BASIC

IMMUNOLOGY

INTRODUCTION
Immunology is the study of host
defence mechanisms.
Immunity is the ability of the host to
protect itself against foreign
organisms.
The immune system comprises the
tissues, cells & molecules which
mount the immune response.

Coagulation
Cascade
Plasma Fibrinogen

XIIa

Fibrinolytic
Cascade

Thrombin

Complement
Cascade

Fibrin

Plasmin

Bradykinin

PCV

Kinin
Cascade

Kallikrein
Cellular mediators

MAC

Immunology
Natural (innate) immune system
Skin, tears, saliva, mucus, acids
Property of all living creatures

Adaptive (acquired) immune system

Specialist cells, cytokines, antibodies
Specific and has memory
Specialised mucosal lymphoid tissue

INTRODUCTION
Immunogenicity is the capacity
to induce an immune response by
foreign, complex, high molecular
weight compounds
Antigenicity is the ability to bind
to Ig or immune cells; an immune
response need not result
Haptens

INTRODUCTION
Epitopes
aka antigenic determinants

Immunological cross-reactivity
the sharing of epitopes by different
substances
toxoids & immunisation

THE INNATE IMMUNE

SYSTEM
Synonyms are the natural or native
immune system
Rapidly mobilised first line of defence
Not dependent on prior exposure to a
foreign invader
Non-specific
May not be sufficient to prevent foreign
material persisting in the host

THE INNATE IMMUNE

SYSTEM

Innate immunity comprises:

physicochemical barriers
molecules normally present in body
fluids e.g. lysozyme, complement,
antiproteases
phagocytic & cytotoxic cells such as
neutrophils, macrophages, natural
killer cells

THE INNATE IMMUNE

SYSTEM
The Respiratory Burst
aka the oxidative burst
membrane-bound NADPH system
produces

superoxide radicals
hyperchlorous acid
H2O2
chloramines

THE INNATE IMMUNE

SYSTEM
A reliable means of protecting the
host in the first instance against
many extracellular organisms
It is a property of every living
organism
Unable to deal with all intracellular
organisms (e.g protozoa, viruses &
certain bacteria are not killed)

THE ACQUIRED IMMUNE

SYSTEM
Specific & has immunologic memory
Dedicated immune cells - the lymphoid
cells (lymphocytes)
Molecules that specifically counteract
antigens (antibodies or immunoglobulins)
Specific immune systems associated with
barrier surfaces e.g. MALT, GALT
Lymphocyte secreted cytokines

T-LYMPHOCYTES
Cell-mediated immunity especially
intracellular organisms, protozoa &
fungi
Graft rejection
Immune surveillance of neoplasia
70-80% of total lymphocytes
Long-lived memory cells
Activity is by cytokine production

T-LYMPHOCYTES
Th - CD4+: Respond to antigen in
association with MHC Class II
Tc - CD8+: Respond to antigen
presented via MHC Class I
Antigen MUST be peptide
Tdth
Ts

T-LYMPHOCYTES
CD4+ cells recognize antigens that
have been taken up by antigen
presenting cells which present
antigen fragments on the cell surface
CD8+ cells recognise cells infected
with virus, which they then kill

T-LYMPHOCYTES
CD4 (Th) cells interact directly with
other cells by releasing cytokines to
control development of the immune
response
Two types of Th cell
Th-1 cells activate macrophages to
destroy material phagocytosed
Th-2 cells help B-cells make antibody

B-LYMPHOCYTES
Specialised for the production of
immunoglobulins after differentiation
into plasma cells
Controls pyogenic bacteria
Prevents blood-borne infections
Neutralise toxins
12% of total lymphocytes

B-LYMPHOCYTES
Can respond to peptide,
carbohydrate & glycolipids
Usually require T-cell help to respond
to antigen (interleukins) but can also
recognise antigen directly through
surface Ig
B cells mature & proliferate in lymph
nodes

B-LYMPHOCYTES
B-cells process & present antigen via
surface MHC class II
Responses are antigen-specific but
effects are not specific - mainly via
complement

