Reviewer
Immunology Lecture
IMMUNITY
 generated by natural exposure to pathogens is
certainly an effective way to resist infections
 Artificial immunization- best weapon against
infectious diseases
NATURAL IMMUNITY
 innate and adaptive protect the host from
pathogens and both of them are essential for
survival
 immunity due to the possession of suitable gen
etical characteristics rather than immunityprod
uced in response to a vaccine or serum.
a) Natural active immunity- acquiring a
natural infection that initiates an
adaptive immune response.
 outcome of exposure to
antigens through infection and
usually results in protective
immunity conferred by
antibodies and T cells.
 Agammaglobulinemia-
disease which patients cannot
produce antibodies because of
genetic defects in their B cells.
 develop normal immune
responses to virus
 antibody mediated
immunity is essential for
protection from
extracellular pathogens.
 DiGeorge’s syndrome- a  immunity cannot be maintained and decays
developmental defect that
prevents maturation of the
thymus and inhibits production
of mature T cells.
 patients suffer from
recurrent infections with
viruses and other
intracellular pathogens.
 AIDS- general lack of an
adaptive immune response.
 infection with HIV if not
controlled will result to
the depletion of TH cells
resulting in a lack of
effective antibody and
cellular immunity
 death from AIDS is
characteristically due to
the secondary infections
by one or more
opportunistic pathogen.
b) Natural passive immunity- is a non-
immune person’s acquisition of
preformed immune cells or antibodies
via natural transfer of cells or
antibodies from an immune person.
 Maternal IgG- transferred from
the placenta
 IgA- breast milk
 these provide protection while
the immune system of the baby
matures.
Active immunity
 exposure to antigen; immunity achieved by
injecting antigen or through infection.
 specific response made by individual
achieving immunity
 immune system activated to antigen;
immune memory in effect
 immune state develops over a period of
weeks.
Passive immunity
 No exposure to antigen; immunity achieved
by injecting antibodies or antigen reactive T
cell
 specific immune response made in the
secondary host which donates antibodies or
T cells.
 no immune system activation; no immune
memory
rapidly
 immunity develops immediately
ARTIFICIAL IMMUNITY AND IMMUNIZATION
 major weapon for the treatment and prevention
of diseases.
 Immunization- the purposeful artificial
induction of immunity to particular infectious
diseases
 Two ways by which artificial immunity can be
induced:
 Vaccination (artificial active immunity)
 purposefully exposed to a
controlled dose of harmless
antigen to induce formation of
antibodies
 Production of large quantities of
antibodies and, more
importantly, a population of
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Immunology Lecture
immune memory cells in the
primary response.
 A second (“booster”) dose of
the same antigen results in a
faster response yielding much
higher levels of antibodies and
effector T cells due to immune
memory.
 Active immunity often remains
throughout life as a result of
immune memory.
 Antiserum injection (artificial passive
immunity)
 the individual receiving the
antibodies played no active part
in antibody production
 Individual never has more
antibodies than are received in
the injection, and these
antibodies gradually disappear
from the body.
 Later exposure to the antigen
does not elicit a secondary
response.
 Artificial passive immunity is
usually therapeutic in which
cells or antibodies from an
immune individual are
transferred to a non-immune
individual to prevent or cure
active disease.
 For example, tetanus antiserum
may be administered to passively
immunize an individual suspected
of being exposed to Clostridium
tetani due to an acute injury such
as a car accident.
 The antigen or antigen mixture used to induce
artificial active immunity is known as a vaccine
or an immunogen.
 designed to produce artificial active immunity
may introduce risks of infection and other
