1. Defense System 1. Introduction 2. Non-specific Defense Mechanism 3. Specific Defense Mechanism 4. Chemotherapy & Antibiotics

2. 1. Introduction Protection against diseases by Non-specific defense mechanism Combat against any type of pathogens on their invasion Specific defense mechanism Depend on specific recognition of the invading pathogen for action

4. 2. Non-specific defense mechanism Physical barriers Skin (stratified squamous epithelium of epidermis) Mucous membranes of the respiratory tract Form a natural physical barrier Prevent the entry of pathogens The first line of defense

5. Chemical barriers Gastric juice in stomach -- powerful sterilizing liquid Lysozyme in tissue fluids -- lyse many bacteria

6. Phagocytosis ‘Eating process’ Phagosome surrounds the pathogen Lysosomes fuse with the phagosome to digest and destroy the pathogen Residues discharged out of the cell

7. Inflammatory Response Large number of phagocytes are attracted to the wound area Engulf and kill the pathogens

8. Infected or injured cells release chemical alarm signals, e.g. histamine ( 組胺 ) causing  Blood vessels dilate  Blood flow to the area increases, making infected area red and warm  Permeability of vessel wall increased  Massive flow of fluids out from the blood into the tissues, resulting in swelling

9.  Phagocytes move out from the blood into the area, neutrophils and monocyte (transform into macrophage) engulf pathogens Functions of blood clotting Prevent loss of blood Prevent entry of bacteria and fungi

10. 3. Specific Defense Mechanism Characteristics Specificity Memory Two specific mechanisms Humoral Immune Response (HIR) Cell-mediated Immune Response (CMIR)

11. Terminology Antibodies Protein produced in response to foreign substances Can destroy or neutralize antigens Antigens Substances that can elicit a specific immune response Pathogens Micro-organisms that can cause diseases

12. Humoral immune response (HIR) Antigens e.g. bacteria, pollen, animal fur, red blood cells etc Characteristics B cells are involved Recognize specific antigen and proliferate into plasma cells and memory cells Results in production of antibodies

13. B B Antigen e.g. bacteria, pollen, animal fur, red blood cells, etc B cell Antibody forming cell Plasma cell Antibodies combat against antigen Memory cell

14. Antibodies Y-shaped Protein in nature Two top ends of the ‘Y’ are specific to the particular antigen Bind to antigen Help to destroy or eliminate antigens by Lysis Enhance phagocytosis Neutralize bacterial toxins

16. Cell-mediated immune response (CMIR) Antigens e.g. intracellular bacteria, viruses, foreign substances like skin, kidney etc Characteristics T cells are involved T cells Recognize specific antigen and proliferate into T-killer cell, T-helper cells and memory cells

17. Antigen (e.g. bacteria, viruses, foreign substances...) T T T T T cell Memory cell T-killer cell / Cytotoxic T cell Kill antigen directly Cytokines B cell Plasma cell T-helper cell B

18. Primary response Elicited when an antigen entered into the body for the first time Secondary response Elicited when subsequent entry by the same antigen Characteristics Shorter lag period Sharper increase and a higher level of antibodies produced High antibody level stays longer

20. 4. Chemotherapy & antibiotics Chemotherapy administration of chemical substances, natural or synthetic, to kill or prevent the reproduction of micro-organisms Some of these substances are produced by micro-organisms, which are called antibiotics e.g. penicillin

21. Action of antibiotics Inhibit cell wall formation Damage cell membrane Interfere protein synthesis Inhibit nucleic acid metabolism Drawback of prolonged use of antibiotics Development of resistant strain of micro- organisms

22. 5. Problems arising from immune response A. Blood transfusion (1) ABO blood group Atypical immune response: Natural antibody is present without previous exposure to antigen, e.g. blood group A person has anti-B antibody in the plasma Incompatibility in blood transfusion cause agglutination of RBCs and blockage of the recipient ’ s blood vessels In large scale transfusion, the antibody of the donor ’ s blood will also attack the RBCs of the recipient.

23. A. Blood transfusion (1) Rh factor Rh factor is a group of antigens on RBC surface Rh positive person contain the antigens (dominant) Rh negative person has no such antigens (recessive) Rh- mother carries an Rh+ foetus, some fetal RBCs may cross the placenta during labour, hence stimulation the mother to produce Rh antibodies In the following pregnancies, the anti-Rh antibodies can cross the placenta to attack the foetal RBCs The risk increases with each Rh+ pregnancy as the mother becomes more sensitized

24. B. Organ transplant Surface antigens present in all body cells Due to difference in genome, different persons have different kinds of antigens (except identical twins) The new transplanted organ from the donor will be attacked by T cells of the recipient, causing rejection So transplanted organ must be matched with the recipient, destruction of bone marrow and lymph tissue, and immunosuppressive drugs must be taken May be solved by introducing stem cells into the body which will initiate no or low level immune response

25. C. Allergy e.g. Asthma – narrowing of the bronchi and bronchioles due to swelling of the mucous membrane and excess mucus secretion that obstuct the air passages Over-reaction of immune response to certain substances (allergens), e.g. pollen, fur, food, dust, etc., that do not stimulate a response in non-allergic persons Allergen engulfed by macrophage, and fragments passes to T cells T cells stimulate B cells to proliferate and differentiate into plasma cells to produce antibodies I g E which attaches to mast cells allergens entered the body attahed to mast cells, stimulating the cells to produce histamine, which cause the symptoms of allergy, e.g. rash, profuse mucus secretion

26. D. Autoimmune Disease The immune system fails to recognize and tolerate self antigens So T cells are activated and results in production of autoantibodies Causing inflammation and organ damage E.g. Rheumatoid Arthritis – destruction of joints E.g. Lupus Erythematosus – affecting joints, skin, kidneys, heart, lungs, blood vessels and brain

27. References N. P. O. Green, G. W. Stout, D. J. Taylor. 1993. Biological Science. (2 nd Edition). Cambridge University Press. McGraw – Hill Biology http://highered.mcgraw- hill.com/sites/0072437316/student_vie w0/ http://highered.mcgraw- hill.com/sites/0072437316/student_vie w0/ HK Bio Web