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Dr. Anuar Sani 17 July 2007

À  nents  Wh le Bl 

(55% of whole blood)

Buffy coat:
leukocyctes and
(<1% of whole blood)
1 Withdraw blood 2 Centrifuge (45% of whole blood)
and place in tube

Figure 17.1
Pr tecti n
‡ Bl  revents inecti n by:
± Synthesizing an utilizing antib ies
± Activating c leent r teins
± Activating WBÀs t een the b y against
 reign invaers
ºeuk cytes (WBÀs)
‡ ºeuk cytes, the nly bl  c  nents that
are c lete cells:
± Are less nuer us than RBÀs
± Make u 1%  the t tal bl  v lue
± Àan leave caillaries via iaeesis
± M ve thr ugh tissue saces
‡ ºeuk cyt sis ± WBÀ c unt ver 11,000 er
cubic illieter
± N ral res nse t bacterial r viral invasi n
ranul cytes
‡ ranul cytes ± neutr hils, e sin hils,
an bas hils
± À ntain cyt lasic granules that stain
seciically (aciic, basic, r b th) with
Wright¶s stain
± Are larger an usually sh rter-live than RBÀs
± Have l be nuclei
± Are all hag cytic cells
Neutr hils

‡ Neutr hils have tw tyes  granules that:

± Take u b th aciic an basic yes
± ive the cyt las a lilac c l r
± À ntain er iases, hyr lytic enzyes, an
eensins (antibi tic-like r teins)
‡ Neutr hils are ur b y¶s bacteria slayers
E sin hils

‡ E sin hils acc unt  r 1±4%  WBÀs

± Have re-staining, bil be nuclei c nnecte via
a br a ban  nuclear aterial
± Have re t cris n (aci hilic) large, c arse,
lys s e-like granules
± ºea the b y¶s c unterattack against arasitic
w rs
± ºessen the severity  allergies by
hag cytizing iune c lees
Bas hils

‡ Acc unt  r 0.5%  WBÀs an:

± Have U- r S-shae nuclei with tw r three
c nsicu us c nstricti ns
± Are uncti nally siilar t ast cells
± Have large, urlish-black (bas hilic)
granules that c ntain histaine
‡ Histaine ± inlaat ry cheical that acts as a
vas ilat r an attracts ther WBÀs (antihistaines
c unter this eect)
Agranul cytes

‡ Agranul cytes ± lyh cytes an

 n cytes:
± ºack visible cyt lasic granules
± Are siilar structurally, but are uncti nally
istinct an unrelate cell tyes
± Have sherical (lyh cytes) r kiney-shae
( n cytes) nuclei
ºyh cytes

‡ Acc unt  r 25% r  re  WBÀs an:

± Have large, ark-urle, circular nuclei with a
thin ri  blue cyt las
± Are  un  stly eneshe in lyh i tissue
(s e circulate in the bl )
‡ There are tw tyes  lyh cytes: T cells
an B cells
± T cells uncti n in the iune res nse
± B cells give rise t lasa cells, which r uce
antib ies
M n cytes

‡ M n cytes acc unt  r 4±8%  leuk cytes

± They are the largest leuk cytes
± They have abunant ale-blue cyt lass
± They have urle-staining, U- r kiney-shae
± They leave the circulati n, enter tissue, an
ierentiate int acr hages
M n cytes

‡ Macr hages:
± Are highly  bile an actively hag cytic
± Activate lyh cytes t  unt an iune
res nse
Suary  F re Eleents

Table 17.2
Suary  F re Eleents

Table 17.2
Pr ucti n  ºeuk cytes

‡ ºeuk  iesis is h r nally stiulate by

tw ailies  cyt kines (heat  ietic
act rs) ± interleukins an c l ny-
stiulating act rs (ÀSFs)
± Interleukins are nubere (e.g., Iº-1, Iº-2),
whereas ÀSFs are nae  r the WBÀs they
stiulate (e.g., granul cyte-ÀSF stiulates
granul cytes)
‡ Macr hages an T cells are the  st
i rtant s urces  cyt kines
‡ Many heat  ietic h r nes are use
F rati n  ºeuk cytes

Figure 17.11

Defends body against pathogens
Can distinguish between self and non-self

General Defence System (innate) Specific Defence System (adaptive)

Non-specific = acts against all pathogens


Skin = barrier. Sweat (acidic pH)
Clotting = also helps protect skin
Lysozyme = enzyme in saliva, sweat, tears. Attacks bacterial cell walls
Mucous (respiratory, digestive, urinary & reproductive tracts) = traps pathogens
Cilia = little hairs that help clear mucous (and pathogens) from respiratory tract

 = lysozyme in saliva, stomach HCl kills many pathogens, specialised
immune areas in the GI tract, very high turnover of epithelial cells, antibodies
•hagocytic white blood cells (leukocytes) = destroy pathogens that enter

•hagocytes ² (•hago= eat; cyte=cell)

attracted to a site of infection (chemotaxis) by chemicals released by injured cells
Three types ² neutrophils (short lived),
monocytes ( blood) and macrophages ( tissue)
Immune organs Macrophages ² very large white cells that can move
around body, or remain in certain tissues. Long lived,
act as scavengers

‡ set of 30 proteins found in plasma that are activated by
‡ complicated chain reaction that leads to the bursting of
viruses and bacteria
‡ made in the liver

‡ set of proteins produced by virally infected cells cells to limit the spread of viral
infections, by inducing a state of resistance in healthy cells.
‡ induced by viruses, bacteria and other signals from the immune system

