Disorders in Immunity pdf - D. Talib

Talaro−Talaro: Foundations
in Microbiology, Fourth

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17. Disorders in Immunity

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502

CHAPTER 17 Disorders in Immunity

CYTOKINES, TARGET ORGANS,
AND ALLERGIC SYMPTOMS

Numerous  substances  involved  in  mediating  allergy  (and  inflam-
mation)  have  been  identified.  The  principal  chemical  mediators
produced by mast cells and basophils are histamine, serotonin, leu-
kotriene, platelet-activating factor, prostaglandins, and bradykinin
(figure 17.4). These chemicals, acting alone or in combination, ac-
count  for  the  tremendous  scope  of  allergic  symptoms.  For  some
theories  pertaining  to  this  function  of  the  allergic  response,  see
Medical Microfile 17.1. Targets of these mediators include the skin,
upper respiratory tract, gastrointestinal tract, and conjunctiva. The
general responses of these organs include rashes, itching, redness,
rhinitis, sneezing, diarrhea, and shedding of tears. Systemic targets

include smooth muscle, mucous glands, and nervous tissue. Be-
cause smooth muscle is responsible for regulating the size of blood
vessels and respiratory passageways, changes in its activity can
profoundly alter blood flow, blood pressure, and respiration. Pain,
anxiety, agitation, and lethargy are also attributable to the effects of
mediators on the nervous system.

Histamine* is the most profuse and fastest-acting allergic

mediator. It is a potent stimulator of smooth muscle, glands, and
eosinophils. Histamine’s actions on smooth muscle vary with lo-
cation. It

constricts the smooth muscle layers of the small bronchi

and intestine, thereby causing labored breathing and increased

Allergen particles enter

Lymphatic vessel

carries them to

Lymph node

B cell recognizes
allergen

Fc fragments

Mast cell in tissue

IgE binds to
mast cell surface

Granules
with
inflammatory
mediators

Time

Sensitization/IgE Production

Degranulation

Mast cells

trigg

ers

Allergen particle is encountered again

End result: Symptoms in various organs

Red, itchy eyes

Hives

Runny
nose

Subsequent Exposure to Allergen

Systemic distribution of
mediators in bloodstream

proliferates
into

Plasma cells

Synthesize

IgE

B cell

(b)

(a)

FIGURE 17.3

A schematic view of cellular reactions during the type I allergic response.

(a) Sensitization (initial contact with sensitizing dose).

(b) Provocation (later contacts with provocative dose).

histamine

(his´-tah-meen) Gr.

histio, tissue, and amine.

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Type I Allergic Reactions: Atopy and Anaphylaxis

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intestinal motility. In contrast, histamine

relaxes vascular smooth

muscle and dilates arterioles and venules. It is responsible for the
wheal*  and  flare reaction  in  the  skin  (see  figure  17.6a),  pruritis
(itching),  and  headache.  More  severe  reactions  (such  as  anaphy-
laxis) can be accompanied by edema and vascular dilation, which
lead  to  hypotension,  tachycardia,  circulatory  failure,  and,  fre-

quently, shock. Salivary, lacrimal, mucous, and gastric glands are
also histamine targets.

Although the role of

serotonin* in human allergy is uncer-

tain, its effects appear to complement those of histamine. In exper-
imental animals, serotonin increases vascular permeability, capil-
lary dilation, smooth muscle contraction, intestinal peristalsis, and
respiratory rate, but it diminishes central nervous system activity.

Dilated blood vessel

Constricted
bronchiole

Smooth muscle

Leukotriene

Glands

Prostaglandin

Typical
response
in asthma

Nerve cell

Dilated
blood vessel

Constricted bronchioles

Headache

Wheal and flare
reaction, itching

Wheezing,
difficult breathing

Excessive mucus and
glandular secretions

Constriction
of bronchioles

Plugged
alveoli

Histamine

Serotonin

Bradykinin

FIGURE 17.4

The spectrum of reactions to inflammatory cytokines and the common symptoms they elicit in target tissues and organs.

Note the

extensive overlapping effects.

serotonin

(ser

-oh-toh-nin) L. serum, whey, and tonin, tone.

wheal

(weel) A smooth, slightly elevated, temporary welt that is surrounded by a

flushed patch of skin (flare).

