Stpm Form 6

STPM FORM 6 (ALL THAT I’VE MISSED OUT) CHAPTER 12 – IMMUNITY 1. INTRODUCTION – Immunity = the body’s ability to recognise foreign materialwhich has invaded the body, and to respond by removing the foreign material quickly and effectively – 1st line of defence of the body includes : ○ Intact skin which  Difficult to penetrate – tough, impermeable and waterproof  Produces antimicrobial chemicals, makes skin slightly acidic – prevent microorganism colonization ○ Exposed epithelial layer (mouth and eyes) bathed in saliva and tears - contains strong hydrolytic enzymes (lysozyme) ○ Mucous membrane of respiratory and alimentary tracts secrete mucus which traps microbes ○ Ciliated epithelium in respiratory tract sweeps mucus towards pharynx to be discarded out of the body or swallowed into the alimentary tract – microbes killed in stomach by enzyme protease and gastric acid – If 1st line of defences is breached, the body’s non-specific internal defences acts against foreign material; consists of 4 ways ○ Phagocytosis Mechanism : neutrophil/monocyte/macrophage attracted by chemicals released by damaged body cells -> moves towards foreign particle by amoeboid movement -> phagocytic vacuole forms when pseudopodia engulf foreign particle -> lysosome (contain lysozyme, acid, hydrolytic enzymes) fuses with phagocytic vacuole -> enzymes digest foreign particle -> soluble product released into into the cytoplasm of the phagocyte • Neutrophils squeeze through blood capillary walls (diapedesis) to move about tissue spaces, lasting only a few days • Monocytes migrate out of the bloodstream, to become larger macrophages, some circulate throughout the whole body; others reside permanently in tissue/organs (liver, spleen, kidney, lymph nodes) • Macrophages – long-lived phagocytes, can engulf larger particles (old RBCs, protozoan parasites) ○ Natural Killer (NK) cells • WBCs that attack virus-infected bodies cells and abnormal body cells that could form tumours • Mechanism : virus-infected cells display viral proteinson surfaces -> recognised by NK cells -> NK cells release perforin molecules by exocytosis -> perforin molecules

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make large holes/pores on target’s cell plasma membrane causing cytoplasmic content leakage -> target cell death • Plasma membrane of NK cells unaffected by perforin molecules ○ Inflammation – caused by physical damaged to skin/mucous membrane • Damaged cells and certain leukocytes produce histamine and prostaglandins • Histamine – cause local vasodilation (capillary dilate, walls become leaky) – more fluid collected around wound, becoming red, swollen and warm (oedema) • Prostaglandins – promote blood flow to site of injury and increase sensation of pain • Following inflammation, phagocytes appear quickly to destroy microbes, dirt and tissue debris ○ Fever – triggered if microbes infect larger areas of the body • Certain leukocytes released pyrogens in response to infection -> stimulates the hypothalamus to increase the body temperature (> 37C) • Beneficial effects of fever : a) Increase the activity of phagocytes – attack invading microbes more effectively b) Increase the production of interferon in virus-infected cells – inhibits viral replication; activate NK cells; stimulates macrophages to destroy tumour and virusinfected cells If non-specific defence mechanisms fail, the body response with specific immune response Specific immune response = immunity against specific microbes; result from interaction among several types of lymphocytes, the molecules they produce and the foreign materials introduced by the microbes Major cells of the specific immune system

Cells B - cells

Description Lymphocytes that produce antibodies when stimulated Produced and mature in the bone marrow Have glycoprotein receptors on cell surface membrane – bind specific antigen

T - cells

Mature cells may become memory cells/plasma cells – secrete large amount of antibodies Lymphocytes that regulate immune response/kill certain types of cells Produced in the bone, mature in the thymus gland Develop specific receptors which recognise specific antigens

TC cells

TH cells TS cells Macropha ges Memory cells

2 main categories : TH cells (CD4 receptors) and TC cells (CD8 receptors) Recognise and destroy cells with foreign antigens on surface Mainly attack virus-infected cells, cancerous body cells and foreign grafted tissue Stimulates and enhance immune responses by both B and TC cells Inhibits immune response by other lymphocytes Phagocytic leucocytes that destroy microbes Alert other immune cells to the infection Derived from B – cells and T – cells Long-lived Confer future immunity against secondary infections by same antigens

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Major molecules of the specific immune system Immune response and their description Antibody are : Molecutes Description Antigens (Ag) Usually proteins, polysaccharides or glycoproteins carried on surface of cells Causes antibody formation The body can distinguish between its own antigens (self) from foreign antigens (non-self) Antibody (Ab) Immunoglobulin that recognises and binds to specific antigens Neutralise the antigen/tag cells that are antigen Epitope Antigenic determinants that confer a specific shape to the antigen molecule which is then recognised by an antibody/t-cell receptor Major histocompatibility complex (MHC)

Cytokines/lympho kines

Complement

Set of closely-linked genes which codes a set of proteins (antigen markers) found on the surfaces of cells Class I – carried by most nucleated cells; important in self/non-self recognition Class II – mostly found in B-cells, macrophages and some T-cells Class III – components of the complement system Regulate many cell activities Act as signals in both the specific and non- specific immune responses Eg. Interferons and interleukins Group of about 20 proteins found in plasma and other body fluids

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Inactive until the body is exposed to antigens Eg. Histamine Immune response and their description Antibody are : Response Description Cell-mediated Primary defence against cancerous cells and infected response cells Destroys foreign/transplanted tissue Depends mainly on action of T-cells Humoral Involves mainly B-cells but stimulation of T-cells also response necessary Once B-cells activated, produce antibodies which circulate in the body fluids (lymph/plasma) Antibody are : a) Y-shaped immunoglobulin b) Made up of 2 heavy chains (H) and 2 light chains (L) c) Each chain has a constant part and a variable part d) The variable part is specific to the antigen that it binds Major classes of antibodies Antibodies destroy extracellular microbes and antigens by several mechanisms : Class Description Ig M Large molecule made up of 5 Y-shaped monomers linked together Has many antigen binding sites – mainly responsible for agglutination reactions The 1st class antibody produced when initially exposed to an antigen IgM does not cross the placental barrier Ig G Small monomer which easiy moves out of blood vessels and into the tissue fluid Crosses the placenta Most abundant circulating In body fluid Ig A Small molecules made by 2 monomers Produced mainly by cells in the mucous membranes Found in the tears, perspiration, saliva and colostrums Prevents bacteria and viruses from attaching to epithelial surfaces Ig D Mainly found on cell surface membrane of B-cells Function as antigen receptors Cannot cross placental barrier Probably responsible for stimulating the differentiation of B-cells into plasma cells or memory cells Ig E Only produced in small amounts Bind to mast cells and basophils and stimulate them to produce histamines Responsible for allergic response

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Antibodies destroy extracellular microbes and antigens by several mechanisms : a) Neutralisation – antibody combines with/covers up active site of toxins b) Agglutination – the binding site of the antibody molecules attach to antigens on different microbes to cause microbes to clump together c) Opsonisation – the antibody molecules coat the surface of a microbe, making it easier for the phagocytic leukocytes to engulf it d) Precipitation – soluble antigens are bound to antibody molecules to form larger complexes which tend to precipitate e) Complement fixation – antibodies activate complement proteins which leads to lysis of foreign cells