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DISORDERS OF THE IMMUNE
SYSTEM:
ALLERGIES
Your Immune System
The organs involved with the immune system are the
lymphoid organs, which affect growth, development,
and the release of lymphocytes.
The blood vessels and lymphatic vessels are important
parts of the lymphoid organs, because they carry the
lymphocytes to and from different areas in the body
Each lymphoid organ plays a role in the production and
activation of lymphocytes. Lymphoid organs include:
adenoids, tonsils, appendix, lymph nodes, spleen,
Peyer’s patches (lymph tissue in your small intestine),
thymus
Disorders of the immune system
When the immune system does not function properly, it leaves
the body susceptible to an array of diseases
Allergies and hypersensitivity to certain substances are
considered immune system disorders
Examples of immune disorders include:
•cancer of the immune system (leukemia)
•autoimmune diseases, such as juvenile diabetes, rheumatoid
arthritis, and anemia
•immune complex diseases, such as viral hepatitis and malaria
•immunodeficiency diseases, such as acquired
immunodeficiency syndrome (AIDS)
Autoimmune diseases
autoimmune rx’s can be directed against
•the brain multiple sclerosis
•the gut in Crohn's disease
•other autoimmune diseases such as systemic lupus
erythematosus (lupus)
•damage to certain tissues by the immune system
may be permanent, as with destruction of insulinproducing cells of the pancreas in Type 1 diabetes
mellitus
Hypersensitivity
 Abnormal
sensitivity to
microorganisms, products or certain
foreign substances
 Sensitivity beyond what is
considered normal
Nature of Hypersensitivity
Chemical nature of the allergen (pollen, food, latex,
metals, synthesized chemicals, penicillin)
 Sensitizing route-ingestion, injection, skin contact
 Individual traits-anatomical and physiological traits
 Once sensitized, another exposure to the Ag
triggers an immune response that damages host
tissue –sensitization can takes years I.e. a lot of
people come to AZ with NO allergies, after 5-7
years they develop allergies

Allergen

Any substance which gives rise to allergy
(antigen)
HYPERSENSITIVITY (allergy)

Excessive (harmful) immune response
 Individuals
previously exposed (sensitized) to
an antigen (allergen)

Four main types (I-IV)
TYPES OF HYPERSENSITIVITY

Type I

Type II
 Anaphylatic
 Cytotoxic
reaction (less than 30 min)
reaction (5 to 12 h)
TYPES OF HYPERSENSITIVITY (cont.)

Type III
 Immune-complex

reaction (3 to 8 h)
Type IV
 Cell-mediated
reactions (24 to 48 h)
TYPE I (ANAPHYLATIC
REACTION)

Ana (against), phylaxis (protection)
 Hay
fever
 Asthma
 Hives
Type I (mechanism)

Antigenic stimulus (Ag’s + Ig’s combine)
 IgE
production is triggered
 IgE’s might trigger a systemic response, producing
sometimes fatal shock and breathing difficulties
 or a localized rx, such as hay fever, asthma or
hives
IgE bind to mast cells and basophils
 Mast cells are prevalent in the connective
tissue of skin, the respiratory tract, and
surrounding blood vessels
 Basophils circulate in the blood

Type I (mechanism) (cont.)

Mast cells and basophils degranulate after
successive antigenic stimuli
 Histamine
--affects blood vessels-causing edema,
erythema, increased mucus
 secretion and smooth muscle contraction, resulting
in breathing difficulties
 Leukotrienes –cause contraction—like the spasms of
asthmatic attacks
 Prostaglandins tend to cause increased secretion of
mucus
Anaphylactic response to bee venom
Type I
(local reactions)
Hay fever (histamine-mediated response to
inhaled antigen)
 Asthma

 Inhalation

Hives (urticaria)
 Ingestion
of food or drug—often difficult to
distinguish btw food hypersensitivity & food
intolerance
Urticaria
wheals on the thigh
Swelling of lips and
eye lids
Can hives occur anywhere
else?
Around 1 in 3 people with hives
can also have swelling of the
tongue and throat. This is called
angioedema, and is caused by
similar swelling deeper in the
tissues. Occasionally the
swellings will occur inside the
stomach and cause tummy pain
or cramps.
Underneath the lining of the skin, gut, lungs, nose and eyes are mast
cells. These are designed to kill worms and parasites. Mast cells are like
"land-mines", and contain "bags" filled with irritant chemicals including
histamine. When these are released in small amounts, they cause local
itch and irritation. In larger amounts, they will cause fluid to leak out of
blood vessels, resulting in swelling of the skin.
Allergic reactions to food, pain killers (such as aspirin or arthritis tablets like
naproxen, diclofenac) or antibiotics can also trigger hives. Sometimes insect
stings, food additives or preservatives can trigger hives
TYPE I
(systemic reactions)