IMMUNOGLOBULINS
The 5 classes of Ig are:
IgM
IgA
IgD
IgG
IgE

IMMUNOGLOBULINS
4-chain structure
2 light chains
2 heavy chains

Chains linked by disulphide bonds

Chains are coiled into domains
110 amino acids
stabilised by intrachain disulphide bond

IMMUNOGLOBULINS
Terminal regions of H & L chains are
the variable regions
The variable region is the site where
Ig combines with antigen
This regions variability is responsible
for wide range of antigen specificity

IMMUNOGLOBULINS
The other domains are the constant
regions which are similar within
isotypes of Ig
Using enzymes, a number of Ig
fragments have been identified.
Important ones are:
Fab
Fc

IMMUNOGLOBULINS
Fc regions formed from H chains &
determine isotype & so biological
function
Hinge region also has effect on
function
These functions are distinct from
antigen binding

IMMUNOGLOBULINS
IgG
neutralises toxins
activates complement
opsonisation
able to cross placenta (only Ig that can)

IMMUNOGLOBULINS
IgA
monomeric & dimeric forms
dimeric = secretory IgA - found in
secretions
important antiviral Ig

IMMUNOGLOBULINS
IgM
pentameric
good agglutinator
good at activating complement

IMMUNOGLOBULINS
IgD
true function unknown
appears to be involved in B-cell
differentiation

IMMUNOGLOBULINS
IgE
parasitic infections
Fc portion binds to mast cells
triggers mast cell degranulation

T- & B-LYMPHOCYTES
T- & B-cells recognise the antigen,
proliferate in response to it, &
migrate back to the site of injury
There they release cytokines that
attract effector cells (cytotoxic Tcells, activated macrophages,
committed B-cells)

THE ACQUIRED IMMUNE

SYSTEM
CD System
WBCs are distinguished according to
groups of molecules they express on
their surfaces - mostly CD molecules
>130 CD molecules identified
may be lineage specific or shared
between different cell types
may only appear during cell
development or only when activated

THE ACQUIRED IMMUNE

SYSTEM
MHC expression
Class I molecules expressed on all
nucleated cells
Class II molecules expressed on a small
group of antigen presenting cells
Class II molecules may also be induced
to be expressed on other cells during
immune reactions by interferon-

THE ACQUIRED IMMUNE

SYSTEM
Cytokines are short-range,
multifunctional, short-acting
mediators of cellular activities,
especially within the immune system
Released primarily by activated Tcells & other immune and nonimmune cells.

THE ACQUIRED IMMUNE

SYSTEM
There are 4 major classes of
cytokines
interleukins (IL-1 to IL-12)
interferons (IF-, IF- & IF-)
colony stimulating factors (CSFs)
tumour necrosis factors (TNF- & TNF-)

NATURAL KILLER CELLS

Natural Killer (NK) cells:
classed as part of the lymphoid system
but have no differentiating surface
markers
they are particularly effective against
virus-infected & tumour cells
also called large granular lymphocytes

ANTIGEN PRESENTING
CELLS
Examples of APCs are:
macrophages
B-cells
dendritic cells

Macrophages & B-cells recognise

antigen through the Ig molecule
Dendritic cells process & present
antigen to nave T-cells via MHC
Class II

THE ACQUIRED IMMUNE

SYSTEM
Macrophages
long-lived
widespread distribution
they express receptors for Ig & activated
complement components which they
use to take up immune complexes

ANTIGEN PRESENTING
CELLS

Antigen Presenting Cells (APCs):

normally, initiation of the acquired
immune response does not take place
at the site of injury or penetration of
foreign organisms
antigen is taken up by APCs at the
site of inflammation & transported to
regional lymph nodes &/or spleen
where it is presented to T- & B-cells

THE ACQUIRED IMMUNE

SYSTEM
Macrophages & B-cells are involved
in the perpetuation of the immune
response
Dendritic cells are implicated in the
initiation of the immune response

