I. Lines of Defense Pathogen: Table 1: Types of Immune Mechanisms. Table 2: Innate Immunity: First Lines of Defense

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1 I. Lines of Defense Pathogen: Table 1: Types of Immune Mechanisms Table 2: Innate Immunity: First Lines of Defense Innate Immunity involves nonspecific physical & chemical barriers that are adapted for preventing the initial entry of pathogens into the body. Represents the body s first line of defense against infection that include: a) Skin (Physical Barrier): secretions from sebaceous & sweat glands act as a chemical barrier, giving the skin a ph ranging from 3-5 to prevent colonization by many microbes. b) Mucus Membranes (Physical Barrier): line digestive, respiratory, genitourinary system & bar entry of pathogens. c) Tears, Sweat (Chemical Barrier): contain antimicrobial agents such as lysozyme to break down bacterial cell walls. Stomach Acid (Chemical Barrier): destroys microbes before entering the intestinal tract.

2 Table 3: Innate Immunity: Second Lines of Defense Another aspect of innate immunity involves nonspecific cellular responses to pathogens that are adapted for limiting the spread of infectious agents should they enter the body. These cellular responses represent the body s second line of defense against infection & is carried out by the following white blood cells: a) Neutrophils: are attracted to sites of infection by chemical signals whereby they may either (1) phagocytose pathogens or (2) secrete a H 2 O 2 & hypochlorite solution to destroy pathogens ( respiratory burst ). b) Eosinophils: defend against parasites (tapeworms, blood flukes) by attaching to their body wall & discharging destructive enzymes. c) Macrophages: extend long pseudopodia that attach to a microbe s surface, upon which it is engulfed in a vacuole & destroyed. Some macrophages migrate throughout the body while others reside permanently in certain tissue (lungs, liver, kidney, brain, spleen, & lymph nodes). Figure 1: Innate Immunity: Second Line of Defense: Inflammatory Response The inflammatory response deals with localized infections & is initiated when leukocytes in connective tissue called Basophils & Mast Cells release Histamine. Histamine increases the permeability of the local capillaries, causing them to leak fluid into neighboring tissues, resulting in heat, redness, & swelling (inflammation). Clotting factors begin to repair tissue damage & help block the spread of microbes to other parts of the body. Neutrophils are the first phagocytes to arrive at the damaged area (respiratory burst), followed by macrophages.

3 Figure 1.1: Innate Immunity: Second Line of Defense: Complement Proteins Complement Proteins work in concert with certain antibodies (IGg) to perforate pathogenic cells. As ions & water rush in, the targeted cell swells, lyses & is destroyed. Complement proteins may function during the inflammatory response as well as during the immune response. Figure 1.2: Innate Immunity: Second Line of Defense: Interferon Proteins Interferons are released by viral infected cells. Once released, they can stimulate production of proteins in neighboring cells that block the transcription of viral mrna & formation of viral proteins. Figure 2: Acquired Immunity: Third Line of Defense: Lymphocytes T Lymphocytes B Lymphocytes Pathogen (Antigens)

4 Acquired Immunity involves specific cellular responses that are adapted to recognizing & destroying specific pathogens. After being exposed to a pathogen, the cells of the immune system become programmed to quickly recognize & attack the same pathogen upon subsequent exposures. a) Cells of the immune system are able to recognize & attack or neutralize specific pathogens due to the presence of molecules called Antigens. An antigen is ANY substance (usually a surface protein) that can stimulate an immune response by a host s immune system. Cells of the Immune System Figure 3: B-Cell Lymphocyte Specificity B Cells: a) Recognize antigens associated with pathogenic microbes via B-Cell Receptors. b) Produce antibodies that neutralize the activity of bacteria or viral particles & other Free Antigens by either (1) binding to dangerous chemical groups or (2) binding several pathogens together, preventing them from infecting a healthy cell. In both cases, the antigen-antibody complex is engulfed by macrophages. Figure 3.1: T-Cell Lymphocyte Specificity T Cells: a) Recognize antigens associated with pathogenic microbes on the surface of infected cells via T-Cell Receptors.

5 Major Histocompatibility Complex Figure 4: Class II MHC & Clonal Selection Class II MHC Clonal Selection (B Lymphocytes) During Clonal Selection, a foreign antigen selectively activates a small fraction of cells from the body s diverse pool of lymphocytes (depending on their specific antigen receptors). This small number of selected cells gives rise to clones of thousands of cells, each specifically designed to eliminate the invading pathogen. Class II MHC: a) Exist on the surface of immune cells such as macrophages & lymphocytes. Incorporate foreign antigens (proteins) of pathogens in order to mobilize specific immune cells for the eradication of the microbe. Figure 4.1: Class I MHC Class I MHC: a) May either present the cell s normal proteins or those of a pathogen in order to advertise to lymphocytes of the immune system the cells health status.

