Assoc. Prof. Ma. Jennifer R.

Tiburcio, MSMT
Department of Med Tech
UST Faculty of Pharmacy
Hypersensitivity

Altered, exaggerated
Harmful to the host

Etiology
Defect in mechanisms
underlying
self-recognition
Anaphylactic

Cytotoxic

Cell mediated
Antibody-mediated Cell-mediated
Type I, II, III and V Type IV

Immune reactions observed Immune reactions delayed

minutes after antigen in time
exposure

Inflammatory reactions – Significant cell infiltration

more fluid erythema w/ resultant cell induration
(Wheal & Flare reaction)
 Type I Immediate/anaphylactic

• Ag stimulates B cells to produce IgE w/ the

help of T cell
• When the Ag subsequently reaches the
sensitized mast cells
• It crosslinks the surface bound IgE
• The Ag specific IgE binds to mast cells via
the Fc receptors, thus sensitizing them
 Type I

• And the cell degranulates

• Releasing mediators
histamine
prostaglandins
leukotriennes
serotonin
• Causing Type I hypersensitivity reactions
 Type II
Cytotoxic

• When the antigenic cell reacts w/ IgG,

opsonization is encouraged
• Because of surface receptor for the Fc
region of the IgG on polymorphs &
macrophages
• Macrophages & killer cells can also cause
contactual damage to IgG sensitized red
cells or other target cells
 Type II

• When the C’ system is activated by IgG or

IgM Abs reacting w/ the cells
• The C3b receptors on the phagocytes
promote immune adherence
• Leading to enhanced phagocytosis or
• The lytic effect may result in membrane
damage
 Type III Immune Complex

• When a certain Ag-Ab ratio exists, the

soluble complexes that form are small &
escape phagocytosis
• These complexes circulate in the blood,
pass between endothelial cells of the blood
vessels
• And become trapped in the basement
membrane beneath the cells
 Type III

• Where they activate the C’ and attract inflammatory

cells such as neutrophils to the site
• The neutrophils discharge enzymes as they react w/
the immune complexes
• Resulting in damage to tissue cells
• Immune complexes can also aggregate platelets &
cause microthrombi
• C3a & C5a can act on basophils releasing
vasoactive amines resulting in increased
permeability
 Type IV Delayed

• Following early priming, memory T cells recognize

the Ag together w/ Class II MHC molecules on
macrophage
• And are stimulated to blast cell transformation &
proliferation
• Continual release of lymphokines from sensitized T
cells leads to accumulation of large numbers of
macrophages
• A proportion of the stimulated T cells release a
number of lymphokines – attracting macrophages
 Type IV

• Separate population of T cells develop cytotoxic

powers
• Many of which give rise to arrays of epithelial
cells
• While others fuse to form giant cells
• Macrophages bearing Ags on their surface may
become targets for killer cells & be destroyed
 Type IV

• Virally infected cells may have an extensive

damaged by cytotoxic cells
• Further tissue damage may occur as a result of
indiscriminate cytotoxicity by LAM & lymphotoxin
itself
• Morphologically, this combination of cell types w/
proliferating lymphocytes & fibroblasts associated
w/ areas of necrosis & fibrosis is termed chronic
granuloma
 Tissue

damage
IL-4, IL-5
EOSINOPHIL
IFN, GM-CSF

SENSITIZED
T-cell

Antigenic GIANT CELL Chronic

granuoloma
stimulation

Cytotoxicity ACTIVATED
? MACROPHAGE EPITHELIOID CELL

Cytotoxicity Tissue

damage
CYTOTOXIC T-CELL
VIRALLY INFECTED CELL
 Type V
Anti-receptor

• Thyroid gland receives instruction from the TSH by

reacting w/ the thyroid gland receptor
• Under abnormal conditions, there’s an excess of self
reactive T and B cells producing autoantibody
• This autoantibody reacts w/ the receptor of the
thyroid gland resulting in
• The thyroid gland receiving signal/information from
the autoantibody
 Type VI Miscellaneous

• C3bBb acts as an antigen

• Antibody (nephritic factor) to C3
convertase – C3bBb
• Observed in the presence of C3a and C5a
(anaphylatoxin) continually activated
forming anaphylactic shock
Type Common Diseases Antigens Mediators

I Allergic rhinitis Pollen, foods (eggs, IgE, mast

chocolates) cells
Bronchial asthma Fungal spores;
animal danders
Drugs or insect bites Penicillin, bee sting

Tropical eosinophilia Parasites

II Transfusion Ags on RBCs IgG, IgA,
reaction IgM and
Penicillin, Complement
Acquired immune quinidine coating
hemolytic anemia RBC

Idiopathic Ags on surface of

thrombocytopenic platelets
purpura

Good Pasteur Ags on basement

syndrome membrane
III SLE Nuclear material IgG, IgA, IgM
RA IgG Complement
Arthus-like Penicillin
reaction
Serum sickness Horse serum
Glomerulonephritis Sheep antigens

IV PTB M. tuberculosis
Leprosy M. leprae
Contact dermatitis Dyes, metal,
catechols
V Grave’s disease TSH receptor of IgG but
acinar cells not C’
fixing
Myasthenia gravis Acetylcholine

VI Gram negative Gram negative

endotoxic shock (LPS) bacteria

Paroxysmal nocturnal Defective red cell

hemoglobinuria membrane
RIST Total IgE concentration

RAST
Specific IgE levels
The pathogenic requirements for immune
complex induced glomerulonephritis include

A. RBC and C’ interaction

B. lymphocytes
C. neutrophils
D. kidney derived antigen
Allergic urticaria is best described as being
a manifestation of

A. an IgE mediated disorder

B. delayed hypersensitivity
C. cytotoxic IgG antibodies
D. cytotoxic T cells
• In order to determine if a patient is allergic
to rye grass, the best test to perform is

A. RAST
B. DAT
C. CF
D. RIST
• In hemolytic disease of the newborn, warm
autoimmune hemolytic anemia and thrombo-
cytopenic purpura, which immune reactant is
responsible for cellular damage?
A. IgE
B. histamine
C. IgG and C’
D. sensitized T cells