MALAMULO COLLEGE OF HEALTH SCIENCES

DEPARTIMENT OF BIOMEDICAL SCIENCES

COURSE NAME : IMMUNOLOGY AND SEROLOGY

LECTURES NAME : C. KAMWENDO

STUDENT NAME : MISHECK MAGANGA

STUDENT ID # :BMS/22/688

ASSIGNMENT : TYPES OF HYPERSENSITIVITY

HYPERSENSITIVITY
Is uncontrolled response to an antigen.
This reaction may cause inflammations, cell destruction or tissue injuries
There classification are based on time after exposure to antigen .E.G. immediate and delayed
hypersensitivity
TYPES OF HPERSENSITIVITY
There are 4 types of hypersensitivity

1. TYPE 2 HYPERSENSITIVITY
This is type were an antibody-mediates immune reaction in which antibodies {igG or igM} are
directed against cellular or extracellular matrix antigens, cell receptor which perceive as non-self
as stated
Type 1, 2, 3 hypersensitivity are known as immediate hypersensitivity reaction because they
occur within24 hours of exposure to the antigen or allergen
They are cytotoxic mediated reaction

THE MECHANISM

The autoantibodies (IgG and IgM) binds to the host antigen of a targeted cell after binding it
produces immune response which leads to destruction or dysfunction of the cell. The destruction
can happen in the following ways; it can activate the complement system, and this complement
system can destroy the host target (which can be either cell or extracellular tissue). Another way
that destruction can occur is through antibody dependent cellular cytotoxicity, this happens after
the binding of the autoantibodies that it triggers the natural killer cells destroy the host target.
The third way in which destruction can occur is through inflammatory cells, where cells like
neutrophil releases there intracellular content to destroy the host antigen or cells like
macrophages phagocytize the hosts’ antigen due to the opsonisation of the autoantibodies.

The following are some examples of type II hypersensitive reactions: these examples can
further be divided into type IIA and type IIB hypersensitivity.
a. Autoimmune Hemolytic Anemia, this is when the body inappropriately perceives its own red
blood cells as foreign and the autoantibodies (IgG and IgM) binds to the red blood cells antigen
which reads to destruction and hence causing anemia. And this is a type IIA reaction.

b. Myasthenia Gravis, this is an autoimmune disease caused by inhibitory antibodies that bind
and block the acetylcholine receptor, causing muscular weakness and fatigue. Which is a Type
IIB hypersensitivity reaction.

c. Good pasture’s syndrome, this is when the autoantibodies attack the basement membrane of
the lungs and the kidneys this reads to hemoptysis (coughing up blood) or hematuria (blood in
urine). And it’s a Type IIB hypersensitivity reaction.

d. Rh factor incompatibility between mother and fetus can also cause a type II hypersensitivity,
this is when the mother to be is Rh negative and the Father to be is Rh positive an there is
incompatibility of the rhesus factor. The unborn baby might be Rh positive and since the blood
of the mother does not directly come to contact with the unborn blood nothing happens but
during delivery the child’s blood come to contact with the mothers blood and the mothers blood
produce Rh antibodies and the coming pregnancies if the baby is Rh positive IgG antibodies
binds and destroy the fetus cells reading to miscarriage.

TREATMENT

 Steroids: these drugs include prednisolone, dexamethasone.

 Intragam infusion: this is infusing the body with antibodies.
 plasmaphoresis: this is removing the blood autoantibodies

TYPE III HYPERSENSITIVITY

In type III hypersensitivity reactions, autoantibodies binds directly to antigens forming
compound called antigen-antibody immune complexes. These are cleared by neutrophil and
macrophages. However this immune complexes can increase and overwhelming the neutrophils
and the macrophages and are disposed in tissues, causing inflammatory lesions. Complement
activation leads to the recruitment of inflammatory cells (monocytes and neutrophils) that release
lysosome enzymes and free radicals at the site of immune complexes deposited, causing tissue
damage.
The mechanism.
After exposure to antigen, an individual's immune system responds by creating antibodies after
4-10 days. The antibody reacts with the antigen, forming immune complexes that circulate and
can diffuse into the vascular walls, where they may initiate fixation and activation of
complement. These immune complexes, along with complement, produce an influx of
polymorph nuclear leukocytes into the site, where tissue damage takes place by the release of
protolytic enzymes. The process takes place in three steps:

Immune complex deposition: The pathogenicity of immune complexes is partly dependent on

the antigen-antibody ratio. When the antibody is in excess, the complexes are insoluble, do not
circulate, and are phagocytosed by macrophages in the lymph nodes and spleen. However, when
the antigen is in excess, the aggregates are smaller. They freely filter out of circulation in organs
where the blood is transformed into fluids such as urine and synovial fluid. Therefore, immune
complexes affect glomeruli and joints. (Autoimmunity). In both cases, the antigens bind to
antibodies, forming circulating immune complexes, later migrating out of plasma and depositing
in host tissues.

