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OVERVIEW OF THE IMMUNE SYSTEM. & TYPES OF IMMUNITY

OVERVIEW OF THE IMMUNE SYSTEM. & TYPES OF IMMUNITY. BY: ABIBAT ADEOLA DAUDA ROLL NO: 623. INTRODUCTION. The main function of the immune system is to prevent or limit infections by microorganisms such as bacteria, viruses, fungi, and parasites .

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OVERVIEW OF THE IMMUNE SYSTEM. & TYPES OF IMMUNITY

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  1. OVERVIEW OF THE IMMUNE SYSTEM.& TYPES OF IMMUNITY BY: ABIBAT ADEOLA DAUDA ROLL NO: 623

  2. INTRODUCTION • The main function of the immune system is to prevent or limit infections by microorganisms such as bacteria, viruses, fungi, and parasites. • The first line of defense against microorganisms is the intact skin and mucous membranes. • If microorganisms breach this line and enter the body, then the innate arm of the immune system (second line of defense) is available to destroy the invaders. • Highly specific protection is provided by the acquired arm of the immune system (third line of defense).

  3. INNATE IMMUNITY • ACQUIRED (ADAPTIVE) IMMUNITY • a. humoraland • b. cell mediated immunity

  4. INNATE IMMUNITY • This is resistance that exists prior to exposure to the microbe (antigen). It is nonspecific and includes : • Keratin layer of intact skin • Acts as mechanical barrier • Lysozyme in tears and other secretions • Degrades peptidoglycan in bacteria cell wall • Respiratory cilia • Elevate mucus-containing trapped organisms • Low pH in stomach and vagina; fatty acids in skin • Retards growth of microbes • Natural killer cells • Kill virus-infected cells • Neutrophils • Ingest and destroy microbes • Macrophages and dendritic cells • Ingest and destroy microbes, and present antigen to helper T cells

  5. Two major functions of innate immunity • killing invading microbes and • activating acquired (adaptive) immune processes. neutrophils, only kill microbes, whereas others, such as macrophages and dendritic cells, perform both functions,

  6. MECHANISM OF ACTION • Components of the innate arm have receptors called pattern-recognition receptors. An example of this pattern recognition are: • 1. The lipid A portion of LPS combines with LPS-binding protein- This binding protein transfers LPS to a receptor on the surface of macrophages called CD14. • LPS then stimulates toll-like receptor 4 (TLR4), which • transmits a signal to the nucleus of the cell. • This induces the production of cytokines, such as IL-1, IL-6, IL-8, and tumor necrosis factor (TNF),protein, B7, which is required to activate helper T cells and to produce antibodies.

  7. . A pattern-recognition receptor called mannan-binding lectin (MBL) binds to the mannan on the surface of the microbes, which then activates complement resulting in death of the microbe. • MBL is a normal serum protein whose concentration in the plasma is greatly increased during the acute-phase response. C reactive protein level is increased too.

  8. PATHOGENESIS • Children with severe combined immunodeficiency disease (SCID), who have intact innate immunity but no acquired immunity, suffer from repeated, life-threatening infections. • Therefore, innate immunity is often successful in eliminating microbes and preventing infectious diseases, it is, in the long run, not sufficient for human survival.

  9. ACQUIRED IMMUNITY • There are two components of acquired immunity: • Cell –mediated immunity • Humoral immunity • The cell-mediated immunity includes: • 1. Helper T cells and macrophages (IC bacteria, fungi) • 2. cytotoxic T cells (viruses) • Humoral immunity has its main defense against extracellular bacteria, toxins, virus.

  10. CELL MEDIATED IMMUNITY • Antigen presenting cells e.g macrophages recognize the bacteria. • The bacterium is broken down, and fragments of it called antigens or epitopes appear on the surface of the macrophage in association with class II major histocompatibility complex (MHC) proteins. • The antigen–class II MHC protein complex interacts with TCR (T cell receptor) • IL-1 produced by macrophages activate T cells while IL-2 produced by T lymphocytes leads to clonal proliferation of TH2. • .