adverse reactions..
 Formaldehyde is also used to inactivate
viruses for vaccines, such as in the inactivated
(Salk) polio vaccine.
 Toxoids- modified exotoxin; such as the one
that is the vaccine for C. tetani exotoxin can be
given safely in doses large enough to induce
protective immunity against the exotoxin.
 Immunization with live cells or virus is usually
more effective than immunization with dead or
inactivated material.
 Attenuated strains- it is often possible to
isolate a mutant strain of a pathogen that has
lost its virulence but still retains the immunizing
antigens
 those who are immunocompromised,
may acquire active disease caused by
the live, attenuated immunizing
pathogen.
 Attenuated vaccines tend to provide
long-lasting T cell mediated immunity,
as well as a vigorous antibody
response and a strong secondary
response upon re-immunization
 Attenuated vaccine strains are difficult
to select, standardize, and maintain.
 Because they are alive, attenuated
vaccines usually have a limited shelf
life and require refrigeration for storage.
 Attenuated vaccine strains are difficult
to select, standardize, and maintain.
 Because they are alive, attenuated
vaccines usually have a limited shelf
life and require refrigeration for storage.
 Killed virus vaccines tend to provide
short-lived immune responses without
the development of a long term
memory response, but are relatively
easy to store and maintain their
potency for long periods of time.
 Infants should be immunized to prevent
key infectious diseases as soon as
possible so that their own active
immunity can replace the maternal
passive immunity.
 A single exposure to antigen does not
lead to a high antibody titer, or antibody
quantity. “Booster” shots are given to
produce a secondary response and a
high antibody titer.
IMMUNITY TO PARASITES
 Parasites- they are organisms that lives in
another organism (known as host)
● They derive nutrients, shelter and
protection at the host’s expense
CLASSES OF PARASITES
 Arthropods - ticks, mites, fleas and mosquitos
 Helminths or worms - roundworms,
flatworms, hookworms, whipworms and
tapeworms
 Protozoans - lacks cell wall;Giardia lamblia
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Immunology Lecture
CLASSIFICATION OF PARASITES IMMUNE RESPONSE TO PARASITIC PROTOZOAN
(LOCALIZATION)
 Ectoparasites - parasites that live outside the ● Similar mechanism as of the bacteria and
host’s body viruses removal
 Ex. bed bugs, mites and ● Includes complement system, NK cells and
ticks phagocytosis
 Endoparasites - parasites that live inside the ● Has many breed and species specific, some
host’s body species may be more susceptible to different
 Ex. Plasmodium vivex, pathogens
Wuchereria bancrofti ● Acquired immune response:
o Humoral (Antibodies,t and b helper
HOW PARASITES ARE ACQUIRED? cells)
 Intake of contaminated water and food; o Cell mediated (macrophages, NK cells,
Ascaris,Giardia, Taenia,Fasciola Cytotoxic t-cells and cytokines)
 Contact and penetration of the skin and eyes; ● TH1 -> targets intracellular
Acanthamoeba, Schistosoma, Necator infections
 Sexual Contact; Trichomonas,Entamoeba ● TH2 -> aids antibodies to
control parasite numbers in the
 Inhalation; Enterobius, Naegleria
blood and tissues
 Vector-Borne; mosquito - Plasmodium
HELMINTHS
wuchereria,
● Multicellular eukaryotic invertebrates
kissing bug - Trypanosoma
● Parasitic worms that inhabits on the intestines
of vertebrates
PARASITE INFECTION
● Hard to control -> evasive maneuver against
 An infection caused by parasites that are immune system
capable of damaging, growing and reproducing
inside the body of the host IMMUNE RESPONSE TO HELMINTHS
● Phagocytes attack the parasites and secretes
 COMMON SYMPTOMS OF PARASITIC microbicidal substance to kill organism
INFECTION ● Defense against many helminthic infections is
 Chronic digestive issue mediated by the TH2 cells -> IgE antibodies
 Various forms of mental distress and activation of mast cells and eosinophils ->
 Autoimmune disorders destruction and expulsion of parasites

