IMMUNOLOGY to

INFECTION
Dr Retno Budiarti, M.Kes
 Innate immunity
Is resistance that is not acquired
through contact with antigen
It is nonspecific and includes barriers
to infectious agent
Skin, mucous membran, natural
killer cells, phagocytosis, inflamation
Vary with age and with hormonal or
metabolic activity
 Innate Immunity Features
Preformed: Rapid-Available on Short
Notice
Standardized

Not Enhanced by Prior Exposure: No

Memory.
Factors relatively Nonspecific

Dependent on species, strain, sex.

 Acquired / Specific Immunity

occurs after exposure to an antigen (eg. An

infectious agent)
spesific
mediated by either antibody or lymphoid
cells
It can be passive or active
 Innate vs. Acquired Immunity
Innate/Natural/ Acquired/Adaptive
Nonspecific /Specific
present from defense
birth mechanisms
tailored to
operates against
individual
any substance
pathogens
not enhanced by enhanced by prior
prior exposure exposure
 Mechanisms/Components of
Innate Immunity
Anatomic barriers
Physiologic barriers

Phagocytic/Cellular Barriers

Inflammatory Barriers
 Anatomic Barriers
External/First line of defenses
Epithelial Barrier
Skin
Mucous membranes
Conjunctivae, GI, resp, urogenital tracts

secretions (saliva, tears, urine, mucus)

wash/trap/inhibit growth
cilia
 Physiological Barriers
Temperature

pH-Stomach, vagina, and skin

Normal microflora of GI tract, skin

Chemical Mediators

Defensins-Secreted by Epithelia
Hydrolytic enzymes of Saliva
Lysozyme in tears
Cellular Barriers
 Innate immunologic mechanisms
Infection in first few hours
engulfment by macrophages
activation of complement release
of cytokines from macrophages and other
mediators that trigger the inflammatory
response hold the spread of pathogen
until a specific adaptive response is
initiated
 A. Reticuloendothelial system
Involves mononuclear phagocytic cells
present in blood, lymphoid tissue, liver,
spleen, bone marrow, lung and other
tissues that are efficient in uptake and
removal of particulate matter from lymph
channels and the bloodstream.
Filtering microorganisms from the
bloodstream
Phagocytosis by RES enhanced by opsonin
 B. Alternative pathway of
complement activation
Can be activated by microbial
surfacers and preceeds in the
absence of antibody
Antimicrobial properties of
complement protein including
opsonization, lysis of bacteria and
amplification of inflamatory
responses through the
anaphylatoxins C5a, C4a and C3a
 C. Phagocytosis
Eating by Cells
Ingestion/Engulfment and Destruction of
Invading Foreign Particles such as Bacteria
The main functions of phagocytic cells
include migration, chemotaxis, ingestion
and microbial killing.
 Professional Phagocytes
Neutrophils
Macrophages :
- derived from monocyte stem cells in
bone marrow
- activated by microbes and their product,
Ag-Ab complexes, inflamation, sensitized T
lymphocytes, cytokines & injury
- activated macrophages release IL-1
(which has activity of inflamation, fever)
and make nitric oxide (nitrogen metabolite
with antimicrobial activity)
 Phagocytosis
Adherence and Opsonization
Ingestion

Destruction
Phagocytosis of Bacteria by
Macrophages
 Factor affecting phagocytosis
More efficient by the presence of
antibodies (opsonins) that coat the surface
of bacteria and facilitate their ingestion by
phagocytes
Opsonization can occur by

Antibody alone can act as opsonis

Antibody plus antigen can activate complement
Opsonin produced by a heat labile system
 Ingestion of foreign particles has
effects on phagocytic granulocytes
O2 consumption increases, increases
superoxide anion and release H2O2
Glycolysis increases

Lysosomes rupture, and hydrolytic

enzymes are discharged into
phagocytic vacuole to form a
digestive vacuole
 D. Inflammatory Response
Infection

Injury

Irritants

Aims of Inflammation
Destroy
Remove the Intruder
Bring the tissue back to normal state
 Cardinal Signs of Acute
Inflammation
Tumor-Swelling

