BMS 251 Ch. 22
BMS 251 Ch. 22 BMS 251-20
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JOUR 201 001
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This 13 page Class Notes was uploaded by Claire Neville on Thursday February 25, 2016. The Class Notes belongs to BMS 251-20 at Grand Valley State University taught by Dr. Tara Alger in Winter 2016. Since its upload, it has received 33 views. For similar materials see Anatomy & Physiology II in Biomedical Sciences at Grand Valley State University.
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Date Created: 02/25/16
Chapter 22 Immune System Immune System • Protects us from infectious agents and harmful substances o Typically without our awareness • Composed of numerous cellular and molecular structures • Function dependent on specific type of infectious agent 22.1 Overview of Diseases-‐ Caused by Infectious Agents • Infectious agents can damage or kill a host o Pathogenic agents are ones that cause harm o Five major categories: § Bacteria § Viruses § Fungi § Protozoans § multicellular parasites • Bacteria: single-‐celled prokaryotes o Small (1 to 2 µm) cell with both a membrane and a cell wall o Varied types: spherical (cocci), rodlike (bacilli), or coiled (spirilla) o Most bacteria harmless; some virulent (cause serious illness) § Examples of virulent bacteria: Clostridium tetani (tetanus), streptococcal bacteria (strep throat) • Viruses: pieces of DNA or RNA in a protein shell o Viruses are not cells—they are much smaller § Only about one-‐hundredth of a micrometer o Obligate intracellular parasites § Virus must enter a cell to reproduce § Direct infected cell to make copies of nucleic acid and capsid (shell) § The virus or immune response may kill the host cell o E.g., common cold, ebola, chickenpox • Fungi: eukaryotic cells with membrane and cell wall o Include molds, yeasts, multicellular fungi that produce spores o Release proteolytic enzymes inducing inflammation o Cause superficial diseases in the integument (e.g., athletes foot) o Can infect mucosal linings (e.g., vaginal yeast infections) or cause internal infections (e.g., histoplasmosis) • Protozoans: eukaryotic cells without a cell wall o Intracellular and extracellular parasites o Disease examples: malaria and trichomoniasis • Multicelluar parasite are nonmicroscopic o Take nourishment from host they live in o E.g., tapeworm • Prions: fragments of infectious proteins o Neither cells nor viruses o Cause disease in nervous tissue o E.g., Variant Creutzfeldt-‐Jakob disease (“mad cow”)-‐ in humans § Can be spread from cows to human by consuming infected meat • Cancer o Immune system is on alert for cancer cells o Still an infection agent! 22.2a Immune Cells and Their Locations • Leukocytes (WBC) o Formed in red bone marrow o Granulocytes: neutrophils, eosinophils, basophils o Monocytes § Become macrophages when they leave blood and enter tissues o Lymphocytes § B-‐lymphocytes, T-‐lymphocytes, NK (natural killer) cells • Structures that house immune system cells o Most leukocytes are in body tissues (instead of blood) o Lymphatic tissue-‐ secondary structures § T-‐ and B-‐lymphocytes, macrophages, dendritic cells, and NK cells housed in lymph nodes, spleen, tonsils, MALT, lymphatic nodules o Select organs house macrophages § May be permanent residents of the organ, or migrating macrophages • Structures that house immune system cells (continued) o Dendritic cells § Located in Epithelial layers of skin and mucosal membranes § These dendritic cells are usually derived from monocytes § Engulf pathogens and migrate into lymph o Mast cell § Located in connective tissue § Mast cells typically in close proximity to small blood vessels § Abundant in dermis and mucosa of respiratory, GI, and urogenital tracts § Also found in connective tissue of organs (e.g., endomysium of muscle) 22.2b Cytokines • Cytokines: small proteins that regulate immune activity o Produced by cells of both innate and adaptive immune system o Chemical messengers released from one cell that bind to receptors of target cells o Effects § Signaling cells § Controlling development and behavior of immune cells § Regulating inflammatory response § Destroying cells • Cytokine examples o Interferons: targeting pathogens and triggering the immune defense § E.g., IFN-‐α o Colony-‐stimulating factor (CSF): development and differentiation of all blood cells § E.g., granulocyte CSF, GM-‐CSF 22.2c Comparison of Innate Immunity and Adaptive Immunity • Two types of immunity differ based on o Cells involved o Specificity of cell response o Mechanisms of eliminating harmful substances o Amount of time for response • Although innate and adaptive immunities are distinct, they work together in body defense • Innate immunity: present at birth o Protects against variety of different substances (nonspecific) § No prior exposure to substance necessary o Includes barriers of skin and mucosal membranes, nonspecific cellular and molecular internal defenses o Respond immediately to potentially harmful agents • _Adaptive immunity_: acquired immunity o Response to antigen involves specific T-‐ and B-‐lymphocytes § These cells are then specific for what they will target (only certain antigens) o Takes several days to be effective 22.3 Innate Immunity • Characteristics of innate immunity o Prevents entry of potentially harmful substances o Responds nonspecifically to a range of harmful substances o First line of defense is skin and mucosal membrane o Second line of defense involves internal processes § Cells: • neutrophils, macrophages, dendritic cells, eosinophils, basophils, and NK cells § Chemicals: • interferon and complement § Processes: • inflammation and fever 22.3a Preventing Entry • Few microbes can penetrate intact skin o Physical barrier of epidermis and dermis o Skin releases antimicrobial substances § lysozyme, sebum, o Has normal nonpathogenic flora (microorganisms) § Help prevent growth of pathogenic microorganisms • Mucosal membranes line body openings o Produce mucin and release antimicrobial substances § Defensins, lysozyme, IgA o Lined by harmless bacteria that suppress growth of more virulent types 22.3b Cellular Defenses • Neutrophils, macrophages, and dendritic cells o Cells of innate immunity that engulf unwanted substances by phagocytosis o Neutrophils and _macrophages_ destroy engulfed particles § Intake vesicle fuses with lysosome forming phagolysosome § Digestive enzymes break down the unwanted substances § Degraded residue is released by exocytosis o _dendritic cells_ destroy particles and then present fragments § Antigens are presented on dendritic cell surface to T-‐lymphocytes • Necessary for initiating adaptive immunity • Basophils and mast cells promote inflammation o Basophils circulate in the blood o Mast cells reside in connective tissue, mucosa, internal organs o They release granules containing chemicals § The chemicals increase movement of fluid from blood to injured tissue § They attract immune cells (are chemotactic) § Histamine increases vasodilation and capillary permeability § Heparin acts as an anticoagulant o Eicosanoids released from their plasma membrane also increase inflammation • Natural Killer cells destroy a variety of unwanted cells o “NK cells” form in bone marrow, circulate in blood, and accumulate in secondary lymphatic structures § Perform immune surveillance—patrol the body detecting unhealthy cells o They destroy virus-‐infected cells, bacteria-‐infected cells, tumor cells, cells of transplanted tissue o They kill by releasing cytotoxic chemicals § Perforin creates a transmembrane pore in unwanted cell § Granzymes enter pore and cause apoptosis (death) of cell • Eosinophils attack multicellular parasites o Degranulate, release enzymes and other toxic substances § Can release proteins that form transmembrane pores in parasite’s cells o Participate in immune responses of allergy and asthma o Engage in phagocytosis of antigen-‐antibody complexes • 22.3c Antimicrobial Proteins • Antimicrobial proteins are molecules that function against microbes • Interferons: a class of cytokines that nonspecifically impede viral spread o IFN-‐a and IFN-‐b produced by leukocytes and virus-‐infected cells § Bind to neighboring cells and prevent their infection § Stimulate NK cells to destroy virus-‐infected cells • Complenment system: group of over 30 