About immunity, its types & cells involved in immunity

2. IMMUNITY
Presented By: KASHF IDREES, KAINAT MALIK & KHUDEJA IDREES
3rd Professional year
Pharm-D
LCWU

3. Immunity:
■ The ability of an organism to resist a particular infection or toxin by the action of
specific antibodies or sensitized white blood cells.
■ The immune system main function is to PREVENT or LIMIT INFECTION.
■ First line of Defence:
■ skin & mucous membranes
■ Second line of Defence:
■ Innate arm (Cells & anti bodies)

4. Immunity
Innate immunity
Acquired
immunity
Cell mediated
immunity
Humoral
immunity
Active
immunity
Passive
immunity

5. Innate immunity:
■ The ability of innate arm to kill microorganisms is not specific.
■ It is also called natural immunity.
■ It is the resistance exist prior to exposure.
■ It includes barrier to infectious agents (skin, mucous membrane) & certain cells.
■ The processes are phagocytosis & inflammation
■ It has no memory & dose not improve after exposure.

6. Functions:
■ Killing invading microbes
■ Activating acquired immunity
■ Pattern recognition receptors:
■ These are the receptors present on surface of components of innate arm which
recognize specific pattern on microbes, they can not distinguish between different
microbes but still differentiate between microbes & human cells.

7. Acquired immunity:
■ It activates after exposure
■ It improves upon repeated exposures
■ It is specific.
■ They have long term memory
■ components:
■ T-cells & Antibodies

8. Functions:
■ Antigen presentation
■ Antibody production
(Note that acquired immunity can be activated only if innate arm recognize the microbe)
■ Types:
■ It can be active or passive immunity.
■ Active immunity:
■ It is the resistance induce after contact with foreign antigens
■ Long term (advantage) & slow onset (disadvantage)

9. ■ Artificial active immunity (vaccination)
■ Natural active immunity (resistance against pathogens)
■ Passive immunity:
■ It is resistance based on antibodies performed in another host
■ Prompt availability (advantage)
■ Short life span (disadvantage)
■ Artificial passive immunity (antibodies against hepatitis etc)
■ Natural passive immunity (IgG mother to fetus, IgA mother to new born through
breast feeding)

10. Comparison b/w Active & Passive
immunity:
Active immunity
■ Antibodies &T cells
■ Long duration(years)
■ Slow onset
Passive immunity
■ Antibodies
■ Short duration
■ Immediately available

11. Comparison B/w Innate & Acquired
Immunity:
Innate Immunity
■ Non specific
■ Effective immediately after
exposure(within minutes)
■ Does not improves after exposure
■ No memory
Acquired Immunity
■ Highly specific
■ Requires several days to become
effective
■ Improves after exposure
■ Long term memory

12. Humoral Immunity:
■ Humoral immunity is the aspect of immunity that is mediated by macromolecules found in
extracellular fluids such as secreted antibodies, complement proteins.
■ It involves substances found in Body fluids
■ Also known as antibody mediated immunity.
■ it includes primary & secondary response.
■ Primary response:
■ When antigen is first encountered, antibodies are detectable after a longer lag period (7-
10days)
■ A small clone of B & plasma cells is formed & antibodies concentration rises continuously.

13. ■ Firstly IgM appears
■ Secondary Response:
■ When second encounter with same antigen (or closely related one) occurs there is
rapid antibody response (lag period of 3-5days)
■ The memory cells proliferate to form larger clone of B & plasma cells.
■ The amount of IgM is similar to primary response while IgG is much larger.
(when two or more antigens administered at same time the host reacts by producing
antibodies to all of them)

14. Cell mediated Immunity:
■ Cell-mediated immunity is an immune response that does not involve antibodies, but
rather involves the activation of phagocytes, antigen-specific cytotoxicT-lymphocytes, and
the release of various cytokines in response to an antigen.
■ It is important in intracellular infections (tuberculosis).
■ Cellular immunity protects the body by:
■ T-cell mediated immunity orT-cell immunity : activating antigen-specific cytotoxicT cells
that are able to induce apoptosis in body cells displaying epitopes of foreign antigen on
their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells
displaying tumor antigens;
■ activating macrophages and natural killer cells, enabling them to destroy pathogens; and
■ stimulating cells to secrete a variety of cytokines that influence the function of other cells
involved in adaptive immune responses and innate immune responses.

15. ■ In primary responseT cells form a clone of cells while in Secondary response the clone
expands & more specificT cells formed.
■ When antigen or simple chemical tend not to elicit cell mediated response,they are
given with an adjuvant (it enhance the uptake of antigen By APC).

17. Antigens:
■ These are molecules which react with antibodies while immunogens are molecules
which induce an immune response.
■ (mostly antigens are immunogens except Haptens)
■ Haptens:
■ A molecule that is not immunogenic itself but can react with specific antibody,mostly
they are small molecules
they are not immunogenic as they can not activate helperT cells because of their
inability to bind MHC proteins (as they are not polypeptide)
■ They are univalent so can not activate B cells
■ They need carrier protein to become immunogenic.

18. The features of molecules that
determine immunogenicity:
■ Foreignness
■ Molecular size (above 100,000)
■ Chemical structure complexity (homopolymers are less immunogenic than
heteropolymers)
■ Epitopes(chemical groups that can elicit & react with antibody,if more than 1
determinant called multivalent)
■ Dose, Route & timing of administration.