ARTHROPOD PARASITES
 They are vectors
 They use saliva to spread parasites on the
host
 Saliva has proteins that induces the immune
response of the host which reduces antigen
presentation or cytokine production

IMMUNE RESPONSE TO ARTHROPOD

PARASITES
1. IL-13 & IL-4 activate Goblet Cell and mast cell
 HOST -> produces an immune response in intestine (IL-13 act on intestinal epithelial
against antigens in saliva cells to induce goblet cell hyperplasia)
 Stimulates TH1 -> basophil infiltration 2. Goblet cells secrete mucin and mucus + anti-
 Stimulates TH2 -> production of IgE helminth protein for expulsion (IL-4 stimulates
intestinal smooth muscle hypercontractility to
PARASITIC PROTOZOANS expel helminth)
 Single celled, eukaryotic microorganisms 3. Mast cell secrete protease
 Lacks cell wall 4. Tight junctions open on intestinal epithelial
 Not all are parasitic cells which allows fluid exit to lumen
5. Peristalsis in the intestine
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Immunology Lecture
• TNF-a (tumor necrosis factor a), IL-1b
6. Expulsion of helminth from the intestine (Interleukin 1b), IL-6, type I inferferons and
7. *IL-4, IL-13, & IL-21 activate macrophage chemokines
8. AAM (Alternative Activated Macrophage)
contributes to enhanced tissue repair & fibrosis Adenovirus
9. *IL-5 activates eosinophil and the latter • Common cold, Sore throat, Bronchitis,
proliferates Pneumonia, Diarrhea, Pink eye, Fever,
10. Degranulation of eosinophil (since this Bladder inflammation or infection, Inflammation
contains granules) of stomach and intestines, Neurologic disease
11. Release of mediator (basic protein) • Release of IL-7
12. Mediator toxic to helminth
Human Immunodefiency Virus
IMMUNE EVASION OF PARASITES • Lentivirus
• Destroys CD4+ T cells, macrophages and
 Motility = hide from localized inflammatory dendritic cells
cells • killing of infected CD4+ T cells by CD8
o ex. Some parasites move to areas like cytotoxic lymphocytes that recognize infected
the cornea of the eye because there cells
are no immune cells present in that • Two pathways of cell to cell transmission:
area. – infected T cell to target T
 Block surface antigen expression to avoid cell
detection (Parasite coats itself with host – productive infection by
proteins) macrophages or capture
 Block surface antigen expression to avoid and transfer or virions by
protection (protozoan) dendritic cells
 Their size alone prevents normal immune
responses such as phagocytosis DEFENSE WALLS AGAINST VIRUSES:
 Their thick extracellular coat is hard to
penetrate 1. Intrinsic - skin, mucus
2. Innate - stops most of the infections ; release of
IMMUNITY TO VIRUSES cytokines
3. Adaptive - action of T cells and B cells
VIRUSES
 do not have cells For viral infection to be successful:
 cannot metabolize  Sufficient virus
 cannot reproduce on their own  Cells at the site of infection must be
 will only be a living organism if a host is accessible, susceptible, and permissive
invaded  Defense systems must be absent or initially
 replicate within cells ineffective.

COMMON VIRAL DISEASES INTRINSIC DEFENSE WALLS - “First Defense Wall”

a) Direct Contact- mucosal linings of the
Rhinovirus respiratory, alimentary, and urogenital tracts,
• cause of common colds the outer surface of the eye and the skin
• proliferates in temperatures between 33–35 °C b) Indirect Contact- microbes left on surfaces
• Rhinovirus A and B bind to ICAM-1 (Inter- c) Vectors- mosquitos
Cellular Adhesion Molecule 1
• Infected cells produces chemokines and INNATE IMMUNITY - “Second Defense Wall”
cytokines  has the ability to detect viruses as “Foreign
• Neutralized by IGA or macrophages Substances”
• Influenza virus  Pattern recognition receptors - distinguish
• Influenza A, B, C Virus viral proteins and nucleic acids from cellular
• high fever, runny nose, sore throat, muscle counterparts
pains, headache, coughing
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Immunology Lecture
PRRS: ADAPTIVE IMMUNITY
RIG-I - retinoic acid-inducible gene I- detects  antigenic specificity, diversity, memory and
dsRNA or ssRNA with a 5′-triphosphate ability to distinguish between self and non-self
 leads to release of interferons  involves Lymphocytes (B-cells and T-cells)
and antigen presenting cells (macrophages,
TLR - Toll-like receptor- which sense viral B-cells, and dendritic cells)
glycoproteins, dsRNA, ssRNA, and the
sequence CpG in viral DNA TWO RESPONSES BY THE ADAPTIVE IMMUNITY:
Cytokines / Interferons - indication that host is a) Cell mediated
infected b) Humoral
 elicit fever, sleepiness, lethargy, muscle pain,
loss of appetite, and nausea.  Some viruses do not activate adaptive
 protects other cells from virus infections immunity well.
- do not stimulate inflammatory response
PATTERN RECORGNITION RECEPTORS - some are non-cytopathic
 Non-cytopathic viruses:
Receptor Ligand Localization - cells are not damaged
- cells do not die of infection
TLR3 dsRNA endosomes/lysosomes
- chronic carriers
TLR7 ssRNA endosomes/lysosomes
 Some viruses do not activate adaptive
TLR8 ssRNA endosomes/lysosomes immunity well because of immune evasion of
RIG-1 ssRNA cytoplasm virus.
 Viruses alter their antigens which means that
 Sentinel cells - cells which act as the body's no vaccine can kill the strains of HIV
first line of defense  Example: HIV
 dendritic cells, macrophages and NK
cells
 Dendritic cells - have phagocytic and
antigen presenting
properties

