1. Chapter 43 ~ The Body’s Defenses
Intro video clip – immunity and cancer
Gout – a type of arthritis, caused by build up of uric acid, sometimes due to excessive meat and alcohol consumption. Uric acid crystals accumulate in the joints, causing inflammation

2. Lines of Defense Nonspecific Defense Mechanisms……
Nonspecific – refers to the mechanism of action against any and all pathogens (same regardless of type of invader)
1st  Skin block and mucous membrane traps pathogens;
2nd  engulf, inhibit (interferon), destroy (complement), activate (inflammation)
3rd  SPECIFIC  response is tailored to each different invader
Nonspecific Defense Mechanisms……

3. Phagocytic and Natural Killer Cells
Neutrophils % WBCs; engulf and destroy microbes at infected tissue
Monocytes 5% WBCs; develop into….
Macrophages
Eosinophils % WBCs; destroy large parasitic invaders (blood flukes) by enzymatic hydrolysis
Natural killer (NK) cells destroy virus-infected body cells & abnormal cells

4. The Inflammatory Response
1- Tissue injury; release of chemical signals
histamine (basophils/mast cells): causes Step  
2/3- Dilation and increased permeability of capillary
chemokines: secreted by blood vessel endothelial cells mediates phagocytotic migration of WBCs
4- Phagocytosis of pathogens
fever & pyrogens: leukocyte-released molecules increase body temp

5. Specific Immunity
Lymphocyctes •pluripotent stem cells... • 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 immunoglobulin, produced by B cells
Antigen receptors: plasma membrane receptors on B and T cells
Each of you has your own unique ID card – each pathogen has its own antigen (“bad guy” ID), usually a surface protein
Antibodies bind antigens like puzzle pieces – they are a perfect “match” tailor made for each different antigen
***B cells produce antibodies
***T cells  Helper T activate B and Tc; Cytotoxic T destroy infected body cells

6. Activating B or T cells
Effector cells: short-lived cells that combat the antigen
Memory cells: long-lived cells that bear receptors for the antigen
Clonal selection: antigen-driven cloning of lymphocytes
“Each antigen, by binding to specific receptors, selectively activates a tiny fraction of cells from the body’s diverse pool of lymphocytes; this relatively small number of selected cells gives rise to clones of thousands of cells, all specific for and dedicated to eliminating the antigen.”

7. Clonal selection occurs when a particular antigen binds a B cell with the matching receptors. Only that cell begins to proliferate (make copies of itself by mitosis); these clones then give rise to plasma cells that secrete antibodies and memory cells.
**Note – antibodies are useful as a warning “flag” to the immune system; alerts that a “bad guy” antigen is present, clumps antigens for easier engulfment by macrophages. 3 types of antibody action = neutralization, opsonization, lysis via complement

8. Induction of Immune Responses
Primary immune response: lymphocyte proliferation and differentiation the 1st time the body is exposed to an antigen
Plasma cells: antibody-producing effector B-cells
Secondary immune response: immune response if the individual is exposed to the same antigen at some later time~ Immunological memory
Primary immune response peaks at ~14 days after exposure; note that a 2nd exposure ~1 month after 1st exposure elicits a MUCH faster and greater response (7-10 days) and the antibodies linger in the body.
What is happening in the body from 0-7 days? 7-14 days? days?
The process repeats in a similar fashion for all antigens.

9. Self/Nonself Recognition
Major Histocompatability Complex (MHC): body cell surface antigens
self genes
Class I MHC: found on all nucleated cells
Class II MHC: found on macrophages, B cells, and activated T cells
Antigen presentation:
cell displays an intracellular protein to antigen receptor on a nearby T cell
Tc  bind class I MHC of APC
Th  bind class II MHC of APC

10. Helper T lymphocytes Function in both humoral & cell-mediated immunity
Stimulated by antigen presenting cells (APCs)

11. Antibody Structure
2 heavy chains and 2 light chains joined by disulfide bridges
Antigen-binding site (variable region)

12. Antibody Function
Neutralization (opsonization): antibody binds to and blocks antigen activity
Agglutination: antigen clumping
Precipitation: cross-linking of soluble antigens
Complement fixation: activation of 20 serum proteins, lyse viruses and pathogenic cells

14. Immunity in Health & Disease
Acquired Immunity
Conferred immunity by recovering from disease
immunization and vaccination; produces a primary response
Passive immunity: transfer of immunity from one individual to another
natural: mother to fetus; breast milk
artificial: rabies antibodies
ABO blood groups (antigen presence)
Rh factor (blood cell antigen); Rh- mother vs. an Rh+ fetus (inherited from father)
Get immunity through surviving illness (which also produces memory cells) or through vaccination (stimulates immune response and results in memory cell production)
Passive immunity – no illness, no vaccination, but obtain antibodies by exposure
ABO blood groups – your body only recognizes proteins present on surface of your RBCs; any others will be recognized as foreign and will stimulate a severe immune response (hence blood typing/donation)
Rh factor – important in pregnancy; Rh-negative mom can have an immune reaction to Rh-positive fetus; mom’s antibodies against Rh+ cells can cross the placenta and attack the fetus blood supply, causing anemia or death

15. Abnormal immune function
Allergies (anaphylactic shock): hypersensitive responses to environmental antigens
Autoimmune disease: multiple sclerosis, lupus, rheumatoid arthritis, insulin-dependent diabetes mellitus
Immunodeficiency disease: SCIDS (bubble-boy); A.I.D.S.
Allergies – severe (peanut allergy) can result in anaphylactic shock
Autoimmune – attack own body’s cells
SCIDS/AIDS – loss of immune function due to viral infection

16. What immune system activities occur in the 1st, 2nd, 3rd lines of defense (primary/secondary/specific responses)?
Describe how histamine works in the inflammatory response.
What are the roles of the different kinds of immune cells (B cells, helper T, cytotoxic T, macrophages, memory cells, etc)?
What is Rh factor and under what circumstances does it pose a risk during pregnancy?
What immune activities occur at each stage of an immune response following exposure to a pathogen?

17. How are the ABO blood groups important in immunity
How are the ABO blood groups important in immunity? (what happens if the wrong blood type is given?)
What genetic process enables antibodies to have variation in their specificity?
What is the function of MHC?
How does phagocytosis work?
How do pathogens evade the second lines of defense?
What are antigens? What types of substances can act as antigens?

18. What mechanisms do pathogens (such as Salmonella) use to evade the immune system and cause infection?
What general activities comprise the overall process of a specific immune response?
What do antibodies do to help fight infection by pathogens?
Distinguish between B and T cells.
Compare/contrast autoimmune disease with immune deficiency disease.

19. How are helper T cells activated?
What is clonal selection and what causes it?
What is the role of histamine in the inflammatory response?