Anaphylactic shock
 Injected
antigens (bee sting)
 weak pulse,low blood pressure, low
temperature-- it may be fatal
 Breathing difficulties
PREVENTION OF
ANAPHYLACTIC REACTIONS
Avoid contact with the allergen
 Skin tests (wheals)



Determine cause
Desensitization (injection of small doses of the
Ag—to induce IgG AB’s production, to serve as
blocking AB’s that intercept & neutralize Ag’s
before they can react with cell bound IgE’s)
TYPE II (cytotoxic reactions)
Cell (RBC or tissue cells) bearing or coated with
antigens
 Antibody-antigen reaction activates
complement
 Complement & MQ destroys antigen bearing
cells

TYPE II (cytotoxic reactions)
Transfusion reactions
 ABO blood group system

 Carbohydrate
antigens A and, or B on RBC
membrane
 O group lacks antigen
Type B
Can receive type B and
O only
Anti A
plasma
AB’s
Anti B
plasma
AB’s
Type O
Type A
Can receive type A &
O only
Innocuous antigens can cause type II hypersensitivity
reactions in susceptible individuals by binding to the
surfaces of circulating blood cells
AB-mediated destruction of RBC (hemolytic anemia) or
platelets (thrombocytopenia) is an uncommon side-effect
associated with the intake of certain drugs such as the antibiotic
penicillin, the anti-cardiac arrhythmia drug quinidine, or the
antihypertensive agent methyldopa.
These are examples of type II hypersensitivity reactions in
which the drug binds to the cell surface and serves as a target for
anti-drug IgG antibodies that cause destruction of the cell.
The cell-bound antibody triggers clearance of the cell from the
circulation, predominantly by tissue macrophages in the spleen,
which bear Fc receptors
TYPE II (cytotoxic reactions)
(cont.)
Blood type hereditary pattern
 Roughly 85% of the human population has
an Ag named Rh factor and they are called
Rh +

TYPE II (cytotoxic reactions)
(cont.)

Antibodies against A and B blood antigens
are naturally present without previous
stimulation, they are type IgM
Person
Antigen
with blood on RBC
type
surface
Antibodies Can receive
in serum
blood type
Can
donate to
type:
A
A
Anti-B
A and O
A and AB
B
B
Anti -A
B and O
B and AB
AB
AB
None to
these
groups
A, B, AB and
O (universal
recipient)
AB
O
Neither
Anti-A
Anti-B
O
A, B, AB
and O
Universal
donor
TYPE II (cytotoxic reactions)
(cont.)

Rh blood group
 Antigen present in 85% of the
population (Rh+)
 Antibodies against Rh blood group
appear only after exposure of Rhindividuals to Rh+ blood (pregnancy)
 Antibodies against Rh blood group are
type IgG
TYPE II (cytotoxic reactions)
(cont.)
 Hemolytic disease of the newborn
 (erythroblastosis fetalis)-destruction
RBC’s
 Rh-
mother pregnant with an Rh+
baby
 Transfusion of an Rh- mother with
Rh+ blood
of
TYPE II (cytotoxic reactions)
(cont.)
 Mother
develops anti Rh+ antibodies
 Later pregnancies with Rh+ babies,
antibodies (IgG) cross the placenta and
destroy baby’s RBC
PREVENTION OF
ERYTHROBLASTOSIS FETALIS
Passive immunization of the mother with
anti-Rh+ antibodies immediately after
childbirth
 Transfusion of fresh blood to the baby

Erythroblastosis fetalis
Rh Mother
First pregnancy with an Rh +
baby (father must be Rh +),
or previous Rh + blood transfusion
Subsequent pregnancies
with Rh + babies
Subsequent pregnancies
with Rh - babies
Passive immunization with
anti-Rh+ antibodies
immediately after birth (Rh+ baby)
Erythroblastosis fetalis
Healthy babies
Subsequent pregnancies
with Rh + babies
Healthy babies,
Passive immunization
should continue
in every delibery of Rh+ babies
Drug Induced Cytotoxic Reactions
Thrombocytopenic purpura occurs when
blood platelets, which are essential for
clotting, are coated w/ drug molecules that
function as haptens
If Ab’s develop against these haptens cause
destruction of the platelets
In hemolytic anemia, the body may form AB’s
against its own blood cells
Immune-caused destruction of WBC’s is
called agranulocytosis
Continuation on
Wednesday
TYPE III (IC reaction)