Immune complex formation: Endogenous or exogenous antigen exposure triggers an antibody

formation. Exogenous antigens are foreign proteins such as infectious microbes or
pharmaceutical products. Endogenous antigens are self-antigens against which autoantibodies are
generated.

Inflammatory reaction: After the deposition of the immune complexes, the final step is
activating the classical pathway, which then recruit macrophages and neutrophils and causes
inflammatory damage to tissues. Depending on the site, symptoms of vasculitis (blood vessels),
arthritis (joints), or glomerulonephritis (glomeruli) develop.

The following are some examples of type III hypersensitive reactions:

a. Serum sickness, on exposure to a foreign serum protein, 6-10 days later antibodies and form
antigen-antibody complexes. If the macrophage activating system is not functioning properly,
these complexes will become saturated in the circulation, leading to immune complex deposition,
most commonly in parenchymal tissues and synovial joint fluid. The deposition of immune
complexes may activate the classical complement pathway, which will trigger histamine release
and increase vascular permeability, which leads to an inflammatory response in the tissues and
joints.
b. Systemic Lupus Erythematosus (SLE): SLE is an autoimmune disease with multisystem
involvement. The condition is characterized by the presence of circulating IgG and IgM
autoantibodies to host tissue components. In most cases, the antibodies are directed against the
parts of the nucleus, such as double-stranded DNA, histone, and ribonuclear proteins. In some
patients, autoantibodies against the cells, including platelets, erythrocytes, neutrophils, and
lymphocytes, can be present.

c. Glomerulonephritis: The glomerular deposition of immune complexes is the one which causes
glomerulonephritis. The presenting features could include microscopic or gross hematuria,
proteinuria, hypertension, edema, and elevation in serum creatinine.

TREATMENT

 Removal of the offending agent is the mainstay of treatment of type III hypersensitivity
reaction.

 Antihistamines and nonsteroidal anti-inflammatory drugs can provide symptomatic relief.

 Corticosteroids are used in severe cases to suppress inflammation.

TYPE IV HYPERSENSITIVITY

This type of hypersensitivity reactions is unique because it does not involve antibodies but it
rather involves T cells hence it is a cell-mediated reaction that can occur in response to contact
with certain allergens. But this process is more delayed than the other hypersensitivity reactions.

The mechanism.
The mechanism takes place in two phases;

i. Sensitization phase
This phase occurs when an antigen is exposed to the body and the antigen presenting
cells bind to the antigen. The antigen presenting cells can be macrophages. This
 macrophage presents the antigen to a helper T cell and the cell turns into a Th1 (memory
T cell) for that specific antigen.

ii. Effector phase

This phase starts when the same antigen is being exposed to the body and the antigen
presenting cells binds to the antigen again and this time around it presents the antigen to a
memory T cell. The memory T cell will release its content which recruits cells like
cytotoxic T cell, macrophages and other helper T cells to the exposed area, this induces
inflammatory response.

The following are some examples of type IV hypersensitive reactions:

a. Poison ivy, molecules are small enough to quickly make its way through the epidermis to
the dermis, which is where it might combine with small proteins, it then might get picked up by
dendritic cells which is a type of antigen presenting immune cell.

b. Contact dermatitis, is an itchy rash caused by direct contact with a substance or an allergic
reaction to it. The rash isn't contagious, but it can be very uncomfortable. Many substances can
cause this reaction, such as cosmetics and plants. The rash often shows up within days of
exposure.

TREATMENT

 medications like corticosteroids

 Avoiding exposure to the triggering antigen.
REFERENCES

 John B. Zabriskie, Essential clinical immunology. 2008, Cambridge University Press,

New York.
 Pichler WJ. Delayed drug hypersensitivity reactions. Ann Intern Med. 2003 Oct
 Linda E Miller, C.D Stevens, Clinical Immunology and Serology, 5th edition, © 2021.
 Rakesh sharda, Hypersensitivity (Department of veterinary microbiology NDVSU
College of veterinary science & a.h).
 Tedner, S. G., Asarnoj, A., Thulin, H., Westman, M., Konradsen, J. R., & Nilsson, C.
(2022). Food allergy and hypersensitivity reactions in children and adults-a
review. Journal of Internal Medicine, 291(3), 283-302.