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

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….

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

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.

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.)

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.

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

B Cells

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”

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

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

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.)

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

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

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

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.

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).

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.