  11. Cytotoxic T lymphocytes are also specific effectors of the cellular immune response • Viral envelope glycoproteins appear on the surface of the infected cell in association with class I MHC proteinswhich is present in every nucleated cell of the body.

  12. HUMORAL IMMUNITY • Antibody synthesis typically involves the cooperation of three cells: macrophages, helper T cells, and B cells.

  13. T CELL INDEPENDENT ANTIGENS: • Only IgM is produced by B cells because it requires interleukins 4 and 5 made by the helper T cell for the B cell to "class switch" to produce IgG, IgA, and IgE.

  14. ACTIVE IMMUNITY • Active immunity is resistance induced after contact with foreign antigens, e.g., microorganisms. This contact may consist of clinical or subclinical infection, immunization with live or killed infectious agents or their antigens, or exposure to microbial products (e.g., toxins and toxoids). • The main advantage of active immunity is that resistance is long-term. • Its major disadvantage is its slow onset, especially the primary response.

  15. PASSIVE IMMUNITY • Passive immunity is resistance based on antibodies preformed in another host. • The main advantage of passive immunization is the prompt availability of large amounts of antibody; • disadvantagesare the short life span of these antibodies and possible hypersensitivity reactions if globulins from another species are used.

  16. AGE & IMMUNE RESPONSE • The reason for the relatively poor immune response in newborns is unclear, but newborns appear to have less effective T-cell function than do adults. In newborns, antibodies are provided primarily by the transfer of maternal IgG across the placenta. • Because maternal antibody decays over time (little remains by 3–6 months of age), the risk of infection in the child is high. Colostrum also contains antibodies, especially secretory IgA, which can protect the newborn against various respiratory and intestinal infection. • In the elderly, immunity generally declines. There is a reduced IgG response to certain antigens, fewer T cells, and a reduced delayed hypersensitivity response..

  17. ANTIGENS vsIMMUNOGENS

  18. TAKE HOME POINT • Antigens are molecules that react with antibodies, whereas immunogens are molecules that induce an immune response. In most cases, antigens are immunogens, and the terms are used interchangeably. • However, there are certain important exceptions, e.g., haptens.

  19. A hapten is a molecule that is not immunogenic by itself but can react with specific antibody. Haptens are usually small molecules. Many drugs, e.g., penicillins, are haptens, and the catechol in the plant oil that causes poison oak and poison ivy is a hapten. • Haptens are not immunogenic because they cannot activate helper T cells. The failure of haptens to activate is due to their inability to bind to MHC proteins; they cannot bind because they are not polypeptides but polysaccharides. • They can only stimulate antibody production when covalently bound to a "carrier" protein . In this process, the hapten interacts with an IgM receptor on the B cell and the hapten-carrier protein complex is internalized.

  20. Many drugs that cause allergic reactions, such as penicillin, act as haptens. When injected or ingested, penicillin reacts chemically with proteins in the body to form a hapten-carrier complex that can lead to the life-threatening anaphylaxis.

  21. REFERENCES • Review of medical microbiology and immunology • Lindquester, Gary J. (2006) Introduction to the History of disease. Disease and Immunity, Rhodes College. • ^ Jump up to: a b c d e f g Silverstein, Arthur M. (1989) History of Immunology (Hardcover) Academic Press. Note: The first six pages of this text are available online at: (Amazon.com easy reader) • ^ Jump up to: a b c d e f g Gherardi E. The Concept of Immunity. History and Applications. Immunology Course Medical School, University of Pavia. • Jump up ^ A "al-Razi." 2003 The Columbia Electronic Encyclopedia, Sixth Edition. Columbia University Press (from Answers.com, 2006.) • ^ Jump up to: a b c Maleissye J (1991). Histoire Du Poison. Paris: Francois Bourin, ISBN 2-87686-082-1 (in French. Translated in Japanese: Hashimoto I, Katagiri T, translators (1996). [History of Poison]. Tokyo: Shin-Hyoron, Ltd., ISBN 4-7948-0315-X C0020).

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