FUNCTIONS OF DENDRITIC CELLS:

- present virus proteins
- release inflammatory cytokines
- phagocytose dead and dying cells

 Dendritic cells
- only matures when viral antigen is present
- will travel to lymph nodes after maturation
- presentation of viral antigen to naive T cells

 Natural Killer Cells

- not phagocytic
- have inhibiting anf activating receptors
 Activating receptor
- binds to the glycoprotein on the cell
surface
 Inhibitory receptor
- binds to the MHC molecule
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Immunology Lecture

IMMUNITY TO EXTRACELLULAR BACTERIA

• Extracellular bacteria are capable of replicating

outside host cells.
• They cause disease by two principal
mechanisms
• Induce inflammation, resulting to tissue
damage HOST DEFENSE MECHANISM
• Produce toxins – Endotoxins & • Secretory IgA antibodies
Exotoxins - Block bacterial attachment to mucosal
• The immune responses against extracellular epithelial cells
bacteria are aimed at eliminating the bacteria • Gram-negative bacteria
and at neutralizing the effects of their toxins - Have pili for attachment
• infections where bacteria can live outside cells - Bordetella pertussis
after entering the body - secrete adhesion molecules that attach
• bacteria do not invade and live inside the cells to both the bacterium
of the host
ANTIGEN-NONSPECIFIC HOST DEFENSE
RESPONSE
• Mucosal defense
Toxin-induced - gastrointestinal tract – the secretion of
Attachment to Invasion to
Proliferation damage to
host cells host tissue
host cells mucus, and the detergent action of bile
limit the number of bacteria
- Mucin - traps microbes and facilitates
their removal
- Defensins - disrupt bac terial
IMMUNE RESPONSE TO EXTRACELLULAR membranes
BACTERIA • Acute Inflammation
- various inflammatory products such as
1. Infection induces production of humoral peptidoglycan, LPS, LTA, exotoxins,
antibodies lipoproteins, and glycolipids
• Antibodies act: • Systemic Response to Bacterial Invasion
- To protect the host from - Fever and accumulation of leukocytes
invading organism at the site of infection
- Inactivation of bacterial toxins
2. Pathogen induces a localized inflammatory ANTIGEN-SPECIFIC HOST DEFENSE RESPONSE
response
 Response of the Host (B Cell) Immune System
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Immunology Lecture
• host develops antibodies to many
different bacterial antigens
 Protective Mechanisms of Antibodies
• Anti-toxin antibodies can protect a host
by blocking the action of the toxins
• increasing the removal rate of the
toxins
Evasion of Bacteria
• Some bacteria evade the IgA response of the
host by changing these surface antigens.
- N. gonorrhoeae – pilin sequences are
rearranged to evade neutralization by
IgA
• Some bacteria possess surface structures that
serve to inhibit phagocytosis.
- Streptococcus pneumoniae –
polysaccharide capsule (84 serotypes)
prevents phagocytosis
- Streptococcus pyogenes – surface
protein projection M protein that inhibits
phagocytosis
- Staphylococci - secrete a coagulase
enzyme that precipitates a fibrin coat
- Gram-negative bacteria
• Long side chains on the Lipid A moiety of the
cell-wall core polysaccharide help to resist
complement mediated lysis
• Pseudomonas- secretes elastase toinactivate
both the C3a and C5a anaphylatoxins, thereby
diminishing the localized inflammatory
reaction.