plasma proteins o Work along with (“complement”) antibodies o Identified with letter “C” and number (e.g., C2) o Synthesized by liver, continuously released in inactive form o Complement activation follows pathogen entry o Especially potent system against bacterial infections o 4 modes of action § Opsonization § Inflammation § Cytolysis § Elimination of immune complexes o Opsonization: complement protein (opsonin) binds to pathogen § Enhances likelihood of phagocytosis of pathogenic cell o Inflammation: is enhanced by complement § Activates mast cells and basophils § Attracts neutrophils and macrophages § Diapedsis and chemotaxis o Cytolysis: complement triggers splitting of target cell § Complement proteins form membrane attack complex (MAC) that creates channel in target cell’s membrane • Fluid enters, causing cell lysis o Elimination of immune complexes § Complement links antigen-‐antibody complexes to erythrocytes § Cells move to liver and spleen where complexes are stripped off 22.3d Inflammation • Inflammation: an immediate response to ward off unwanted substances o Local, nonspecific response of vascularized tissue to injury o Part of innate immunity • Events of inflammation o Injured tissue, basophils, mast cells, and infectious organisms (bacteria) release chemicals that initiate response § The chemicals include histamine, and chemotactic (chemical lure) factors o Released chemicals cause vascular changes § Vasodilation § Increased capillary permeability § Increased endothelial expression of molecules for leukocyte adhesion • Cell-‐adhesion molecules, CAMs o Recruitment of leukocytes § Margination adherence of leukocytes to endothelial CAMs § Diapedesis: cells escape blood vessel walls § Chemotaxis: leukocytes migrate toward chemicals released from damaged, dead, or pathogenic cells • Leukocytes release cytokines stimulating leukopoiesis in marrow • Macrophages may release pyrogens (fever-‐inducing molecules) o Delivery of plasma proteins to site § Immunoglobulins, complement, clotting proteins, and kinins § Clotting proteins form clots that wall off microbes • Effects of inflammation o Fluid moves from blood to injured or infected area § Liquid contains fluid, protein, and immune cells to eliminate pathogens and promote healing § Vasodilation brings more blood to the area § Loss of plasma proteins decreases capillary osmotic pressure, thus decreasing fluid reabsorption into blood § Extra fluid is taken up by lymphatic capillaries in the area (“washing”) • Carries away debris and allows lymph node monitoring of its contents o Within 72 hours, inflammatory response slows § Monocytes exit blood becoming macrophages § Macrophages eat bacteria, damaged host cells, dying neutrophils § Tissue repair begins as fibroblasts form new connective tissue • Cardinal signs of inflammation o Redness from increased blood flow o Heat from increased blood flow and increased metabolic activity within the area o Swelling from increase in fluid loss from capillaries o Pain from stimulation of pain receptors o Loss of function from pain and swelling in severe cases • Duration of acute inflammation: about 8 to 10 days 22.3e Fever • Fever (pyrexia): abnormal body temperature elevation o 1°C or more from normal (37°C) o Results from the release of pyrogens (e.g., IL-‐1) from immune cells or infectious agents • Events of fever o Pyrogens circulate through blood and target hypothalamus o Hypothalamus raises temperature set point leading to fever o Fever stages: onset, stadium, and defervescence o Onset: temperature begins to rise § Hypothalamus stimulates dermis blood vessels to constrict (less heat loss) § Shivering of muscle generates more heat (may be in response to chills) o Stadium: elevated temperature is maintained § Metabolic rate increases to promote elimination of harmful substance § Liver and spleen bind zinc and iron thereby slowing microbial reproduction o Defervescence: time when temperature returns to normal § Hypothalamus no longer stimulated by pyrogens § Hypothalamus stimulates mechanisms to release heat • E.g., vasodilation of skin blood vessels, sweating • Benefits of fever o Inhibits reproduction of bacteria and viruses o