THE ACQUIRED IMMUNE

SYSTEM
Antigen specificity is the single most
important aspect of the acquired immune
system (mediated by lymphocytes)
Each clone of a lymphoid cell responds
only to a single antigen
T-cells deal with surface bound antigen
(usually cell associated)
B-cells deal with soluble (extracellular)
antigen

THE ACQUIRED IMMUNE

SYSTEM
Specific immunity is termed humoral
when antibodies are involved in
removing the antigen
It is termed cell-mediated when Tcells & macrophages are involved

THE ACQUIRED IMMUNE

SYSTEM
Immunity after infection is termed active
immunity (because the host has
responded actively to the stimulus)
Immunity may be transferred passively
by antibodies or cells (breast milk,
vaccination)
Vaccination may be passive (using Ig) or
active (using antigen or attenuated
organism)

THE ACQUIRED IMMUNE

SYSTEM
The development of acquired
immunity begins with a primary
immune response:
an afferent phase involving APCs
T-cell transformation from a resting to
an active state
an effector phase - induction of other
cells (B-cells & macrophages) by active
T-cells

THE ACQUIRED IMMUNE

SYSTEM
The primary immune response is
accompanied by the appearance of
antigen-specific T-cells & Ig-secreting Bcells
The secondary immune response:
on second (& subsequent) exposure to
the same antigen, antigen-specific
memory T- & B-cells are recruited
much sooner & more efficiently
Ig levels are consequently much
higher

INNATE & ACQUIRED

IMMUNITY
Extracellular foreign antigen is normally
cleared by the innate immune system,
with some assistance from B-cell activity
Intracellular foreign antigen is handled by
the acquired immune system in which self
& foreign antigen are jointly recognised
All cellular defence mechanisms involve
interactions of cell surface molecules
(receptors) with complementary
molecules (ligands)

COMPLEMENT
The complement system
comprises at least 9 plasma proteins &
some regulatory factors, that mediate
several functions of the inflammatory
process
synthesised by macrophages or
hepatocytes
usually circulate as inactive proenzymes
heat labile (c.f. Ig is heat stable)

COMPLEMENT
Complement pathways
Cascade of sequential activation
converts each proenzyme into its active
state & amplifies the response.
Two main pathways:
Classical pathway - bound IgG, IgM
Alternative pathway - certain
antigens (LPS, endotoxin, IC)

COMPLEMENT
Functions
opsonisation, chemotaxis, immune
adherence (MAC)
acceleration of acute inflammation
immune cytolysis
virus neutralisation

IMMUNOLOGICAL
DISORDERS

OBJECTIVES contd---Discuss the Definition, Causes, Pathophysiology, Clinical

manifestations of the following allergic disorders

Describe the diagnostic, medical and surgical management of

the below mentioned disorders.
Apply nursing process including assessment, diagnosis,
implementation and evaluation of care provided to the client
with the following allergic disorders;
Allergic rhinitis
Atopic dermatitis
Anaphylaxis
Serum sickness
Summarization
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central and peripheral lymphoid

organs and tissues

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Hypersensitivity (allergy)
Definition:
Itisanabnormal,heightenedreactiontoanytypeofstimuli.
(Smeltzer,etal,2004)
Immuneresponsethatresultsintissueinjuryorother
physiologicalchangesarecalledhypersensitivity(allergic)
reactions.
(Mellors,1999).

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Typesofhypersensitivityreactions
Hypersensitivity reactions are classified into four types:
TypeI:anaphylactichypersensitivity
TypeII:cytotoxichypersensitivity
TypeIII:immunecomplexhypersensitivity
TypeIV:cellmediatedhypersensitivity

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Types of hypersensitivity
reactions
Type I: Anaphylactic hypersensitivity:
Itisanimmediatereactionbeginningwithinminutesof
exposuretoanantigen.
ItismediatedbyI.e.antibodies.
Itrequirespreviousexposuretospecificantigen.
Itusuallyaffectsonskin,lungsandgastrointestinaltract.
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Anaphylactic (type I)
Hypersensitivity