6 The Immune Response Figure 5: Initiation of Immune Response: Function of Macrophages (APC s) A pathogen is engulfed by a macrophage, upon which its antigens combine with class II MHC s that are presented on its surface. The macrophage, now an Antigen Presenting Cell (APC), interacts with specific Helper T Cells (T H ), which have a specialized receptor protein called CD 4 that binds to the class II MHC. This interaction stimulates the APC to secrete Interleukin-1, which in turn, stimulates the T H to grow & divide to produce a clone army of T H cells. Figure 5.1: Initiation of Immune Response: Function of Helper T Cells (T H ) These activated T H cells secrete Interleukin-2, stimulating the rapid division of pathogen-specific B cells & T c to initiate the cell-mediated (T-cell mediated) & humoral (B-cell mediated) aspects of the immune response. During both responses, B & T c cells proliferate into the following groups: a) Effector Cells: are the only cells active during the primary exposure to a pathogen. Effector B-cells, called Plasma Cells, secrete specific antibodies to neutralize the invading pathogen. Effector T-cells attach to the class I MHC of infected cells via a specialized protein receptor called CD8, upon which they release the protein Perforin that lyses the infected cell. b) Memory Cells: mounts a defense against a pathogen upon a second exposure multiply rapidly to produce more effector & memory cells. Memory cells can last for years some, such as those produced during an exposure to mumps or chicken pox, may last forever, granting lifetime immunity against these diseases.

7 c) B Cell vs. T-Cell Activation: with regards to B-cell activation, the antigen will bind to membrane antibodies on the surface of a B-cell. The antigen is taken into the cell, processed, & displayed on a class II MHC. Helper T-cells bind to the MHC-antigen complex & stimulate the B-cell to proliferate into effector & memory (plasma) cells. Helper T- cells can also bind to MHC s on infected cells & stimulate the proliferation of effector & memory cytotoxic T-cells. Figure 6: Humoral & Cell Mediated Immune Responses (Summary) Figure 6.1: Action of Effector B Cells: Antibody (Immunoglobulin) Structure Only sites at the end of the antibody molecule can potentially bind to specific regions of an antigen molecule, called the Epitope. Each class of immunoglobulin (IgG, IgM, IgA, IgE) is specific to a particular antigen s epitope region.

8 Figure 6.2: Action of Effector B Cells: Antibody (Immunoglobulin) Functions Figure 6.3: Action of Effector Cytotoxic T Cells: Perforin Function Cytotoxic T cells bind to the class I MHC complex of infected body cells by way of their CD8 receptor. This stimulates the release of proteins called Perforins that create pores in the infected cell s membrane. As a result, ions & water rush into the cell, causing it to lyse.

9 Figure 7: Primary vs Secondary Immune Response III. Vaccination Vaccination: a) A Vaccine is a mixture of dead or modified pathogen. It triggers an immune response without symptoms of infection. For days after a vaccination the immune system develops antibodies & memory cells against the pathogen. Some diseases, such as influenza, can still cause infection even though an individual has previously contracted the disease mutations can alter the surface antigens so that the pathogen is not recognized by memory cells (antigen shifting). Types of Immunity Figure 8: Active vs Passive Immunity

10 Active Immunity: Passive Immunity: IV. Blood Type Compatibility & Transfusions Figure 9: ABO Blood Groups & Plasma Antibodies Figure 9.1: Blood Type Compatibility & Transfusions Blood Type Incompatibility If donor blood is incompatible with the blood type of the recipient, it will be recognized & acted on by either anti-a or anti-b antibodies upon transfusion. The antibodies will bind to the donor blood cells, causing them to clump together, which can result in blood clots that can lead to the potentially fatal blocking of major blood vessels. Because blood-group antigens are polysaccharides, they induce T-independent immune responses, which elicit no memory cells & produce IgM antibodies (very large). Thus if fetal blood crosses the placenta as may happen late in pregnancy or during childbirth, IgM antibodies produced by the mother cannot cross the placenta to harm the child.

11 Figure 9.3: Rh Factors & Blood Type Compatibility First Pregnancy: Mom (Rh-), Fetus (Rh+) Labor of First Pregnancy Subsequent Pregnancies: Mom (Rh-); Fetus (Rh+) Other red blood cell antigens, called Rh Factors pose a problem because they elicit a T-dependant immune response, which produces memory cells & IgG antibodies (small). Thus if Rh+ fetal blood crosses the placenta during childbirth, an Rh- mother mounts a humoral response against the Rh factor. The danger occurs in subsequent pregnancies involving an Rh+ fetus when the mother s memory B cells are exposed to the Rh factor, upon which they produce IgG antibodies which can cross the placenta & destroy fetal red blood cells. To prevent this, the mother is injected with anit-rh antibodies after delivering her first Rh positive baby.

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