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in Microbiology, Fourth

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CHAPTER 17 Disorders in Immunity

Before the specific types were identified,

leukotriene* was

known  as  the  “slow-reacting  substance  of  anaphylaxis”  for  its
property  of  inducing  gradual  contraction  of  smooth  muscle. This
type of leukotriene is responsible for the prolonged bronchospasm,
vascular permeability, and mucous secretion of the asthmatic indi-
vidual.  Other  leukotrienes  stimulate  the  activities  of  polymor-
phonuclear leukocytes.

Platelet-activating factor is a lipid released by basophils,

neutrophils,  monocytes,  and  macrophages  that  causes  platelet
aggregation and lysis. The physiological response to stimulation by
this  factor  is  similar  to  that  of  histamine,  including  increased
vascular  permeability,  pulmonary  smooth  muscle  contraction,
pulmonary edema, hypotension, and a wheal and flare response in
the skin.

Prostaglandins* are a group of powerful inflammatory

agents.  Normally,  these  substances  regulate  smooth  muscle  con-
traction  (for  example,  they  stimulate  uterine  contractions  during
delivery).  In  allergic  reactions,  they  are  responsible  for  vasodila-
tion, increased vascular permeability, increased sensitivity to pain,
and bronchoconstriction. Certain anti-inflammatory drugs work by
preventing the actions of prostaglandins.

Bradykinin* is related to a group of plasma and tissue

peptides known as kinins that participate in blood clotting and
chemotaxis. In allergy, it causes prolonged smooth muscle contrac-
tion of the bronchioles, dilatation of peripheral arterioles, increased
capillary permeability, and increased mucous secretion.

SPECIFIC DISEASES ASSOCIATED WITH IgE-
AND MAST CELL-MEDIATED ALLERGY

The mechanisms just described are basic to hay fever, allergic
asthma, food allergy, drug allergy, eczema, and anaphylaxis. In this
section, we cover the main characteristics of these conditions, fol-
lowed by methods of detection and treatment.

Atopic Diseases

Hay fever is a generic term for allergic rhinitis,* a seasonal reac-
tion to inhaled plant pollen or molds, or a chronic, year-round
reaction to a wide spectrum of airborne allergens or inhalants (see
table 17.2). The targets are typically respiratory membranes, and
the symptoms include nasal congestion; sneezing; coughing; pro-
fuse mucous secretion; itchy, red, and teary eyes; and mild bron-
choconstriction.

Asthma* is a respiratory disease characterized by episodes

of impaired breathing due to severe bronchoconstriction. The air-
ways  of  asthmatic  people  are  exquisitely  responsive  to  minute
amounts of inhalant allergens, food, or other stimuli, such as in-
fectious agents. The symptoms of asthma range from occasional,
annoying bouts of difficult breathing to fatal suffocation. Labored
breathing, shortness of breath, wheezing, cough, and ventilatory
rales* are present to one degree or another. The respiratory tract
of an asthmatic person is chronically inflamed and severely over-
reactive  to  allergy  chemicals,  especially  leukotrienes  and  sero-
tonin  from  pulmonary  mast  cells.  Other  pathologic  components
are thick mucous plugs in the air sacs and lung damage that can
result in long-term respiratory compromise. An imbalance in the
nervous  control of the  respiratory  smooth  muscles is  apparently
involved in asthma, and the episodes are influenced by the psy-
chological state of the person, which strongly supports a neuro-
logical connection.

The number of asthma sufferers in the United States is esti-

mated at 10 million, with nearly one-third of them children. For
reasons that are not completely understood, asthma is on the in-
crease, and deaths from it have doubled since 1982, even though
effective agents to control it are more available now than they
have ever been before. A recent study of inner-city children has
correlated high levels of asthma to contact with cockroach anti-
gens in their living quarters. Nearly 40% of children age 10 or
younger showed extreme sensitivity to the droppings and remains
of these insects.

MEDICAL MICROFILE

17.1

Of What Value Is Allergy?

this  system  is  to  defend  against  helminth  worms  that  are  ubiquitous
human parasites. In chapter 14, we learned that inflammatory mediators
serve  valuable  functions,  such  as  increasing  blood  flow  and  vascular
permeability to summon essential immune components to an injured site.
They are also responsible for increased mucous secretion, gastric motil-
ity,  sneezing,  and  coughing,  which  help  expel  noxious  agents.  The
difference  is  that,  in  allergic  persons,  the  quantity  and  quality  of  these
reactions are excessive and uncontrolled.