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Anaphylactic (type I)
Hypersensitivity
Examples:

Asthma
Allergicrhinitis
Systemicanaphylaxis.
Atopicdermatitis

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Types of hypersensitivity
reactions
Type II: cytotoxic hypersensitivity
Itoccurswhenthesystemmistakenlyidentifiesa
normalconstituentofthebodyasforeign.
Thisreactionmaybearesultofcross-reacting
antibody,possiblyleadingtocellandtissuedamage
ItinvolvesactivationofcomplementbyIgGorIgM
antibodybindingtoanantigeniccell.
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Cytotoxic(typeII)Hypersensitivity

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Cytotoxic(typeII)Hypersensitivity
Examples:
Myastheniagravis
BloodTransfusionreaction
Thrombocytopenia

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Types of hypersensitivity
reactions
Type III: Immune complex hypersensitivity
Itinvolvesintheformationofimmunecomplexes
whenantigenbindstoantibodies.
ThesetypeIIIcomplexesdepositintissuesor
vascularendotheliumandleadstoinjurywiththe
helpofvasoactiveaminesandtheincreasenumberof
circulatingcomplexes.
Thejointsandkidneysareparticularlysusceptible.
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Immune complex (type III) hypersensitivity

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Immune complex (type III)

hypersensitivity
Examples:
Systemiclupuserythematous
Rheumatoidarthritis
Serumsickness

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Types of hypersensitivity
reactions
Type IV: Cell mediated hypersensitivity
Alsoknownascellularhypersensitivity
Itoccurs24-72hrsafterexposuretoanallergen
ThereactionismediatedbysensitizedTcellsand
macrophages.
ThereactionresultsIntissuedamagebyreleasing
lymphokines,macrophagesandlysozymes.
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Cell mediated (type IV) HYPERSENSITIVITY

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Cell Mediated (type IV)

HYPERSENSITIVITY
Examples:
Contactdermatitis
Tuberculintest.

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Allergic Rhinitis

ItisalsocalledasHay Fever
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ALLERGIC RHINITIS
Definition:
Itisaninflammationofthenasalmucosabyan
allergen.
(Smeltzer,2004).
Incidence:
Itaffectsabout8-10%ofU.S.population.
(Smeltzer,2004).

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Types of allergic rhinitis:

Perennial
Year-roundwithallergic
triggers
Sneezing,itching,
waterydischargefrom
noseandeyes

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Seasonal
Earlyspring,earlyfall,
earlysummer
Intensesymptoms
triggeredbyair-borne
pollens,housedustand
animalfeather.

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Pathophysiology:

ALLERGIC

RHINITIS
Inhalationofanantigen(sensitization)
Re-exposure
Nasalmucosareacts(histamineismediator)
Slowingofciliaryaction,edemaformationand
leukocyteinfiltration
Tissueedemaandincreasecapillarypermeability
(vasodilatation).
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Clinical manifestations: ALLERGIC RHINITIS

Nasalcongestion
Cleartogreenishrhinorrhea
Intermittentsneezingandnasalitching
Headache
PainoverParanasalsinuses
Epistaxis
Fatigue,lossofsleepandpoorcoordination.
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Allergic rhinitis
Diagnostic tests:
Nasalsmears(nasaleosinophilia)
TotalserumIgE
Medical management:
Oralantihistamines(blockstheactionofhistamine)
Adrenergicnasaldecongestant
Mastcellstabilizers.
Analgesicsandantipyretics.
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Allergic rhinitis
Nursing management:
Assessment
Examination(Assesssymptoms)
Historyofpatient(Allergyassessment)
Diagnosis
Ineffectivebreathingpatternrelatedtoallergic
reactions
Knowledgedeficitrelatedtoallergyandthe
recommendedmodificationsinlifestyleandself-care
practices
Ineffectiveindividualcopingwithconditionandneed
forenvironmentalmodification.
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Allergic rhinitis
Nursing interventions:
1. Patientisinstructedtomodifytheenvironmentto
reducetheseverity.
2. Encouragefordeepbreathingandcoughfrequently
foradequategasexchange.
3. Encourageforsteaminhalation
4.Promoterest.
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Atopic dermatitis (eczema)

