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
 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 virus-
infected 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 Description
B - cells Lymphocytes that produce antibodies when stimulated

Produced and mature in the bone marrow

Have glycoprotein receptors on cell surface membrane – bind

specific antigen

Mature cells may become memory cells/plasma cells –

secrete large amount of antibodies
T - cells 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

 2 main categories : TH cells (CD4 receptors) and TC cells (CD8
receptors)
TC cells Recognise and destroy cells with foreign antigens on surface

Mainly attack virus-infected cells, cancerous body cells and

foreign grafted tissue
TH cells Stimulates and enhance immune responses by both B and TC
cells
TS cells Inhibits immune response by other lymphocytes
Macropha Phagocytic leucocytes that destroy microbes
ges
Alert other immune cells to the infection
Memory Derived from B – cells and T – cells
cells
Long-lived

Confer future immunity against secondary infections by same

antigens

– 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 Set of closely-linked genes which codes a set of

histocompatibility proteins (antigen markers) found on the surfaces of
complex (MHC) 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
Cytokines/lympho Regulate many cell activities
kines Act as signals in both the specific and non- specific
immune responses
Eg. Interferons and interleukins
Complement Group of about 20 proteins found in plasma and
other body fluids
 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
– 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