Promotes interferon activity o Increases activity of adaptive immunity o Accelerates tissue repair o Increases CAMs on endothelium of capillaries in lymph nodes o Recommended to leave a low fever untreated • Risks of a high fever o High fevers potentially dangerous § 103ºF in children, slightly lower in adult o Changes in metabolic pathways and denaturation of proteins pose risks o Possible seizures o Irreversible brain damage at greater than 106ºF o Death likely if temperature greater than 109ºF 22.4 Adaptive Immunity: An Introduction • Adaptive immunity involves specific lymphocyte responses to an antigen o Contact with antigen causes lymphocyte proliferation o Immune response consists of lymphocytes and their products o Longer response time than innate immunity § Since it takes days to develop, adaptive immunity is considered the third line of body’s defense • Two branches of adaptive immunity o Cell-‐mediated immunity involving T-‐lymphocytes o Humoral immunity involving B-‐lymphocytes, plasma cells, and antibodies 22.4a Antigens • Pathogens are detected by lymphocytes because they contain antigens • Antigen: substance that binds a T-‐lymphocyte or antibody o Antigen is usually a protein or large polysaccharide o Examples of antigens § Protein capsid of viruses § Cell wall of bacteria or fungi § Bacterial toxins § Abnormal proteins or tumor antigens • Foreign antigens versus self-‐antigens o Foreign antigen differ from human body’s molecules § Bind body’s immune components o Self-‐antigen are body’s own molecules § Typically do not bind immune components o Immune system generally able to distinguish § However in autoimmune disorders the system reacts to self-‐antigens as if foreign • Antigenic determinant o Specific site on antigen recognized by immune system o Each has a different shape o Pathogenic organisms can have multiple determinants • Immunogen: antigen that induces an immune response • Immunogenicity: ability to trigger response § Increases with antigen’s degree of foreignness, size, complexity, or quantity • Haptens: small foreign molecules that induce immune response when attached to a carrier molecule in host o E.g., toxin in poison ivy o Account for hypersensitivity reactions § E.g., to drugs such as penicillin, pollen 22.4b General Structure of Lymphocytes • T-‐ and B-‐lymphocytes have unique Receptor complexes o About 100,000 per cell o Each complex binds one specific antigen o TCR (T-‐cell receptor) is antigen receptor of T-‐lymphocyte o BCR (B-‐cell receptor) is antigen receptor of B-‐lymphocyte 22.4b General Structure of Lymphocytes • Lymphocyte contact with antigen o B-‐lymphocytes make direct contact with antigen o T-‐lymphocytes have antigen presented by some other cell § Antigen is processed and presented by another cell type § T-‐lymphocyte coreceptors (e.g., CD proteins) facilitate the interaction • T-‐lymphocyte subtypes o Helper T-‐Lymphocytes are CD4+ cells § Assist in cell-‐mediated, humoral, and innate immunity • E.g., activate NK cells and macrophages o Cytotoxic T-‐lymphocytes are CD8+ cells § Release chemicals that destroy other cells o Other types include memory T-‐cells 22.4c Antigen-‐Presenting Cells and MHC Molecules • Antigen Presentation: cells display antigen on plasma membrane o so T-‐cells can recognize it o Two categories of cells present antigens § All nucleated cells of the body § Antigen Presenting Cells (APCs) • Immune cells that present to both helper T-‐cells and cytotoxic T-‐cells • Include: dendritic cells, macrophages, B-‐lymphocytes o Requires attachment of antigen to Major Histocompatibility complex (MHC) § MHC is group of transmembrane proteins § MHC I is found on all nucleated cells § MHC I & II is found on APCs • Synthesis and display of MHC class I molecules on nucleated cells o MHC class I molecules § Have genetically determined structure that is unique to individual § Display fragments of proteins on the surface of the cell • If fragments are from endogenous proteins, immune system recognizes them as “self ” and ignores them • If fragments are from an infectious agent, immune system considers the antigen “nonself ” o Communicates to cytotoxic T-‐cells that they