Why would humans and other mammals evolve an allergic response that
is capable of doing so much harm and even causing death? It is unlikely
that this limb of immunity exists merely to make people miserable; it
must have a role in protection and survival. What are the underlying bio-
logical functions of IgE, mast cells, and the array of potent cytokines?
Analysis has revealed that, although allergic persons have high levels of
IgE, trace quantities are present even in the sera of nonallergic individu-
als, just as mast cells and inflammatory chemicals are also part of normal
human physiology. It is generally believed that one important function of

leukotriene

(loo

-koh-try-een) Gr. leukos, white blood cell, and triene, a chemical

suffix.

prostaglandin

(pross

-tah-glan-din) From prostate gland. The substance was

originally isolated from semen.

bradykinin

(brad

-ee-kye-nin) Gr. bradys, slow, and kinein, to move.

rhinitis

(rye-nye

-tis) Gr. rhis, nose, and itis, inflammation.

asthma

(az

-muh) The Greek word for gasping.

rales

(rails) Abnormal breathing sounds.

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Atopic dermatitis is an intensely itchy inflammatory condi-

tion of the skin, sometimes also called

eczema.* Sensitization

occurs  through  ingestion,  inhalation,  and,  occasionally,  skin  con-
tact  with  allergens.  It  usually  begins  in  infancy  with  reddened,
vesicular,  weeping,  encrusted  skin  lesions.  It  then  progresses  in
childhood and adulthood to a dry, scaly, thickened skin condition
(figure 17.5). Lesions can occur on the face, scalp, neck, and inner
surfaces  of  the  limbs  and  trunk.  The  itchy,  painful  lesions  cause
considerable discomfort, and they are often predisposed to second-
ary bacterial infections. An anonymous writer once aptly described
eczema as “the itch that rashes’’ or “one scratch is too many but one
thousand is not enough.’’

Food Allergy

The ordinary diet contains a vast variety of compounds that are po-
tentially allergenic. It is generally believed that food allergies are
due to a digestive product of the food or to an additive (preservative
or flavoring). Although the mode of entry is intestinal, food aller-
gies can also affect the skin and respiratory tract. Gastrointestinal
symptoms include vomiting, diarrhea, and abdominal pain. In se-
vere cases, nutrients are poorly absorbed, leading to growth retar-
dation and failure to thrive in young children. Other manifestations
of food allergies include eczema, hives, rhinitis, asthma, and occa-
sionally, anaphylaxis. Classic food hypersensitivity involves IgE
and degranulation of mast cells, but not all reactions involve this

FIGURE 17.5

Atopic dermatitis, or eczema.

Vesicular, encrusted lesions are typical

in afflicted infants. This condition is prevalent enough to account for 1%
of pediatric care.

eczema

(eks

-uh-mah; also ek-zeem-uh) Gr. ekzeo, to boil over.

mechanism. The most common food allergens come from peanuts,
fish, cow’s milk, eggs, shellfish, and soybeans.

Drug Allergy

Modern chemotherapy has been responsible for many medical ad-
vances. Unfortunately, it has also been hampered by the fact that
drugs  are  foreign  compounds  capable  of  stimulating  allergic
reactions. In fact, allergy to drugs is one of the most common side
effects  of  treatment  (present  in  5–10%  of  hospitalized  patients).
Depending upon the allergen, route of entry, and individual sensi-
tivities, virtually any tissue of the body can be affected, and reac-
tions range from mild atopy to fatal anaphylaxis. Compounds im-
plicated  most  often  are  antibiotics  (penicillin  is  number  one  in
prevalence), synthetic antimicrobics (sulfa drugs), aspirin, opiates,
and anaesthetics. The actual allergen is not the intact drug itself but
a hapten given off when the liver processes the drug. Some forms
of penicillin sensitivity are due to the presence of small amounts of
the drug in meat, milk, and other foods and to exposure to

Penicil-

lium mold in the environment.

ANAPHYLAXIS: AN OVERPOWERING
SYSTEMIC REACTION

The term

anaphylaxis, or anaphylactic shock, was first used to

denote  a  reaction  of  animals  injected  with  a  foreign  protein. Al-
though  the  animals  showed  no  response  during  the  first  contact,
upon reinoculation with the same protein at a later time, they ex-
hibited  acute  symptoms—itching,  sneezing,  difficult  breathing,
prostration,  and  convulsions—and  many  died  in  a  few  minutes.
Two clinical types of anaphylaxis are distinguished in humans.

