Immune System & Disease Defense

Cards (47)

  • Pathogens as the Cause of Infectious Diseases
    Infectious diseases are caused by a variety of microorganisms known as pathogens. These tiny invaders can wreak havoc on our bodies, much like unwanted guests crashing a party.
  • Types of pathogens:
    1. Viruses
    2. Bacteria
    3. Fungi
    4. Protists
  • Interestingly, while Archaea are microorganisms, they are not known to cause diseases in humans.
  • The Germ Theory of Disease

    The understanding that microorganisms cause diseases wasn't always known. This concept, known as the germ theory of disease, was a revolutionary idea in the 19th century.
  • Primary Defences Against Pathogens
    Our body's first line of defence against these microscopic invaders includes:
    1. Skin
    2. Mucous membranes
  • The Skin as a Barrier
    Think of your skin as a fortress wall protecting a castle. It serves as both a physical and chemical barrier:
    1. Physical Barrier: The skin's tough, keratinized outer layer prevents pathogens from entering.
    2. Chemical Barrier: The skin produces substances that create an inhospitable environment for pathogens.
  • Mucous Membranes

    Mucous membranes line various body cavities that are exposed to the external environment, such as the respiratory and digestive tracts. They produce mucus, which:
    1. Traps pathogens
    2. Contains enzymes that can destroy some pathogens
  • Nature of Science (NOS) Connection
    This topic beautifully illustrates how careful observation can lead to significant scientific progress. The discoveries made during the childbed fever epidemic in Vienna and the cholera outbreak in London were pivotal in developing our understanding of infectious diseases and their control.
  • Blood Clotting
    Sealing Cuts in Skin: When our skin barrier is breached, our body has a remarkable mechanism to quickly seal the gap: blood clotting. This process is like an emergency repair team rushing to fix a broken pipe.
  • The blood clotting process involves:
    1. Release of clotting factors from platelets
    2. Cascade pathway activation
    3. Conversion of fibrinogen to fibrin
    4. Trapping of erythrocytes to form a clot
  • Clotting Factor Release 
    When platelets encounter damaged blood vessels, they release clotting factors. Think of these as the first responders at an accident scene.
  • Cascade Pathway 

    This is a series of chemical reactions, each triggering the next, like a line of dominoes falling.
  • Fibrinogen to Fibrin Conversion 
    The enzyme thrombin rapidly converts fibrinogen (a soluble protein) into fibrin (an insoluble protein).
  • Clot Formation 
    Fibrin forms a mesh-like structure, trapping red blood cells (erythrocytes) to form a clot.
  • Our immune system is like a two-tiered defense force: 

    The innate immune system (the general infantry) and the adaptive immune system (the specialized forces).
  • Innate Immune System
    • Responds to broad categories of pathogens
    • Does not change during an organism's lifetime
    • Fast-acting but less specific
  • Example of Innate Immune System
    Phagocytes, a component of the innate immune system, engulf and destroy a wide variety of pathogens without needing prior exposure.
  • Adaptive Immune System
    • Responds specifically to particular pathogens
    • Builds up a memory of encountered pathogens
    • Becomes more effective over time
    • Slower initial response but highly specific
  • Example of Adaptive Immune System

    After recovering from chickenpox, your adaptive immune system remembers the virus, providing long-lasting immunity.
  • Key differences of Immune System
    1. Specificity: Innate (broad) vs. Adaptive (specific)
    2. Memory: Innate (no memory) vs. Adaptive (builds memory)
    3. Response Time: Innate (fast) vs. Adaptive (slower initially, faster in subsequent exposures)
    4. Effectiveness Over Time: Innate (constant) vs. Adaptive (improves)
  • Infection Control by Phagocytes
    Phagocytes are like the "pac-men" of our immune system, actively seeking out and devouring pathogens
  • Amoeboid Movement
    • Phagocytes move from blood to infection sites using amoeboid movement.
    • This movement is similar to how an amoeba moves, by extending pseudopodia.
  • Pathogen Recognition
    • Phagocytes can identify various pathogens as foreign invaders
  • Engulfment by Endocytosis
    • Once a pathogen is recognized, the phagocyte surrounds and engulfs it.
    • This process is called phagocytosis, a type of endocytosis.
  • Digestion using Lysosomal Enzymes
    • After engulfment, lysosomes within the phagocyte fuse with the vesicle containing the pathogen.
    • Lysosomal enzymes then break down the pathogen.
  • Lymphocytes in the Adaptive Immune System
    Lymphocytes are the specialized forces of our adaptive immune system, working together to produce antibodies. There are two main types of lymphocytes: B-lymphocytes (B-cells) and T-lymphocytes (T-cells), but we'll focus on B-cells here.
  • Key points about lymphocytes:
    1. Location:
    • Circulate in the blood
    • Contained in lymph nodes
    1. B-lymphocytes and Antibodies:
    • Each individual has a vast number of B-lymphocytes
    • Each B-lymphocyte produces a specific type of antibody
    1. Diversity: The large number of different B-lymphocytes allows for a wide range of antibodies to be produced
  • The Antibody Production Process
    1. A B-lymphocyte encounters a specific antigen (part of a pathogen)
    2. If the antigen matches the B-cell's specific antibody, the B-cell is activated
    3. The activated B-cell multiplies and differentiates into plasma cells
    4. Plasma cells produce large quantities of the specific antibody
  • This process explains why our immune system can respond to such a wide variety of pathogens - we have a diverse array of B-lymphocytes ready to recognize and respond to many different antigens.
  • Antigens as Recognition Molecules
    Antigens are like molecular "name tags" that trigger our immune system to produce antibodies.
  • Nature of Antigens
    • Most antigens are glycoproteins or other proteins
    • Usually located on the outer surfaces of pathogens
  • Location and Function
    • On pathogen surfaces: Helps immune system identify invaders
    • On erythrocytes (red blood cells): Important for blood typing
  • Activation of B-lymphocytes by Helper T-lymphocytes

    This process is like a carefully choreographed dance between different immune cells.
    1. Antigen-Specific Cells
    • B-cells and helper T-cells are antigen-specific
    • Each recognizes a particular antigen
    1. B-cell Activation Requirements
    • Direct interaction with the specific antigen
    • Contact with an activated helper T-cell (that has recognized the same antigen)
    1. Results of B-cell Activation
    • Production of antibodies
    • Formation of memory cells
  • The Activation Process
    1. An antigen enters the body
    2. A B-cell recognizes and binds to the antigen
    3. A helper T-cell also recognizes the same antigen
    4. The activated helper T-cell interacts with the B-cell
    5. This dual recognition activates the B-cell
    6. The activated B-cell multiplies and differentiates into:
    • Plasma cells (antibody-producing cells)
    • Memory B-cells (for future rapid responses)
  • This two-step activation process helps ensure that the immune response is both specific and regulated, preventing unnecessary immune reactions.
  • Multiplication of Activated B-lymphocyte
    When B-lymphocytes are activated, they undergo a process of rapid multiplication to form clones. This process is crucial for producing sufficient quantities of antibodies to combat an infection effectively.
  • Initial Scarcity:
    There are relatively few B-cells that can respond to a specific antigen.
  • Clonal Expansion:
    Activated B-cells divide by mitosis to produce many identical cells.
  • Plasma Cell Formation: 

    These cloned cells differentiate into plasma B-cells.
  • Antibody Production:
    Plasma cells are capable of producing large quantities of the same type of antibody.