should destroy cell • Display of MHC class II molecules on professional antigen-‐presenting cells o MHC class II molecules § Exogenous antigens brought into cell through endocytosis § Phagosome merges with lysosome, forming phagolysosome § Substance digested into peptide fragments § Fragments “loaded” onto MHC class II molecules within vesicle § Vesicle merges with plasma membrane with antigen bound to MHC molecule • Provides means of communicating with helper T-‐lymphocytes 22.4d Overview of Life Events of Lymphocytes • Three main events in life of lymphocyte o Formation and maturation of lymphocytes § Occurs in primary lymphatic structures (red marrow and thymus) § Become able to recognize one specific foreign antigen o Activation of lymphocytes § In secondary lymphatic structures they are exposed to antigen and become activated § Replicate to form identical lymphocytes o Effector response: action of lymphocytes to eliminate antigen § T-‐lymphocytes migrate to site of infection § B-‐lymphocytes stay in secondary lymphatic structure (as plasma cells) • Synthesize and release large quantities of antibodies • Antibodies are transported to infection site through blood and lymph 22.5 Formation and Selection of Lymphocytes • Lymphocytes are formed in red marrow • They are then tested for immunocompetence o Immunocompetent cells bind and respond to antigen o Testing occurs during development and shortly after birth § Occurs in primary lymphatic structures 22.5a Formation of T-‐lymphocytes • T-‐lymphocytes originate in red bone marrow o Migrate to thymus as pre-‐T-‐lymphocytes to complete maturation o Initially have both CD4 and CD8 proteins o Possess unique, randomly produced TCR receptor o Each cell has its TCR “tested” through a process of selection § Whether it can bind MHC with antigen § Whether it binds only foreign (“nonself ”) antigen 22.5b Selection of T-‐lymphocytes • Thymic selection eliminates 98% of T-‐cells produced • Positive selection o Selects for the ability of T-‐cells to bind thymic epithelial cells with MHC molecules (those that can bind survive) • Negative selection o Tests ability of T-‐lymphocyte to NOT bind self-‐antigens (self-‐tolerance) o Thymic dendritic cells present self-‐antigens and T-‐cells that bind to them are destroyed 22.5c Differentiation and Migration of T-‐Lymphocytes • T-‐lymphocytes differentiate o Helper T-‐lymphocytes lose CD8 protein o Cytotoxic T-‐lymphocytes lose CD4 protein • T-‐lymphocytes migrate from thymus to secondary lymphatic structures o They are immunocompetent o Naïve T-‐lymphocyte not yet exposed to antigens they recognize 22.6 Activation and Clonal Selection of Lymphocytes • Clonal Selection: forming clones in response to an antigen o All formed cells have same TCR or BCR that matches specific antigen • Antigen Selection: first encounter between antigen and lymphocyte o Usually occurs in secondary lymphatic structures § Antigen in blood taken to spleen § Antigen penetrating skin transported to lymph node § Antigen from respiratory, GI, urogenital tracts, in tonsils or MALT 22.6a Activation of T-‐Lymphocytes • Activation of helper T-‐lymphocytes o First Signal: direct contact with MHC molecule of APC § APC presents exogenous antigen with MHC class II molecules § Occurs in secondary lymphatic structure § Specific TCR site of T-‐cell binds to antigen peptide fragment • Interaction stabilized by CD4 molecule of helper T-‐lymphocyte § If it doesn’t recognize antigen, T-‐cell disengages quickly § If it does recognize antigen, contact lasts several hours • Activation of helper T-‐lymphocytes (continued) o Second Signal § Other receptors of APC and T-‐cell interact § Helper T-‐cell secretes interleukin-‐2, stimulating itself § Helper T-‐cells proliferate forming clones of helpers T-‐cells (with same TCR) • Some cells become activated helper T-‐lymphocytes that continue to produce IL-‐2 • Some cells become memory helper T-‐lymphocytes, available for future encounters 22.6b Activation of B-‐Lymphocytes • B-‐lymphocytes need to be activated, but can respond to antigens outside of cells o First signal § Intact antigen binds to BCR, cross-‐linking 2 BCRs § Stimulated B-‐cell