ItisatypeIimmediatehypersensitivity
Definition:
Inflammationoftheskin
Incidences/Causes:
Familialtendency
Itishighestininfantsandchildren
1%populationissufferingfromthisdisease
Aggravatedinlowhumidityandinwinter.
(smeltzer,2004)
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Pathophysiology: Atopic
dermatitis
Allergen/Sensitizingantigen
Effecttheskin(changesinlipidcontent,sebaceousglandactivityand
sweating)
Skinreducedwater-bindingcapacityintheskin
Highertransepidermalwaterlossanddecreasedwatercontent
Dryskin
Itching,rubbingleadstoinfection

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Clinical manifestations: Atopic dermatitis

Redoozingcrustingrash(inchildhood)
Drythickbrownishgreyandscalyskin(later
stage)
Pruritis
Lesionaremostlyfoundonhand,foot,backof
theknees,neck,face,eyelidsandelbowbands.

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Medical Management:
Atopic dermatitis

Moisturizers
Topicaland
systemicsteroids
Antibiotics
Antihistamines
Performallergen
test

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Nursing management: Atopic dermatitis

Assessandmaintainhygiene(dailybath)
Determinedietaryandotherallergen(cowmilk,egg,Soya,
wheat,nut,fish)
Teachtoavoidallergen
Keepwoundareamoist
Teachproperuseofmedicines
Avoidscratching(wearcottonfabrics,washingwithmild
detergent)
Preventfromsecondaryinfection
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Anaphylaxis
Definition:
Itisanimmediatelifethreateningsystemicreactionthatcan
occuronexposuretoparticularsubstances
Itisanimmediate(typeIhypersensitivity)immunologic
reaction,resultsfromIgEantibody
Thisreactionaffectsmanytissuesandorgans.

Deathmayoccurduetorespiratorytractspasmandconstriction
orcollapse.
.

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Causes: Anaphylaxis
Food(peanuts,fish,milk,eggs,wheatandchocolate).
Medications(penicillin,NSAIDs)
Insectsstings(bees,ants)

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Pathophysiology: Anaphylaxis
InteractionofforeignantigenwithIgEantibodies
Releaseofhistamine
Activationofplatelets,eosinophilsandneutrophils
smoothmusclespasm,bronchospasm,mucosaledemaand
inflammation.

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Clinical manifestations: Anaphylaxis

Mild
Occurswithinfirst
2hrsofexposure

Moderate
Same

Severe
Same

Peripheraltingling Flushing
Sensationof
Itching
warmth

Broncospasm
Laryngealedema

Fullnessinmouth
andthroat

bronchospasm

SevereDyspnea,
cyanosis

Nasalcongestion

Edemaoflarynx

Hypotension

Periorbital
swelling

Dyspnea

Cardiacarrestand
comamayfollow.

Pruiritis
Sneezing

Cough

wheezing

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Medical management: Anaphylaxis

1. Ifcardiacarrestthencardiopulmonaryresuscitation
initiated.
2. Antihistaminetopreventrecurrencereaction
3. Startintravenousfluidstomaintainhemodynamics.
4. Giveaminophyllineforbronchospasm
Nursing management: Anaphylaxis
1.
2.
3.
4.
5.

Assessforsignsofanaphylaxis.
Restoreeffectivebreathing
Reduceanxietybyreassuringthepatient
Provideoxygen,andmaintainairway
Monitorvitalsigns.

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Serum sickness
ItisatypeIIIhypersensitivityreaction.
ThereactionresultfromadministrationoftherapeuticAntiSeratakenfromanimalsourceforthetreatmentand
preventionofinfectiousdiseasesliketetanus,rabies,
diphtheria

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Clinical manifestations
Serum sickness

Localized:
Inflammatoryreactionatthesiteofinjection.