Rubor-Redness

Calor-Heat

Dolor-Pain

Functio Leasa-Loss of function

Acute Inflammatory Response
 E. Fever
Direct mechanical injury or application of
chemical subtances to the
thermoregulatory center in the
hypothalamus result in fever
Subtances capable of inducing fever
(pyrogen) : endotoxin gram negative
bacteria and cytokines released from
lymphoid cells, such as IL-1
Ab production & T cell proliferation are
more efficient at higher body temperature
 F. Interferon
Viral infection induces the expression
of antiviral proteins known as
interferons
Alpha & beta interferons help control
viral replication by inhibiting protein
synthesis in cells
 G. Natural Killer (NK) cells
Play a role in antibody dependent cellular
cytotoxicity (ADCC) & have a role in the
early phase of infection with herpes
viruses and other intracellular pathogens
Can lyse target cells that undergone
malignant transformation and play role in
immune surveillace against tumor
establishment.
Can kill certain virus infected cells
Lytic activity of NK cells is enhaced by
high levels of & interferons
 MECHANISMS OF SPECIFIC
HOST DEFENSE
Ag-taken up by APC make complexes
with MHC (Major histocompatibility
complex) presented to T
lymphocytes.
MHC-Ag complexes are recognized
by specific receptors on the surface
of T cells, and then produce variety
of cytokines
 A. Antibody (humoral)
mediated defense
Helper (CD4) T lymphocytes recognize
pathogens-Ag complexed with class II
MHC proteins on the surface of APC
produce cytokines that activate B cells
produce specific Ig (Ab)
Important to against pathogens that
produce toxins or have polysaccharide
capsules that interfere with phagocytosis
applies mainly to extracellular pathogens
and their toxins
 Antibody (humoral)
mediated defense
Primary response
- when exposure to Ag at the 1st time, Ab
to that Ag is detectable in the serum
within days or weeks depend on the dose
& route of administration
- serum Ab continues to rise for several
weeks & then declines
- the first Ab formed are IgM followed by
IgG, IgA
 Antibody (humoral)
mediated defense
Secondary response
- in the 2nd encounter with the same Ag
months or years after primary response,
the Ab response is more rapid & rise to
higher levels than during the primary
response
- this change of response is attributed to
the persistence of Ag sensitive memory
cells following the first immune response
- the amount of IgM is qualitatively similar
to that produced after 1st contact with Ag.
- Level of IgG tends to persist much longer
than in the primary response
 Antibody (humoral)
mediated defense
Protective functions of Ab
- Ab can produce resistance to infection by
opsonizing (coating) organisms, which
makes them more readily ingested by
phagocytes
- Ab can bind to viruses and reduce their
ability to invade host cells
- Ab can neutralize toxins of
microorganisms & inactivate their harmful
effects
 Active immunization
Ab can be induced actively in the
host by administering appropriate Ag
or preparations containing them
(toxoids of diphtheria, tetanus)
Results are delayed until the Ab
reach helpful concentrations
 Passive immunization
Ab can be administered passively
(preformed in another host), which
makes them immediately available
for preventive or therapeutic purpose
Used in the management of clinical
diphtheria, tetanus and botulism
Important in the prevention of some
viral infections, rabies, hepatitis,
varicella zoster
 B. Cell mediated defense
Ag-MHC class I complex is
recognized by cytotoxic (CD8) T
lymphocytes.
Cytotoxic T cell activity is aimed
mainly at the destruction of cells in
tissue grafts, tumor cells or cells
infected by some viruses
Mainly to intracellular pathogens
 Cell mediated immunity (CMI)
important in toxin induced
disorders, in microbial infections
which polysaccharide capsules, and
in the prevention of some viral
infections
Important in defense against
parasites, tumor, and foreign cells
Includes several cell types and their
products.
Immune evasion by bacteria
Immunity to extracellular bacteria
Immunity to intracellular bacteria
Immunity to intracellular bacteria
Immunity to viral infection
Thank you