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* Immune System Basics Immunity: The capacity to resist infectious pathogens. Pathogens: Disease-causing organisms Self vs. Non-self recognition Major.

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Presentation on theme: "* Immune System Basics Immunity: The capacity to resist infectious pathogens. Pathogens: Disease-causing organisms Self vs. Non-self recognition Major."— Presentation transcript:

1 * Immune System Basics Immunity: The capacity to resist infectious pathogens. Pathogens: Disease-causing organisms Self vs. Non-self recognition Major Histocompatibility Complex (MHC 1) Antigen- a particle or piece of pathogen the immune system recognizes as foreign. MHC 1 Antigens

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3 * 1st defense: Non-Specific Immune System Its your first line of defense Called “non-specific” since it works the same regardless of threat- Does not need to identify/know the pathogen. Made of three general parts: – 1. Barrier Defenses – 2.Inflammatory Defenses – 3. Cellular and Molecular Defenses

4 * Non-Specific Defenses 1.Barrier Defenses: Skin: 20m 2 of skin shields your internal systems from pathogens. Probably the single most important way your body avoids infection. Ex- patients will severe burns usually die of infection without their skin to serve as a barrier Mucous membranes: Areas w/o skin are vulnerable to infection, but still covered by a sticky mucous barrier- ex. Lungs, eyes, nose, genital opening all produce mucous coatings

5 2. Inflammatory Defenses: Histamines: If barrier defense is breached, a signaling molecule called histamine is released at the site of damage. Histamine increases blood flow to area and causes fluids and white blood cells to leak into the area- white blood cells (WBC’s) are designed to destroy invading pathogens For these reasons, release of histamine in an area causes redness, swelling, fluid release, and itchiness. Does that sound like an allergy???? Allergies are your bodies reaction to a perceived breach of mucous membranes. Ex- pollen grains embed in your nose and eyes- your body releases histamine. What do you think anti-histamine medications do?

6 3.Cellular and Molecular Defenses: Macrophages: -White blood cells that use pocket transport (phagocytosis) to destroy foreign particles. Natural Killer Cells (NK): Release enzymes onto target cells to rupture/destroy them. Interferon: A chemical released by cells already infected with viruses that helps other cells resist infection. Complement: Groups of proteins floating throughout the blood stream that stick to foreign particles and prevent them from infecting cells.

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8 * Final Defense: Specific Immune System Recognizes pathogens and develops a sustained immune response. Comprised of two parts: 1.Cell- Mediated Response 2.Humoral Response White blood cells characters (lymphocytes): Macrophage Helper T cells (T h ) Killer T cells (T c ) B cells

9 * Specific Immunity- The Battle Begins! * Macrophages search body tissues for pathogens. * Consume pathogens with phagocytosis, kill it with lysosomes, and save the antigens. * Antigens placed into MHC 2 receptors and displayed on macrophage’s membrane. * The macrophage is now considered an antigen- presenting cell (APC). *

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11 * Specific Immunity Cont. * Macrophage chemically signals Helper T to attach to it. * Helper T attaches to the MHC 2 receptor (with foreign antigen stuck in it) with its CD4 receptor. * Helper T cells have incredible variety of receptors that act like a “lock and key” in regards to the displayed antigen. * If the Helper T’s “key” fits the displayed antigen’s “lock”, the Helper T is activated. * Activation results in Helper T releasing cytokines (ex. Interleukin)- chemicals that cause lymphocytes to start mitosis.

12 Fig Antigen- presenting cell Peptide antigen Cell-mediated immunity (attack on infected cells) Class II MHC molecule CD4 TCR (T cell receptor) Helper T cell Humoral immunity (secretion of antibodies by plasma cells) Cytotoxic T cell Cytokines B cell Bacterium

13 * Cell-Mediated Response Seek and Destroy * Body cells can be infected by viruses that will hide inside the cell. * As the virus reproduces inside cells, pieces of it fall off and are put into new MHC 1 receptors that the cell puts on its own membrane. * Killer T cells can bind to an infected cell’s MHC 1 receptors with their CD8 receptors. * If Killer T binds to MHC 1 receptors with antigen attached, it releases a chemical called perforin. * Perforin ruptures the infected cells membrane and exposes the virus to other immune cells. ure=related ure=related

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16 Fig Antigen Top view: binding surface exposed to antigen receptors Plasma membrane of infected cell Antigen Class I MHC molecule

17 Fig Cytotoxic T cell Perforin Granzymes TCR CD8 Class I MHC molecule Target cell Peptide antigen Pore Released cytotoxic T cell Dying target cell

18 Fig Infected cell Antigen fragment Class I MHC molecule T cell receptor (a) Antigen associates with MHC molecule T cell recognizes combination Cytotoxic T cell(b)Helper T cell T cell receptor Class II MHC molecule Antigen fragment Antigen- presenting cell Microbe

19 * Humoral System Bring in the artillery! B cells have receptors called antibodies (100,000/cell). Different B cells have uniquely shaped antibodies that match specific antigens. If a B cell’s antibody is able to bind with a specific antigen (lock and key effect), the B cell receives a message from Helper T’s to become activated. Activated B cells divide into Plasma B and Memory B cells. U&feature=related U&feature=related

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21 * Humoral System Cont. Plasma B cells produce and secrete 10,000 “keyed” antibodies per hour. Due to their shape, each can bind to several antigens at once. Antigen/Antibody binding has three effects. Neutralization Macrophage signaling Complement pore formation w w

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23 Fig Viral neutralization Virus Opsonization Bacterium Macrophage Activation of complement system and pore formation Complement proteins Formation of membrane attack complex Flow of water and ions Pore Foreign cell

24 * Memory B cells These cells do not actively produce antibodies Instead, they remain in the bloodstream and maintain their cell life cycle independently from T h commands. If the same pathogen/antigen complex presents itself in the future, these cells are already activated and ready to produce antibodies. There are also Memory versions of T h and T c cells that serve a similar function.


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