Generalized:
Skinrashes
Tendernessandswellingofjoints
vasculitismostlyinkidneysresultsinproteinuria
Glomerulonephritis
Peripheralneuritisleadstotemporaryparalysis
Fever
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Serumsickness
Medical management:
Antihistamines
Corticosteroids

Nursing management:
EncourageforROMexercises,provideDVTstockings
(adeepveinthrombosisandpulmonaryembolismare
treatstothesepatients.

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Disorders of
the immune
system

Functions of the immune

system
to protect against disease or other
potentially damaging foreign bodies.
identifies a variety of threats, including
viruses, bacteria and parasites, and
distinguishes them from the body's own
healthy tissue

What can go wrong with the

immune system?
When your immune system doesn't work
the way it should, it is called an immune
system or immunodeficiencydisorder.

Someone may be..

Beborn with a weak immune system. This
is called primary immune deficiency.
Get a disease that weakens your immune
system. This is called acquired immune
deficiency.
Have animmune system that is too active.
Have animmune system thatturns
against you. Conditions called
autoimmune disease occur.

An overactive immune
system/hypersensitivity
If you are born with certain genes, your
immune system may react to substances
inthe environment that are normally
harmless.

Four principal TYPES OF

HYPERSENSITVITY
Type I (Anaphylactic)
< 30 min symptoms occur.
IgE binds to mast cells or basophils: causes
degranulation of mast cell or basophil and
release of reactive substances such as
histamine
Examples:
Anaphylactic shock from drug injections and
insect venom ,hay fever, asthma

Anaphylactic responses can be

systemic reactions
shock and breathing difficulties
localized reactions
hay fever, asthma, and hives (slightly
raised, often itchy and reddened areas of the
skin).

Asthma
The response in your lungs can cause
coughing, wheezing, and trouble
breathing. Asthma can be triggered
by a common allergen like dust or
pollenor by an irritant like tobacco
smoke.

Allergic rhinitis
Sneezing, a runny nose, sniffling, and
swelling of your nasal passages from
indoor allergens like dust and pets or
outdoor allergens like pollens or molds.

Eczema
An allergen causes an itchy rash known as
atopic dermatitis

Skin testing

Type II (Cytotoxic)
Clinical symptoms occur 5-12 hours
Antigen causes formation of IgM and IgG
antibodies that bind to target cell , when
combined with action of complement,
destroys target cell
-Examples: Transfusion reactions, Rh
Incompatibility, HDNB

Blood Transfusions and Rh Incompatibi

lity
If blood from an Rh + donor is given to an
Rh - recipient, the donor's RBCs stimulate
the production of anti-Rh antibodies in the
recipient. If the recipient then receives Rh
+ RBCs in a subsequent transfusion, a
rapid, serious hemolytic reaction will
develop.

Hemolytic disease of the

newborn
Also called erythroblastosis fetalis
incompatibility between the blood types of
the mother and the baby.
HEMOLYTIC- breaking down of red blood
cells.
Erythroblastosis-making of immature red
blood cells.

HDNB is usually prevented today by

passive immunization of the Rh - mother at
the time of delivery of any Rh + infant with
anti-Rh antibodies(RhoGAM).

Drug-Induced Cytotoxic
Reactions

Thrombocytopenic purpura

Blood platelets (thrombocytes) are

destroyed by drug-induced cytotoxic
reactions.

 Drugs may bind similarly to white or red

blood cells, causing local hemorrhaging
and yielding symptoms described as
"blueberry muffin" skin mottling.

Blueberry muffin (skin

mottling)

Agranulocytosis
-immune-caused destruction of
agranulocytic white cells and it affects the
body's phagocytic defenses.

Hemolytic anemia
-when RBCs are destroyed

Type III (Immune

Complex)
clinical symptoms occur 3-8 hours
Antibodies and antigens form complexes
that cause damaging inflammation
Examples: Arthus reactions, serum
sickness

 Arthus Reaction- an acute response to a

second injection of vaccines (boosters)or
drugs at the same site as the first
injection.
Serum sickness-condition appeared in
soldiers after repeated injection of horse
serum to treat tetanus. It can also be
caused by injection of animal hormones
and drugs.