‡ infected cells (mast cells) release histamine, which is a vasodilator. This causes
localised swelling, redness, heat, pain. Can also cause high temperature.
‡ brings white cells to the area of infection
‡ Anti-histamines
À leent Pathways

Figure 21.5
Interer n (IFN)

Figure 21.4
Inlaat ry Res nse: Phag cytic
M bilizati n

4 Positive
diffusing from
the inflamed
site act as
1 ÿeutrophils agents
enter blood
from bone 3 Diapedesis
marrow 2 Margination

Capillary wall
Basal lamina
Figure 21.3
Iun c etent B r T cells
è  Key: = Site of lymphocyte origin
= Site of development of immunocompetence
as B or T cells; primary lymphoid organs
= Site of antigen challenge and final
Immature differentiation to activated B and T cells
Circulation in lymphocytes
1 1 Lymphocytes destined to become T
  cells migrate to the thymus and develop
immunocompetence there. B cells

 develop immunocompetence in red
bone marrow.

2 2 After leaving the thymus or bone

   marrow as naive immunocompetent
    cells, lymphocytes ³seed´ the lymph
   nodes, spleen, and other lymphoid
tissues where the antigen challenge

3 Mature (antigen-activated)
3 3 immunocompetent lymphocytes
circulate continuously in the
Activated bloodstream and lymph and
immunocompetent throughout the lymphoid organs of
B and T cells the body.
recirculate in blood
and lymph

Figure 21.8
Antigen-Presenting Àells (APÀs)

‡ Maj r r lls in iunity are:

± T engul  reign articles
± T resent ragents  antigens n their wn
suraces, t be rec gnize by T cells
‡ Maj r APÀs are enritic cells (DÀs),
acr hages, an activate B cells
‡ The aj r initiat rs  aative iunity
are DÀs, which actively igrate t the
lyh n es an sec nary lyh i
rgans an resent antigens t T an B cells
Macr hages an Denritic Àells

‡ Secrete s luble r teins that activate T cells

‡ Activate T cells in turn release cheicals
± Rev u the aturati n an  bilizati n  DÀs
± Pr  acr hages t bec e activate
acr hages, which are insatiable hag cytes
that secrete bactericial cheicals

Antigens ² foreign molecules that

body production

Antibodies (immunoglogulins) ² proteins

produced by lymphocytes in response
to antigens

Monocytes ² develop into macrophages which phagocytose foreign particles (antigens)

Lymphocytes -
Àlasses  Antib ies
‡ IgD ±  n er attache t the surace  B cells,
i rtant in B cell activati n
‡ IgM ± entaer release by lasa cells uring
the riary iune res nse
‡ Ig ±  n er that is the  st abunant an
iverse antib y in riary an sec nary
res nse; cr sses the lacenta an c ners assive
‡ IgA ± ier that hels revent attachent 
ath gens t eithelial cell suraces
‡ IgE ±  n er that bins t ast cells an
bas hils, causing histaine release when
Mechaniss  Antib y Acti n

Figure 21.13
Maj r Tyes  T Àells

Figure 21.14

Mature in Thymus, which is most active just before and after birth.
The thymus starts to shrink during puberty.

Helper T-Cells Killer T-Cells Suppressor T-Cells Memory T-Cells

‡Recognise antigens on Also called cytotoxic ‡Control the ‡Can survive a long time
surface of leukocytes, ‡Destroy abnormal body immune system and give lifelong
especially macrophages cells, e.g. virus infected when the antigen immunity from
‡Enlagre and form a or cancer cells /pathogen has infection
clone of T-helper cells ‡Stimulated by cytokines been destroyed ‡Can stimulate memory
‡Secrete interferon and (THcells) ‡Only recently B-cells to produce
cytokines which ‡Release perforin, which discovered so antibodies
stimulate B-cells and forms pores in target little is known ‡Can trigger production
stimulate killer -cells cells. This allows water about them of killer T cells
‡Can be infected by HIV and ions in = lysis
Killer T-cell How T-cells work«
Abnormal cell e.g recognises antigen
cancer cell, infected cell

Killer T-cells release
perforin pores
Clones of killer T-cell
attach to antigen

Normal cell

Helper T-cell stimulates
correct killer T-cell to
X Abnormal cell gains
Helper T-cell also water, swells and
stimulates B-cells bursts
to make antibodies

Memory T-
cells stay in
Suppressor T-cells
turn off immune

Memory B-cells circulate for a long time. If the same pathogen infects the
body again, these B-cells can produce large amounts of specific antibody
very quickly. This is why you usually don·t suffer from the same infection
Memory T-cells survive a long time and trigger an immune response

‡Sometimes the body produces antibodies against its own tissues e.g. autoimmune
diseases e.g. rhumatoid arthritis, Crohn·s disease, SCID (bubble boy disease),

‡Allergies occur when the body reacts to materials which should not
be antigenic e.g. peanuts

‡Tumours ² in most cases the body recognises tumours as being bad, because they
express abnormal molecules on the cell surface. However sometimes the body doesn·t
notice and cancers can develop

Active immunity •assive immunity

•roduction of a person·s own An individual is given antibodies by another
antibodies. Long lasting Short-term resistance (weeks- 6months)

Natural Active Artificial Active Natural •assive Artificial •assive

When pathogen 
 ² usually Baby in utero Gamma globulin
enters body in the contains a safe antigen (placenta) injection
normal way, we from the pathogen. Breast-fed babies Extremely fast, but
make antibodies •erson makes short lived (e.g. snake
antibodies without venom)
becoming ill


Edward Jenner