Cu-

taneous anaphylaxis is the wheal and flare inflammatory reaction to
the local injection of allergen.

Systemic anaphylaxis, on the other

hand, is characterized by sudden respiratory and circulatory disrup-
tion that can be fatal in a few minutes. In humans, the allergen and
route of entry are variable, though bee stings and injections of an-
tibiotics or serum are implicated most often. Bee venom is a com-
plex material containing several allergens and enzymes that can
create a sensitivity that can last for decades after exposure.

The underlying physiological events in systemic anaphylaxis

parallel those of atopy, but the concentration of chemical mediators
and the strength of the response are greatly amplified. The immune
system of a sensitized person exposed to a provocative dose of al-
lergen responds with a sudden, massive release of chemicals into
the tissues and blood, which act rapidly on the target organs. Ana-
phylactic persons have been known to die in 15 minutes from com-
plete airway blockage.

DIAGNOSIS OF ALLERGY

Because allergy mimics infection and other conditions, it is impor-
tant to determine if a person is actually allergic. If possible or nec-
essary, it is also helpful to identify the specific allergen or allergens.
Allergy diagnosis involves several levels of tests, including non-
specific, specific,

in vitro, and in vivo methods.

A new test that can distinguish whether a patient has experi-

enced an allergic attack measures elevated blood levels of tryptase,
an enzyme released by mast cells that increases during an allergic
response. Several types of specific

in vitro tests can determine

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CHAPTER 17 Disorders in Immunity

the allergic potential of a patient’s blood sample. The leukocyte
histamine-release test measures the amount of histamine released
from the patient’s basophils when exposed to a specific allergen.
Serological tests that use radioimmune assays (see chapter 16) to
reveal the quantity and quality of IgE are also clinically helpful.

Skin Testing

A useful

in vivo method to detect precise atopic or anaphylactic

sensitivities is skin testing. With this technique, a patient’s skin is
injected, scratched, or pricked with a small amount of a pure al-

lergen extract. Hundreds of these allergen extracts contain com-
mon airborne allergens (plant and mold pollen) and more unusual
allergens  (mule  dander,  theater  dust,  bird  feathers).  Unfortu-
nately, skin tests for food allergies using food extracts are unreli-
able in most cases. In patients with numerous allergies, the aller-
gist maps the skin on the inner aspect of the forearms or back and
injects  the  allergens  intradermally  according  to  this  predeter-
mined  pattern  (figure  17.6

a). Approximately 20 minutes after

antigenic challenge, each site is appraised for a wheal response
indicative of histamine release. The diameter of the wheal is

(a)

Environmental Allergens

1. Acacia gum
2. Cat dander
3. Chicken feathers
4. Cotton lint
5. Dog dander
6. Duck feathers
7. Glue, animal
8. Horse dander
9. Horse serum
10. House dust #1
11. Kapok
12. Mohair (goat)
13. Paper
14. Pyrethrum
15. Rug pad, ozite
16. Silk dust
17. Tobacco dust
18. Tragacanth gum
19. Upholstery dust
20. Wool

No. 1 Standard Series

1. Ant
2. Aphis
3. Bee
4. Housefly
5. House mite
6. Mosquito
7. Moth
8. Roach
9. Wasp

10. Yellow jacket

Airborne mold spores

11.

Alternaria

12.

Aspergillus

13.

Cladosporium

14.

Hormodendrum

15.

Penicillium

16.

Phoma

17.

Rhizopus

18. .........................

No. 2 Airborne Particles

+++
+++
++++
++++
++
+
+
++

+++
+
+
+
++++
+++
+
+
+
+++++
+++

ID 8/85

+++
+++++
++++
++++

+++
++++
+++
++

ID 8/85

++
+++
++
+++
0
+
+++

0
+

+++

++++

- not done
- no reaction
- slight reaction

- mild reaction
- moderate reaction
- severe reaction

FIGURE 17.6

A method for conducting an allergy skin test.

The forearm (or back) is mapped and then injected with a selection of allergen extracts.