19. Antibody:
■ These are globulin( gamma) proteins that react specifically with antigen that
stimulated their production
■ Make up 20% protein of blood plasma
■ Structure:
■ They are glycoproteins
■ Made of Light (mol.Wt. 25000) & Heavy (mol.wt.50000-70000) chains
■ Two heavy & two light chains are linked with disulphide bonds
■ Light & heavy chains are further divided into Variable( for antigen binding) &
Constant( for biological functions) regions.

20. Antibodi
es
Heavy
chain
type
Physical
state
J
(joining)
chain
Molecula
r weight
Sub
classes
%age in
blood
Comple
ment
fixation
Placenta
crossing
Site
found
Function
IgG gamma monome
r
no 150,000 4 80% + + Body
fluids
Neutraliz
e toxin,
ease in
phagocyt
osis
IgM mu pentame
r
yes 900,000 1 6% +++ no blood In
primary
response,
in
agglutina
tion
IgA alpha Polymer,
monome
r, dimer
yes 160,000 2 13% - no Serum,
body
secretion
s
Protect
mucous
IgD delta monome
r
no 180,000 1 1% - no Serum,
lymphoc
yte
surface
Antigen
receptor
IgE epsilon monome
r
no 185,000 1 0.002% - no serum In
immediat

22. Cellular basis for Immunity:
■ From bone marrow stem cells differentiate into Erythroid, Myeloid & Lymphoid series.
Lymphoid series:
■ It has B &T cells.
T-Cells:
They are 65-80% of lymphocytes
■ Life span; months or years
■ Formation:
■ In embryonic life liver & yolk cell while in postnatal life in bone marrow.
■ T cells precursor differentiation occur within the thymus.

23. ■ T cells differentiate into HelperT Cells( CD4) & Cytotoxic T Cells (CD8).
■ InThymusT cells undergo Clonal deletion
■ HelperT-Cells: (CD4)
■ They have two sub classes; Th-1 cells & Th-2 cells
■ Th-1 cells; produce Interlukin-2 & gamma interferon
■ IL-2 help activating CD8 cells & delayed HS while gamma interferon activates
macrophages.
■ Th-2 Cells; produce IL-4 & IL-5 which help B-cells to produce antibodies.
■ (IL-12 by macrophages keeps balance b/wTh-1 &Th-2,IL-12 increases the no.ofTh-1)

24. Functions:
■ Delayed hypersensitivity (effector role)
■ Antibody production (regulatory role)
■ Cell mediated immunity
■ CytotoxicT-Cells (CD8):
■ Most cytotoxicT cells expressT-cell receptors (TCRs) that can recognize a specific antigen.
An antigen is a molecule capable of stimulating an immune response, and is often
produced by cancer cells or viruses.Antigens inside a cell are bound to class I MHC
molecules, and brought to the surface of the cell by the class I MHC molecule, where they
can be recognized by theT cell. If theTCR is specific for that antigen, it binds to the
complex of the class I MHC molecule and the antigen, and theT cell destroys the cell.

25. THEY KILL BY
INDUCING
APOPTOSIS OR
RELEASE OF
PERFORINSWHICH
DESTROY CELL
MEMBRANE
SUPPRESSION OF
CERTAIN IMMUNE
RESPONSE.

26. MemoryT-Cells:
■ MemoryT cells protect against previously encountered pathogens
■ They secrete IL that enhance antibody production
■ B-CELLS:
■ In embryonic life formed in liver while in adults formed in bone marrow
■ Life span; days or weeks
■ Form 30% of lymphocytes
■ Found in spleen & lymph nodes

27. Clonal
Selection:
■ The antigen binds to B-CELLs
( having IgM or IgD) the B
cells formed a clone of cells,
the selected B cells become
Plasma cells which secrete
antibodies
■ They also act as APC (
antigen presenting cells)
■ MEMORY B-CELLS have
surface IgG

28. Natural Killer
Cells (NK):
■ They are also lymphocytes
make up5-10% of it
■ They kill virus infected cells &
tumor cells by secreting
cytotoxins
■ They are active without prior
exposure to virus

29. Myeloid Series:
MACROPHAGES:
■ Their main functions are:
■ Phagocytosis; they have surface Fc
receptor which interact with Fc
portion of antibodies & enhance
uptake of opsonized organisms (kill
by reactive O2 & N)
■ Antigen presentation; foreign
martial is ingested & degraded,
presented on surface of macrophage
in conjunction with class 2 MHC
proteins.
■ Also involve in Cytokine production

30. Dendritic Cells:
■ They are APC.
■ Neutrophils:
■ They are stained pale pink (Wright’s stain)
■ They have bactericidal action, involved in
phagocytosis

31. Eosinophils:
■ They are stained red, important in Parasitic & HS diseases
■ Contain histaminase (enzyme degrade histamine)
■ Basophils & Mast Cells:
■ Basophils are stained blue
■ Both release Histamine, causes inflammation such
as systemic anaphylaxis

32. Reference:
■ Medical microbiology & immunology, Book by Ernest Jawetz andWarren E. Levinson,
seventh edition.

33. THANKYOU….