1. Immune Systems Part 2—Specific Defense and Blood Typing…
AP Biology
Immune Systems
Part 2—Specific Defense and Blood Typing…

2. Remember… Single Transduction Pathway… Reception…Transduction…Response
Glycoproteins and Glycolipids are important Cellular Communication
Direct Contact is a type of Cellular Communication
Local (paracrine) and long distance communication between cells is accomplished by chemical means….

3. Antibodies attaching to the antigen
binding
sites
Epitopes
(antigenic
determinants)
Antibody A
Antigen
Antigens and Immune Response
An Antigen is a surface protein on a pathogen that causes antibodies to be generated by WBC’s.
B. Antigen receptors – These are “recognitition hands” on lymphocytes. (The glycoproteins or glycolipids of the ECM.)
1. When a pathogen is “identified” that triggers Clonal Selection in that Lymphocyte.
Antibody B
Antibody C

4. Primary vs Secondary Response
1. When a pathogen is “identified” that triggers Clonal Selection in that Lymphocyte.
a. Clonal selection makes effector cells (fighters) and memory cells (for future fights).
b. Primary Immune Response (This refers to the first encounter with a pathogen.)
i. It generally takes 10 – 17 days to find right DNA sequence and make antibodies for fighting.
c. Secondary Immune Response (This is a second, third, etc. encounter with that same pathogen.)
i. It takes only 2 – 7 days to get better because of memory cells.

5. 3rd Line: Acquired (active) Immunity
Specific defense with memory
lymphocytes
B cells
T cells
antibodies
immunoglobulins
Responds to…
antigens
cellular name tags
specific pathogens
specific toxins
abnormal body cells (cancer)
Antigens
cellular name tag proteins
“self” antigens
no response from WBCs
“foreign” antigens
response from WBCs
pathogens: viruses, bacteria, protozoa, parasitic worms, fungi, toxins
non-pathogens: cancer cells, transplanted tissue, pollen
II. Specific Immune Responses - Using Lymphocytes to fight infections
A. This immunity is the attack of specific pathogens using the Lymphocyte WBC. (These are like specialized assassins.)

6. B (bursa) Lymphocytes –These “kill” by producing antibodies
B (bursa) Lymphocytes –These “kill” by producing antibodies. Antibodies are like protein tongs.
2. T (thymus) Lymphocytes – These “kill” by using chemicals to kill infected cells.
a. Cytotoxic T cells – These actually kill infected cells. (“toxic” means “deadly”)
b. Helper T cells – These help turn “on” B cells to make antibodies and Cytotoxic T cells to kill.
i. These are the cells that are infected, and rendered useless by the AIDS virus.

7. B cells
Attack, learn & remember pathogens circulating in blood & lymph
Produce specific antibodies against specific antigen
Types of B cells
plasma cells
immediate production of antibodies
rapid response, short term release
memory cells
continued circulation in body
long term immunity

8. B Cells

9. What if the attacker gets past the B cells in the blood & actually infects (hides in) some of your cells?
You need trained assassins to recognize & kill off these infected cells!
Attack of the Killer T cells!
Major histocompatibility (MHC) proteins
proteins which constantly carry bits of cellular material from the cytosol to the cell surface
“snapshot” of what is going on inside cell
give the surface of cells a unique label or “fingerprint”

10. Infected cells digest some pathogens
MHC proteins carry pieces to cell surface
foreign antigens now on cell membrane
called Antigen Presenting Cell (APC)
macrophages can also serve as APC
tested by Helper T cells
Attack, learn & remember pathogens hiding in infected cells
recognize antigen fragments
also defend against “non-self” body cells
cancer & transplant cells
Types of T cells
helper T cells
alerts rest of immune system
killer (cytotoxic) T cells
attack infected body cells
memory T cells
long term immunity

14. Self tolerance situations:
A. Recognition of normal body cells and WBCs.
B. ABO blood groups and WBCs.

15. Rh factor and Pregnancy
C. Rh Factor on RBCs. (Pregnancy? – second pregnancy can be deadly if mother is Rh - and baby is Rh +.)
1. Antibodies could have been made because of an Rh+ first birth. (Blood mixes during birth, antibodies made.)
D. Tissue grafting and organ transplants. (Must have matching MHC’s to work; Suppression of immune system is needed.)

16. Immune system malfunctions
Auto-immune diseases
immune system attacks own molecules & cells
lupus
antibodies against many molecules released by normal breakdown of cells
rheumatoid arthritis
antibodies causing damage to cartilage & bone
diabetes
beta-islet cells of pancreas attacked & destroyed
multiple sclerosis
T cells attack myelin sheath of brain & spinal cord nerves
Allergies
over-reaction to environmental antigens
allergens = proteins on pollen, dust mites, in animal saliva
stimulates release of histamine

17. Abnormal Immune System Function
Allergy---False Alarm—Mast cells over produce histamine—runny nose…Sneeze…
Lupus---Butterfly Rash---Kidneys malfunctioning
Rheumatoid Arthritis—WBC breakdown connective tissue
Insulin-Dependent Diabetes-Type I-Juvenile
Multiple Sclerosis (MS) WBC attack the Schwann Cells and myelin sheath of Neurons

18. Immunodeficiency Diseases (Having no immune system)
SCID Infants born with no immune system
(AKA Bubble People)
Hodgkin’s Lymphoma (This is a cancer of the lymphocyte white blood cells) (Lymph nodes destroyed)
Stress—Weakens Immune System
HIV/AIDS---This is caused by a retrovirus—Host Cell is T Helper Cell

19. Gene-to-gene recognition
No Avr allele;
virulent pathogen
R allele; plant cell
becomes diseased
Avr allele
Avr allele;
virulent pathogen
No R allele; plant cell
becomes diseased
II. Plant defenses against plant pathogen invasion: (virulent – means “deadly”)(non-virulent – means “just harmful”.)
Gene – for- gene recognition (Result of coevolution.)(Resistance genes – like bacteria have.)
1. If receptor protein matches the infecting ligand; no infection occurs.
No Avr allele;
virulent pathogen
No R allele; plant cell
becomes diseased
If there is no gene-for-gene recognition because of one of the above three conditions, the pathogen will be virulent, causing disease to develop.

20. Plant Defense
1. If receptor protein matches the infecting ligand; no infection occurs.
B. Elicitors (These plant cell wall pieces traveling down the phloem indicating damage.)
1. Oligiosaccharines released to cells causing them to produce phytoalexins and PR proteins(antibiotics).

21. Hypersensitive Immune Response
C. Hypersensitive response – Massive release of phytoalexins and PR proteins to injured infected cells.
Causes a “sealing off” effect in leaves. (This tries to keep pathogen from advancing further.)
2. This creates a “Dead Zone” that the pathogen may not be able to move past.
D. Systemic (whole plant) Acquired Resistance (SAR) - Accomplished by releasing salicylic acid production.