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Transcript
4/2/13 Lymphoid Organs Body Defenses Lymphoid tissues and organs – provide defense against disease by: Housing and facilitating the maturation of lymphocytes Cleansing the lymph of pathogens Keri Muma Bio 6 Body Defenses Body Defenses Body defense mechanisms are aimed at eliminating abnormal cells or any foreign materials that are not self Invading pathogens (viruses, bacteria, ect.) Removal of worn out cells, damaged tissue Identification and destruction of abnormal or cancerous cells Rejection of foreign tissue Inappropriate responses can lead to allergies or autoimmune diseases Innate (nonspecific) system responds quickly and consists of: First line of defense – physical barriers; intact skin and mucosa prevent entry of microorganisms Second line of defense – antimicrobial proteins, phagocytes, and other cells Inhibit spread of invaders throughout the body Inflammation is its hallmark and most important mechanism The body has two defense systems – that differ in timing and specificity yet are interactive and interdependent Body Defenses Lymph nodes Tonsils MALTs (mucus associated lymph tissue) Spleen Thymus Bone Marrow Innate immunity Adaptive or Acquired immunity Engulfing and Destroying Pathogens Neutrophil and macrophage destruction of bacteria Phagocytosis: Engulfs foreign material into a vacuole Enzymes from lysosomes digest the material 1 4/2/13 Innate Immunity The inflammatory response is triggered whenever body tissues are injured physically or by infection Prevents the spread of damaging agents to nearby tissues Disposes of cell debris and pathogens Sets the stage for repair processes Inflammation is mediated by phagocytes Toll-like receptors (TLRs) present on phagocytes recognize and bind to foreign microbes and those that have been marked by an opsonin (complement protein or antibody) Activated TLRs triggers the phagocyte to: Engulf and destroy the pathogen And/or release chemicals that promote inflammation The four cardinal signs of acute inflammation are redness, heat, swelling, and pain Inflammatory Response Inflammation Inflammatory chemicals are released into the extracellular fluid by injured tissue, phagocytes, lymphocytes, and mast cells Inflammatory chemicals: Include kinins, histamine, prostaglandin, complement, and cytokines. Cause local blood vessels to dilate, resulting in hyperemia (heat and redness) Capillaries become “leaky” (edema and pain) Attract other WBCs to the area Mobilization of WBC Inflammatory Response Mobilization of WBC – leukocytes emigrate from the blood into the tissues Additional neutrophils are released from the bone marrow in response to leukocytosis-inducing factors released by injured cells Margination – neutrophils cling to the walls of capillaries in the injured area Diapedesis – neutrophils squeeze through capillary walls Chemotaxis – inflammatory chemicals attract neutrophils to the injury site and they begin phagocytosis Inflammation 2 4/2/13 Other Secreted Chemicals Pyrogens – secreted by macrophages Cause hypothalamus to elevate the body’s set temperature (fever) Moderate fever can be beneficial, as it causes: Antimicrobial Proteins Enhance the innate defenses by: The liver and spleen to sequester iron and zinc (needed by microorganisms to grow and divide) Increase rate of chemical reactions which speeds up tissue repair Antimicrobial proteins Innate Immunity Attacking microorganisms directly Hindering microorganisms’ ability to reproduce The most important antimicrobial proteins are: Interferon Complement proteins Defense Cells Interferon Released by virus infected cells and binds to receptors on neighboring healthy cells Interferon protects these neighbors by activating genes for PKR (an antiviral protein) PKR nonspecifically blocks viral reproduction in the cell if it becomes infected Also slows division of tumor cells Enhances natural killer cells Antimicrobial Proteins Natural killer cells Lyse and kill cancer cells and virus- infected cells on first exposure to them Immediate and nonspecific response Immunosurveillance Body Defenses Complement 25 or so proteins that circulate in the blood in an inactive form Forms membrane attacking complex that punch holes in foreign cell’s membrane Also act as opsonins and chemotaxins Activated by: Exposure to carbohydrate chains on the surface of micro-organisms Exposure to antibodies produced by the adaptive immune response against the micro-organism Adaptive (specific) defense system Third line of defense – mounts attack against particular foreign substances Takes longer to react than the innate system Targets invaders that the body has previously been exposed to Involves lymphocytes Works in conjunction with the innate system 3 4/2/13 Characteristics of Adaptive Immunity The adaptive immune system is: antigen-specific - requires the production of specific lymphocytes and antibodies against a specific antigen systemic - not restricted to the initial infection site has memory -second encounter causes a more rapid and vigorous response Antigens - any substance capable of provoking an immune response Adaptive Immunity Antigens include foreign protein, nucleic acid, some lipids, and large polysaccharides It has two separate but overlapping branches: Lymphocytes - originate from stem cells in the red bone marrow Each lymphocyte is equipped with: Immunocompetent – cells display a unique type of receptor that responds to a distinct antigen Become immunocompetent before they encounter antigens they may later attack Are exported to secondary lymphoid tissue where encounters with antigens occur Mature into fully functional antigen-activated cells upon binding with their recognized antigen a unique receptor that binds