The  allergist  must  be  very  aware  of  potential  anaphylaxis  attacks  triggered  by  these  injections.  (a) Close-up  of  skin  wheals  showing  a  number  of
positive  reactions  (dark  lines  are  measurer’s  marks).  (b) An  actual  skin  test  record  for  some  common  environmental  allergens  with  a  legend  for
assessing  them.

(b)

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in Microbiology, Fourth

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17. Disorders in Immunity

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Type I Allergic Reactions: Atopy and Anaphylaxis

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measured and rated on a scale of 0 (no reaction) to 4

" (greater

than 15 mm). Figure 17.6

b shows skin test results for a person

with extreme inhalant allergies.

TREATMENT AND PREVENTION OF ALLERGY

In general, the methods of treating and preventing type I allergy in-
volve (1) avoiding the allergen, though this may be very difficult in
many instances; (2) taking drugs that block the action of lympho-
cytes, mast cells, or chemical mediators; and (3) undergoing desen-
sitization therapy.

It is not possible to completely prevent initial sensitization,

since there is no way to tell in advance if a person will develop an
allergy to a particular substance. The practice of delaying the intro-
duction of solid foods apparently has some merit in preventing food
allergies in children, though even breast milk can contain allergens
ingested by the mother. Although rigorous cleaning and air condi-
tioning can reduce contact with airborne allergens, it is not feasible
to isolate a person from all allergens, which is the reason drugs are
so important in control.

Therapy to Counteract Allergies

The  aim  of  antiallergy  medication  is  to  block  the  progress  of  the
allergic response somewhere along the route between IgE produc-
tion  and  the  appearance  of  symptoms  (figure  17.7).  Oral  anti-
inflammatory  drugs  such  as  corticosteroids  inhibit  the  activity  of
lymphocytes and thereby reduce the production of IgE, but they also
have dangerous side effects and should not be taken for prolonged
periods.  Some  drugs  block  the  degranulation  of  mast  cells  and
reduce the levels of inflammatory cytokines. The most effective of
these  are  diethylcarbamazine  and  cromolyn. Asthma  and  rhinitis
sufferers  can  find  relief  with  a  new  drug  that  blocks  synthesis  of
leukotriene and a monoclonal antibody that inactivates IgE (Xolair).

Widely used medications for preventing symptoms of

atopic allergy are

antihistamines, the active ingredients in most

over-the-counter  allergy-control  drugs.  Antihistamines  interfere
with histamine activity by binding to histamine receptors on tar-
get organs. Most of them have major side effects, however, such
as drowsiness. Newer antihistamines lack this side effect because
they do not cross the blood-brain barrier. Other drugs that relieve
inflammatory  symptoms  are  aspirin  and  acetaminophen,  which
reduce pain by interfering with prostaglandin, and theophylline, a
bronchodilator  that  reverses  spasms  in  the  respiratory  smooth
muscles. Persons who suffer from anaphylactic attacks are urged
to  carry  at  all  times  injectable  epinephrine  (adrenaline)  and  an
identification  tag  indicating  their  sensitivity. An  aerosol  inhaler
containing epinephrine can also provide rapid relief. Epinephrine
reverses constriction of the airways and slows the release of aller-
gic mediators.

Approximately 70% of allergic patients benefit from con-

trolled injections of specific allergens as determined by skin tests.
This technique, called

desensitization or hyposensitization, is a

therapeutic  way  to  prevent  reactions  between  allergen,  IgE,  and
mast cells. The allergen preparations contain pure, preserved sus-
pensions of plant antigens, venoms, dust mites, dander, and molds
(but so far, hyposensitization for foods has not proved very effec-
tive). The immunologic basis of this treatment is open to differ-
ences  in  interpretation.  One  theory  suggests  that  injected  aller-
gens  stimulate  the  formation  of  high  levels  of  allergen-specific
IgG  (figure  17.8).  It  has  been  proposed  that  these  IgG

blocking

antibodies remove allergen from the system before it can bind to
IgE, thus preventing the degranulation of mast cells. It is also pos-
sible that allergen delivered in this fashion combines with the IgE
itself and prevents it from reacting with the mast cells. Some ex-
perts suggest that the therapy induces specific clones of suppres-
sor T cells to block the production of IgE by B cells.

Avoidance
of allergen

Corticosteroids
keep the plasma cell
from synthesizing IgE
and inhibit T cells.