 Glomerulonephritis is an immune
complex condition, usually resulting from
an infection, that causes inflammatory
damage to the kidney glomeruli.

Type IV (Delayed CellMediated, or Delayed

Hypersensitivity)

clinical signs occur 24-48 hours

Antigens activate T cells that kill target
cell
Examples: Rejection of transplanted
tissues, contact dermatitis ,tuberculosis

ALLERGIC CONTACT
DERMATITIS

Autoimmune
disease
Inautoimmune diseases, the body
attacks normal, healthy tissues. The
cause is unknown. It is probably a
combination of a person's genes and
something in the environmentthat
triggers those genes.

Cytotoxic
Autoimmune
Graves' disease
Reactions
The immune system
produces antibodies
that stimulate the thyroid gland to release
excess amounts of thyroid hormone into
the blood (hyperthyroidism).
Symptoms: bulging eyes weight loss,
nervousness, irritability, rapid heart rate,
weakness, and brittle hair.
Treatment:Destruction or removal of the
thyroid gland

Graves disease

Myasthenia gravis
Antibodies bind to nerves and make them
unable to stimulate muscles properly.
Weakness that gets worse with activity is
the main symptom of myasthenia gravis.
Mestinon (pyridostigmine) is the main
medicine used to treat myasthenia gravis.

Myasthenia gravis

Immune Complex
Autoimmune Reactions
Systemic lupus erythematosus
(lupus)
People with lupus develop autoimmune
antibodies that can attach to tissues
throughout the body.
The joints, lungs, blood cells, nerves, and
kidneys are commonly affected in lupus.
Treatment often requires daily oral
prednisone.

Systemic lupus
erythematosus

Rheumatoid arthritis
The immune system produces antibodies
that attach to the linings of joints.
Immune system cells then attack the
joints, causing inflammation, swelling, and
pain
Treatments for rheumatoid arthritis can
include various oral or injectable
medications that reduce immune system
over activity.

Rheumatoid arthritis

Cell-Mediated Autoimmune
Type 1 diabetes
Reactions
In this type of diabetes,the immune
systemattacksthe cells inthe pancreas
that make insulin.

Psoriasis
In psoriasis, overactive immune system
blood cells called T-cells collect in the skin.
The immune system activity stimulates
skin cells to reproduce rapidly, producing
silvery, scaly plaques on the skin.

psoriasis

Reactions Related to the

Human
Leukocyte Antigen (HLA)
Complex
Human Leukocyte
Antigen (HLA)
-Is the locus of genes that encode for proteins
on the surface of cells that are responsible for
regulation of the immune system in humans.

Certain HLAs are related to an

increased susceptibility to specific
diseases.

HLA typing

-used to identify and compare HLAs.

Another important medical application of HLA typing is
in
transplant surgery, in which the donor and the
recipient must be matched by tissue typing
Serological tissue typing
-the laboratory uses standardized antisera or
monoclonal antibodies that are specific for particular
HLAs.

Tissue typing
-Lymphocytes from the person being tested
are incubated with laboratory test stocks of
anti -HLA antibodies specific for a particular
HLA. If the antibodies react with the
antigens on a lymphocyte then complement
damages the lymphocyte and they can
enter the cell.

Polymerase Chain Reaction

-new technique for analysing HLA is the use
of the polymerase chain reaction, to amplify
the cell's DNA

Diseases Related to Specific

Human Leukocyte Antigens
(HLAs)
Disease
Increased
Description
Risk of
Occurrence
with
Specific
HLA"
Inflammatory Diseases
Multiple sclerosis

5 times

Rheumatic fever

4- 5 times

Endocrine Diseases
Addison's disease

4- 10 times

Graves' disease

10- 12 times

Malignant Disease
Hodgkin's disease

1.4- 1.8 times Cancer of lymph nodes

Progressive inflammatory disease

affecting nervous system
Cross-reaction with antibodies
against streptococcal antigen
Deficiency in production of
hormones by adrenal gland
Antibodies attached to certain
receptors in the thyroid gland
cause it to enlarge and produce
excessive hormones