This is caused when soluble antigen-antibody (IgG
or IgM) complexes, which are normally removed
by macrophages in the spleen and liver, form in
large amounts and overwhelm the body
 These small complexes lodge in the capillaries,
pass between the endothelial cells of blood vessels especially those in the skin, joints, and kidneys - and
become trapped on the surrounding basement
membrane beneath these cells
 IC circulate in the blood
 Pass
between blood vessel cells (endothelial)
 The antigen/antibody complexes then activate the
classical complement pathway and cause inflammation
TYPE III (Immune complex rx’s)
Antibody-soluble antigens (immune complexes) in
serum escape phagocytosis b/c they are too small
 These circulating AB-AG complexes get deposited in
organs and can cause inflammation and damage
 Glomerulonephritis is an immune complex condition
that causes inflammatory damage to kidney
glomeruli

TYPE III (IC reaction) (cont.)

Glomerulonephritis
 Is
caused by the response of the immune
system to the M protein of Streptococci
pyogenes (Group A Streptococci—GAS)
 May lead to a fatal kidney failure
What is glomerulonephritis?
-Glomerulonephritis is the term used to
describe a group of diseases that
damage the part of the kidney that filters
blood
-other terms used are nephritis and
nephrotic syndrome
•Acute glomerulonephritis
•develops suddenly
• may get it after an infection in your throat or on your
skin (Streptococcus-- M protein)
The early signs of the acute disease are
•puffiness of your face in the morning
•blood in your urine (or brown urine)
•urinating less than usual
Rheumatoid
Arthritis is an
Auto Immune rx
IC are
deposited
in the joints
-it is a systemic disease
•In RA, the inflammatory
process continues on,
creating excessive
inflammation that
can cause damage
TYPE IV (Cell mediated reactions)
Type I-III hypersensitivities involved IgE, IgG or IgM
 Type IV rx’s involve cell-mediated rx’s caused by T
cells/or MQ
 Delayed reactions (24-48 h)







During the delayed rx-- MQ and lymphocytes migrate &
accumulate near the foreign AG
Foreign Ag is phagocytized by MQ—presented to T cell
surface receptors
T cells involved in this type of rx are TD but may include Tc
ells
A principal factor is the release of lymphokines by T cells rx
w/ the target Ag
TD and TC cells
Two examples (PPD test and poisen ivy)
Tuberculin Hypersensitivity .
•observed when soluble AG from organisms such as
Mycobacteria bovis (PPD test) were administered
subcutaneously
•fever, general unwellness, plus an area of red, hard swelling
•This type of rx is induced by a series of cellular migrations
and activations
1.T-cell migration from capillaries
2.Disruption of collagen in dermis
3.Macrophage infiltration
4.Granulomatous appearance, no edema, self-limiting
What is a granuloma?
•When macrophages fail to destroy the mycobacteria, the
human immune systems next line of defense is to form
granulomas around the infected macrophages
•Layers of two different types of T cells surround the
infected macrophage, sealing it inside a barrier from which
it cannot escape
•This barrier is known as a granuloma
•Since the infecting mycobacteria is "contained" inside the
granuloma, this form of mycobacterial disease is known as
the contained form. Contained mycobacterial disease is
typified by low numbers of infecting mycobacteria and high
levels of inflammation
PPD skin test
•T cells are responsible for the formation of these granulomas
•PPD stands for Purified Protein Derivative. The subject mycobacteria
are killed, using heat or ultrasound
•PPD for every mycobacterium is different.
•PPD for M. tuberculosis is called "tuberculin", that for M leprae is
called "lepromin" or "leprosin
•site of injection is then checked one or two days later.
• skin around the injection site is inflamed, or has formed a granuloma,
then this shows that the patient is currently infected with the
mycobacterium
• Because the reaction only shows up after a day or two, this type of
reaction is called Delayed Type Hypersensitivity (DTH)
TYPE IV (Cell mediated reactions)

Re-exposure to antigen

Memory T cells activate
 Release of cytokines when in contact with the AG
 Allergic contact dermatitis are usually caused by haptens
that combine w/ proteins in the skin
 Typical foreign AG are poisen ivy, cosmetics, latex and
metals such as nickel in jewlery
 The patch test, in which samples of suspected material
are taped to the skin, may determine the offending
environmental factor
Enjoy your Christmas break, before it’s time to hustle and stress again!!