a specific antigen and a MHC receptor that distinguishes and recognizes “self” Cells of the Immune System Immunocompetent B or T cells Humoral, or antibody-mediated immunity Cellular, or cell-mediated immunity B lymphocytes become immunocompetent in the bone marrow Responsible for antibody-mediated immunity Defend against extracellular pathogens by producing antibodies T lymphocytes become immunocompetent in the thymus Responsible for cell-mediated immunity Defend against intracellular pathogens and cancer Maturation of T Cells T cells mature in the thymus under negative and positive selection pressures Negative selection – eliminates T cells that are strongly anti-self Positive selection – selects T cells with a weak response to self-antigens, which thus become both immunocompetent and self-tolerant 4 4/2/13 T Cell Selection in the Thymus Antibody-Mediated Response B-cells with specific receptors bind to a specific antigen The binding event activates the lymphocyte to multiply (clonal selection) Most B cells become plasma cells that produce antibodies to destroy antigens Some B cells become long-lived memory cells that will remain in the body to respond to the antigen if exposed again Figure 21.7 Antibody-Mediated Response Antibodies (immunoglobulins) Antibodies – proteins that travel in the plasma and combine with a specific antigen Example: blood types Mark the antigens for destruction by specific or nonspecific mechanisms Y shaped molecules with variable region on the tips of each arm that binds a specific antigen Antibody Function Antibodies inactivate antigens in a number of ways: Complement fixation – bind and lyse cell Opsonization – mark antigen for phagocytosis Neutralization – block harmful effects of toxins Agglutination – clumping of foreign cells Precipitation – clumping of antigens Attract natural killer cells 5 4/2/13 Antibody Function Cell Mediated Response Cell Mediated Response T cells can recognize and bind antigens that are presented to them by antigen presenting cells (macrophages) APCs are macrophages that engulf pathogens and then present pieces of the antigen to lymphocytes. Mechanisms of Cytotoxic T cells Antigens must be presented by APC to a THelper cell which triggers the cell to release cytokines that stimulate division of various cells: Enhances proliferation of B-cells and Cytotoxic T-cells which specialize in killing cancer and virus infected cells Mechanisms of Cytotoxic T cell Cytotoxic T cells bind to virus infected and cancerous cells and destroy them by releasing: Perforins that punch holes in the target cells membrane Granzymes that cause the cell to undergo apoptosis 6 4/2/13 Immunological Memory Immunity – ability to defend against specific invaders Primary immune response – cellular differentiation and proliferation, which occurs on the first exposure to a specific antigen Immunological Memory Lag period: 3 to 6 days after antigen challenge Peak levels of plasma antibody are achieved in 10 days Antibody levels then decline Primary and Secondary Responses Secondary immune response – re-exposure to the same antigen Sensitized memory cells respond within hours Antibody levels peak in 2 to 3 days at much higher levels than in the primary response Antibodies bind with greater affinity, and their levels in the blood can remain high for weeks to months Figure 21.10 Immunological Memory Active Immunity - B cells encounter antigens and produce antibodies against them Naturally acquired – response to a bacterial or viral infection Artificially acquired – response to a vaccine of dead or attenuated pathogens Vaccines – spare us the symptoms of disease, and their weakened antigens provide antigenic determinants that build our immunity Immunological Memory Passive Immunity -differs from active immunity in that: B cells are not challenged by antigens Immunological memory does not occur Protection ends when antigens naturally degrade in the body Naturally acquired – from the mother to her fetus via the placenta or IgA antibodies in breast milk Artificially acquired – from the injection of serum that contains the immunoglobulins 7 4/2/13 Acquired Immunity Immune Disorders Hypersensitivity Allergies Hypersensitivity - abnormal, vigorous immune responses (overzealous immune system) Immediate hypersensitivity – occurs within seconds to 20 minutes Allergies and Asthma Plasma cells produce IgE antibodies which attach to mast cells Mast cells release histamine – which causes inflammation and itching Also releases a leukotriene called slow reactive substance – causes smooth muscle contraction in air ways Treated with anti-histamines and newer drugs that block leukotrienes such as Singular Hypersensitivity that is life-threatening Allergen directly enters blood Systemic histamine and SRS releases may result in: Immunodeficiencies Anaphylactic Shock - systemic allergic response Constriction of bronchioles Sudden vasodilation and fluid loss from the bloodstream Hypotensive shock and death Immunodeficiency - production or function of immune cells is lacking or abnormal Treated with epinephrine Delayed hypersensitivity - symptoms appear after 1-3 days Severe combined immunodeficiency disease (SCID) Deficiency of B and T-cells Acquired Immune Deficiency Syndrome HIV destroys THelper cells Inflammation caused by cytotoxic T-cells release of lymphokines Treated with corticosteroids 8 4/2/13 Autoimmune Diseases Autoimmune - the immune system does not distinguish between self and non-self The body produces antibodies and cytotoxic T-cells that attack its own tissues Possible causes: Inefficient lymphocyte programming Appearance of new self-antigens Antibodies produced against foreign antigens react with self-antigens (example: streptococcus and rheumatic fever) 9