1. The Body’s Defenses
Chapter 43

2. Lines of Defense Innate Immunity: Rapid Response
Acquired Immunity: Slower Response

3. Skin and secretions create a hostile environment for microbes
1st Line Nonspecific Defense Mechanisms: Innate Immunity Barrier Defenses
Skin & mucous membrane linings of: digestive, respiratory, urinary, and reproductive systems
Mucus – thick fluid to trap microbes and particles
Skin and secretions create a hostile environment for microbes

4. Natural killer (NK) cells
2nd Line Nonspecific Defense Mechanisms: Innate Immunity Phagocytic WBC’s and Natural Killer Cells
Neutrophils
60-70% WBCs; engulf and destroy microbes at infected tissue
Macrophages
engulf and enzymatically destroy microbes (big eaters)
Eosinophils
1.5% WBCs; discharge enzymes to destroy multicellular parasitic invaders (blood flukes)
Natural killer (NK) cells
destroy virus-infected body cells & abnormal cells (tumor cells)

5. 2nd Line Nonspecific Defense Mechanisms: Innate Immunity Inflammatory Response
1. Tissue injury; release of chemical signals
histamine released from mast cells and signals from macrophages increases blood flow & blood vessel permeability to injured area
2. Swelling occurs
Increased blood flow causes excess fluid to exit capillaries causing swelling, heat, and redness
3. Phagocytosis of pathogens
Phagocytic WBC’s enter the injured site from the blood stream and inactivate any microbes
An accumulation of WBC’s forms pus – fluid rich in WBC’s, dead microbes, and cell debris
Toxins released by pathogens and pyrogens released by macrophages can cause fever

6. Antibodies: antigen-binding protein, produced by B cells
3rd Line Specific Defense Mechanisms: Acquired Immunity What’s Involved?
Lymphocytes: from pluripotent stem cells in marrow; recognize and inactivate foreign cells and molecules
B Cells (bone marrow)
T Cells (thymus)
Antigen: a foreign molecule that elicits a response by lymphocytes (virus, bacteria, fungus, protozoa, parasitic worms)
Antibodies: antigen-binding protein, produced by B cells
Antigen receptors: plasma membrane receptors on B and T cells
B cells make antibodies that bind directly to the pathogen’s antigens
T cells bind to antigens that are displayed by antigen-presenting cells on their MHC’s (infected body cells) causing them to lyse

7. Self-tolerance: capacity to distinguish self from non-self
3rd Line Specific Defense Mechanisms: Acquired Immunity Self vs. Non-Self Recognition
Major Histocompatibility Complex (MHC): body cell surface proteins that can present foreign antigen fragments; coded for by a family of genes
Class I MHC molecules: found on all nucleated cells; display foreign peptide antigens synthesized from viral/bacterial mRNA; signals to cytotoxic T cells; death of cell
Class II MHC molecules: found on dendritic cells, macrophages, & B cells; display antigen epitopes from pathogen’s that have been engulfed; signals cytotoxic T cells and helper T cells
Self-tolerance: capacity to distinguish self from non-self
Autoimmune diseases: failure of self-tolerance; multiple sclerosis, lupus, rheumatoid arthritis, insulin-dependent diabetes mellitus
Class I MHC molecules present peptide fragments of antigens that are produced in virus hijacked cells. Viruses insert their DNA or RNA into a host cell and the host cell begins manufacturing the antigens/glycoproteins for the membrane. These antigens are broken down by proteasomes and the fragments (small amino acid fragments – aka peptides) are attached to a Class I MHC molecule and sent to the cell membrane for display

8. Class I MHC
Class II MHC

9. Activated B and T cells divide many times producing:
3rd Line Specific Defense Mechanisms: Acquired Immunity B and T Cell Activation: Clonal Selection
Activated B and T cells divide many times producing:
Effector cells: short-lived cells that combat the antigen and any pathogens producing that antigen (B cells = plasma cells; T cells = cytotoxic and helper)
Memory cells: long-lived cells that bear receptors for the antigen
These cells are specific for the particular antigen

10. Acquired Immune Responses
Primary immune response: lymphocyte activation the 1st time the body is exposed to an antigen; includes clonal selection
Secondary immune response: immune response if the individual is exposed to the same antigen at some later time - immunological memory (memory cells)

11. Types of Acquired Immune Responses
Humoral Immune Response
Activation and clonal selection of:
Effector B cells (plasma cells), which produce antibodies that circulate in the blood & lymph
Memory B cells
Cell-mediated Immune Response
Effector T cells (cytotoxic & helper), which identify and destroy infected cells
Memory cytotoxic & helper T cells

12. Helper T Cells Function in enhancing humoral & cell-mediated responses
Stimulated by antigen-presenting cells (Class II MHC)
Dendritic cells, macrophages, & B cells
CD4 surface protein enhances activation
Secreted cytokines stimulate helper T cell to clone additional activated helper T cells with the same antigen receptor
New helper T cells then release other cytokines to activate B cells and cytotoxic T cells

13. Cytotoxic T Cells
Destroy cells infected by intracellular pathogens and cancer cells
Stimulated by nucleated body cells presenting foreign antigen fragments (Class I MHC)
CD8 surface protein enhances activation
Cytotoxic T cell releases perforin, a protein that forms pores in the infected cell’s membrane; cell lyses and pathogen is exposed to circulating antibodies marking it for disposal
Cytotoxic T cell can move on and destroy more infected cells

14. Active and Passive Immunity
Active immunity: develops naturally in response to an infection or artificially by immunization (vaccines)
Passive immunity: transfer of immunity from one individual to another
natural: mother to fetus via breast milk
artificial: rabies antibodies via 1 painful shot followed by 4 vaccine shots to develop active immunity
Rabies post-exposure vaccinations consists of a dose of human rabies immune globulin and four doses of rabies vaccine given on the day of the exposure, and then again on days 3, 7, and 14. The vaccine is given in a muscle, usually in the upper arm. This set of vaccinations is highly effective at preventing rabies if given as soon as possible following an exposure.
Administration of rabies immunoglobulin (RIG) should be infiltrated into the depth of the wound and around the wound as much as anatomically feasible. Any remainder should be injected at an intramuscular site distant from that of vaccine inoculation e.g. into the anterior thigh. Amount given depends on your weight.

15. Abnormal Immune Function
Allergies (anaphylactic shock): hypersensitive responses to environmental antigens (allergens); causes dilation and blood vessel permeability (by histamines) which lowers blood pressure; epinephrine
Autoimmune disease: multiple sclerosis, lupus, rheumatoid arthritis, insulin-dependent diabetes mellitus
Immunodeficiency disease: SCIDS (bubble-boy); A.I.D.S.
HIV attacks helper T cells rendering them nonfunctional and then HIV multiplies within the deactivated T cells
When the immune system can no longer fight normal infections then the person is diagnosed with A.I.D.S.