Allergen

Cromolyn acts
on the surface
of mast cell;
no degranulation

IgE

Antihistamines, aspirin,
epinephrine, theophylline
counteract the effects
of cytokines on targets.

Monoclonal drugs
that inactivate IgE

FIGURE 17.7

Strategies for circumventing allergic attacks.

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in Microbiology, Fourth

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17. Disorders in Immunity

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CHAPTER 17 Disorders in Immunity

Type II Hypersensitivities: Reactions
That Lyse Foreign Cells

The diseases termed type II hypersensitivities are a complex group
of syndromes that involve complement-assisted destruction (lysis)
of cells by antibodies (IgG and IgM) directed against those cells’
surface antigens. This category includes transfusion reactions and
some types of autoimmunities (discussed in a later section). The
cells targeted for destruction are often red blood cells, but other
cells can be involved.

HUMAN BLOOD TYPES

Chapters 14 and 15 described the functions of unique surface re-
ceptors or markers on cell membranes. Ordinarily, these receptors
play essential roles in transport, recognition, and development, but
they become medically important when the tissues of one person
are placed into the body of another person. Blood transfusions and
organ donations introduce alloantigens (molecules that differ in the

same species) on donor cells that are recognized by the lympho-
cytes of the recipient. These reactions are not really immune dys-
functions as allergy and autoimmunity are. The immune system is
in fact working normally, but it is not equipped to distinguish
between the desirable foreign cells of a transplanted tissue and the
undesirable ones of a microbe.

THE BASIS OF HUMAN ABO
ANTIGENS AND BLOOD TYPES

The existence of human blood types was first demonstrated by an
Austrian pathologist, Karl Landsteiner, in 1904. While studying in-
compatibilities in blood transfusions, he found that the serum of one
person could clump the red blood cells of another. Landsteiner iden-
tified four distinct types, subsequently called the ABO blood groups.

Like the MHC antigens on white blood cells, the ABO anti-

gen markers on red blood cells are genetically determined and com-
posed of glycoproteins. These ABO antigens are inherited as two
(one from each parent) of three alternative

alleles:* A, B, or O. A

and B alleles are dominant over O and codominant with one an-
other. As table 17.3 indicates, this mode of inheritance gives rise to
four blood types (phenotypes), depending on the particular combi-
nation of genes. Thus, a person with an

AA or AO genotype has

type A blood; genotype BB or BO gives type B; genotype AB

Type I hypersensitivity reactions result from excessive IgE production in

response to an exogenous antigen.

The two kinds of type I hypersensitivities are atopy, a chronic, local

allergy, and anaphylaxis, a systemic, potentially fatal allergic response.

The predisposition to type I hypersensitivities is inherited, but age,

geographic locale, and infection also influence allergic response.

Type I allergens include inhalants, ingestants, injectants, and contactants.

The portals of entry for type I antigens are the skin, respiratory tract,

gastrointestinal tract, and genitourinary tract.

Type I hypersensitivities are set up by a sensitizing dose of allergen and

expressed when a second provocative dose triggers the allergic
response. The time interval between the two can be many years.

The primary participants in type I hypersensitivities are IgE, basophils,

mast cells, and agents of the inflammatory response.

Allergies are diagnosed by a variety of in vitro and in vivo tests that

assay specific cells, IgE, and local reactions.

Allergies are treated by medications that interrupt the allergic response at

certain points. Allergic reactions can often be prevented by
desensitization therapy.

CHAPTER CHECKPOINTS

Allergen

IgG
"blocking
antibodies"

B Cell / Plasma Cell

Mast Cell

IgE

No IgE

FIGURE 17.8

The blocking antibody theory for allergic
desensitization.

An injection of allergen

causes IgG antibodies to be formed instead of
IgE; these blocking antibodies cross-link and
effectively remove the allergen before it can react
with the IgE in the mast cell.

TABLE 17.3

Characteristics of ABO Blood Groups

Phenotype A
or B* RBC

Prevalence in

Serum Content

Genotype

Antigen

Population**

of Antibodies

Neither

Most common

Both anti-a

and anti-b

AA, AO

Second most

Anti-b

common

BB, BO

Third most

Anti-a

common

Least common

Neither

antibody

*Capital letters generally denote antigen; lowercase denotes antibody.
**True of most large populations of mixed racial and ethnic groups.

allele

(ah-leel

) Gr. allelon, of one another. An alternate form of a gene for a given trait.