engulfs, processes, and presents antigen to helper T-‐cell for recognition o Second signal § Activated helper T-‐cell releases IL-‐4, stimulating B-‐lymphocyte • B-‐lymphocyte activation o Causes B-‐lymphocytes to proliferate and differentiate o Most differentiate into Plasma Cells that produce antibodies o Remainder become memory B-‐lymphocytes § Retain BCRs and activate with reexposure to same antigen § Have much longer life span than plasma cells o In some cases activation occurs without T-‐cells § But production of memory B-‐cells and various antibodies requires helper T-‐cell involvement in activation 22.6c Lymphocyte Recirculation • Lymphocyte recirculation o After several days, a lymphocyte exits secondary lymphatic structure § Circulates through blood and lymph § Different lymphocytes delivered to secondary lymphatic structures § Makes it more likely lymphocyte will encounter specific antigen 22.7 Effector Response at Infection Site • Effector Response o Mechanism used by lymphocytes to help eliminate antigen o Each lymphocyte type has its own § Helper T-‐lymphocytes • Release IL-‐2 and other cytokines • Regulate cells of adaptive and innate immunity § Cytotoxic T-‐lymphocytes • Destroy unhealthy cells by apoptosis § Plasma cells (B-‐lymphocytes) • Produce antibodies 22.7a Effector Response of T-‐Lymphocytes • Effector response of helper T-‐lymphocytes o After exposure to antigen (in secondary lymphatic structures), activated and memory helper T-‐ cells migrate to infection site § Continually release cytokines to regulate other immune cells o Help activate B-‐lymphocytes o Activate cytotoxic T-‐lymphocytes with cytokines o Stimulate activity of innate immune system cells • Effector response of cytotoxic T-‐lymphocytes o After exposure to antigen, activated and memory cytotoxic T-‐cells migrate to infection site o They destroy infected cells that display the antigen § Make physical contact with unhealthy or foreign cell § After recognizing antigen, cytotoxic T-‐cell releases granules containing perforin and granzymes (cytotoxic chemicals) § Perforin forms channel in target cell membrane § Granzymes enter channel and induce death by apoptosis o Because this works against antigens associated with cells, the system is called cell-‐mediated immunity 22.7b Effector Response of B-‐Lymphocytes • Most activated B-‐lymphocytes become plasma cells • Plasma cells synthesize and release antibodies o The cells remain in the lymph nodes o Antibodies circulate through lymph and blood until encountering antigen 22.8a Structure of Immunoglobulins • Antibodies: immunoglobulin proteins produced against a o particular antigen o Antibodies “tag” pathogens for destruction by immune cells o Good defense against viruses, bacteria, toxins, yeast spores • Structure: Y-‐shaped, soluble proteins o Composed of four polypeptide chains § Two identical heavy chains and two identical light chains § Held together by disulfide bonds to form antibody monomer § Two important functional areas, variable and constant regions • Variable regions o Located at the ends of the antibody “arms” § Contain antigen-‐binding site (most antibodies have two sites) • Constant Region o Contains the Fc region, which determines biological function 22.8b Actions of Antibodies • Neutralization o Antibody physically covers antigenic determinant of pathogen o Makes it ineffective in establishing infection § E.g., covers region of virus used to bind cell receptor • Agglutination (clumping) o Antibody cross-‐links antigens of foreign cells causing clumping § Especially effective against bacterial cells • Preciptation o Antibody cross-‐links circulating antigens (e.g., viral particles) o Forms antigen-‐antibody complex that becomes insoluble and precipitates out of body fluids o Precipitated complexes recognized by phagocytes • Fc region (of constant region) actions o Complement fixation § Fc region can bind complement for activation (classical complement activation) o Opsonization § Fc region makes it more likely target cell will be “seen” by phagocytic cells § Some phagocytes have receptors for these Fc regions • Bind to Fc region and engulf antigen and antibody o Activation of NK cells § Fc region can trigger NK cells to release cytotoxins § This destroys abnormal cells 22.9a Immunologic Memory • Memory results from formation of a long-‐lived army of lymphocytes upon immune activation o Adaptive immunity activation requires contact between lymphocyte and antigen § There is lag time between first exposure and direct contact o Activation leads to formation of many memory cells against specific antigen 22.9b Measure of Immunologic Memory • Initial exposure and the primary response o Initial exposure can be active infection or vaccine o Primary Response: antibody production to first exposure § Lag or latent phase: initial period of no detectable antibody § Production of antibody: plasma cells produce antibodies • Occurs within 1 to 2 weeks • Antibody levels peak, then decline over time • Subsequent exposures and the secondary response o Next exposure can occur after variable length of time o Measurable response to subsequent exposure is the Secondary Response § Lag or latent phase • Much shorter than primary response due to memory lymphocytes § Production of antibody • Antibody levels rise rapidly 22.9a Immunologic Memory • With subsequent antigen exposure o Many memory cells make contact with antigen more rapidly o Produce powerful secondary response § Pathogen typically eliminated before disease symptoms develop § E.g., person who develops measles will not have it again, even if exposed • Virus eliminated by memory T-‐ and B-‐lymphocytes, antibodies before causing harm o Vaccines are typically effective in developing memory 22.9c Active and Passive Immunity • Active Immunity o Results from direct encounter with pathogen § Occurs naturally by direct exposure to antigen § Can occur artificially through exposure through vaccine o Memory cells against specific antigen are formed 22.9c Active and Passive Immunity • Passive Immunity obtained from another individual o Natural passive immunity arises from transfer of antibodies from mother to fetus (through placenta or milk) o Artificial passive immunity occurs when serum containing antibodies transferred from one person to another § E.g., antibodies to snake venom can be transferred this way o Neither form of passive immunity produces memory cells § Lasts only as long as antibody proteins present Clinical View: Pus and Abscesses • Pus o Contains destroyed pathogens, dead leukocytes, macrophages, cellular debris o Removed by lymphatic system or through skin o If not completely cleared, may form abscess § Pus walled off with collagen fibers § Usually requires surgical intervention to remove Clinical View: Organ Transplants and MHC Molecules • Transfer of organ from one individual to another o E.g., kidney, liver, heart • Individuals tested prior to donation for MHC antigens and ABO group o No two individuals with exactly same MHC molecules • Components of innate and adaptive immune system o Attempt to destroy transplanted tissue o Recipient’s immune system suppressed with drugs Clinical View: Vaccinations u Weakened or dead microorganism or component u Stimulate immune system to develop memory B-‐lymphocytes u Provide relatively safe means for initial exposure to microorganism u If later exposed, secondary response triggered u Immune system response predominantly from the humoral branch u May provide lifelong immunity Clinical View: Hypersensitivities u Acute hypersensitivity, Allergy u Overreaction of immune system to a noninfectious substance, Allergen u E.g., pollen, latex, peanuts u May cause multiple symptoms u Runny nose and watery eyes u Red welts and itchy skin (hives) u Labored breathing and coughing (allergic asthma) u Vomiting and diarrhea u Systemic vasodilation and inflammation u May go into anaphylactic shock Clinical View: HIV and AIDS u Acquired immunodeficiency syndrome u Life-‐threatening condition u Result of human immunodefiency virus u Infects and destroys helper T-‐lymphocytes u Resides in body fluids of infected individuals u Can be transmitted by intercourse, needle sharing, breastfeeding u Prevention through safe sex u No cure for HIV u Treatments alleviate symptoms and help prevent spread
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