recognition that myeloma proteins were a model for the study of the structure of normal immunoglobulins had a global impact on investigations of the structure, function and inheritance of these molecules. The elucidation of the chain structure of gamma globulin and the recognition that immunoglobulins possessed individual antigenic specificity (idiotypes) were internationally recognized discoveries. Dr. Kunkel was the recipient of many awards and honors, including membership in the National Academy of Sciences, honorary degrees from Universities of Uppsala and Harvard, and recipient of the Lasker and Gairdner Awards and the Kovalenko Medal of the National Academy of Sciences. Henry Kunkel Society Officers Henry Kunkel Society Lecturers President ................Westley Reeves 1992. Louis Kunkel 2003. .Fred Rosen Vice President ...............Keith Elkon 1993. .David Ho 2004. .Diane Mathis Secretary ........... Michel Nussenzweig 1994. Benvenuto Pernis 2005. Charles Weissman Treasurer ...............Anne Marshak- 1996. Jeffrey Ravetch 2006. Ralph M. Steinman Rothstein 1997. Anthony Fauci 2007.