Rheumatic fever

Adissons disease

hodgkinss disease

Reactions to transplantation
Transplants recognized as non self are
rejected- attacked by T
cells that directly lyse the grafted cells.

types of transplants

bone marrow
lungs
heart
liver
cornea

Privileged Sites and

Privileged Tissue
Immunologically privileged site.
A part of the body wherein antibodies
usually do not circulate, meaning transplants
do not stimulate immune response.
Ex: Corneal transplant

Privileged tissue
An example is replacing a person's
damaged heart valve with a valve
from a pig's heart.

Stem Cells
Embryonic Stem Cells (ESCs)
These cells can be isolated from the very
earliest stage of an embryo, usually from
discarded embryos created for attempts at
in vitro fertilization.
ESCs are capable of generating many
different types of tissue cells and cell lines
such as muscle, nerve, or blood cells

Grafts
AUTOGRAFT
-when one's own tissue is grafted to
another part of the body.

ISOGRAFT
Identical twins have the same genetic
makeup; therefore, skin or organs
such as kidneys may be transplanted
between them without provoking an
immune response.

ALLOGRAFTS
Grafts between people who are not
identical twins.

XENOTRANSPLANTATION
Tissues or organs that have been
transplanted from animals.

Hyperacute rejection occurs in

human-to-human transplants only
when antibodies have been
preformed because of previous
transfusions, transplantations, or
pregnancies.

Bone Marrow Transplants

The recipients are usually individuals
who lack the capacity to produce B
cells and T cells vital for immunity or
who are suffering from leukemia.

Graft-Versus-Host(GVH) Disease
the transplanted bone marrow contains
immunocompetent cells that mount primarily
a cell-mediated immune response against the
tissue into which they have been transplanted
.

immunosupression
-to suppress cell-mediated immunity, the
most important factor in transplant
rejection.

Cyclosporine and Tacrolimus (FKS06)

-suppresses the secretion of
interleukin-2 (IL-2), disrupting cell
-mediated immunity by cytotoxic T
cells.

Cyclosporine and Tacrolimus (FKS06)

suppresses the secretion of interleukin-2
(IL-2), disrupting cell -mediated immunity
by cytotoxic T cells.
both has much effect on antibody
production by the humoral immune system.

Sirolimus(Rapamune)
-are among those that inhibit both cellmediated and humoral immunity.

Mycophenolate Mofetil
-inhibit the proliferation of T cells and
B cells.
Some biological agents such as the
chimeric monoclonal antibodies
basiliximab and daclizumab also block
IL-2 and are useful
immunosuppressives.

cancer

cancer
New growth of abnormal cells.
Benign tumor -self contained mass within
an organ that does not spread into
adjacent tissues.
Malignant tumor -uncontrolled growth of
abnormal cells within normal tissues.

Immunotherapy for
Cancer
Herceptin
consists of monoclonal antibodies against
a breast cancer growth factor.
Immunotoxins
are chemical poisons linked to a
monoclonal antibody ; the antibody
selectively locates the cancer cell for
release of the poison.

Immunotherapy for
cancer

1.Non specific immune stimulation

2.Adoptive cell transfer
3.Immune checkpoint blockage
4.Vaccination strategies

Immunodeficiencies
The absence of a sufficient immune
which can be
either congenital or acquired.

Congenital Immunodeficiency
defects in, or the absence of a
number of inherited genes.

Severe combined
immunodeficiency
(SCID).This is an example of an
immune deficiency that is present
at birth. Children with SCID are
missing important white blood
cells.

Bubble baby disease

Acquired
Immunodeficiency
a variety
of drugs, cancers, or
infectious agents

Selective IgA
immunodeficiency
B, T cells
Affects about 1 in 700, causing
frequent mucosal infections
specific cause uncertain

Mucosal Infections

Common variable
hypogammaglobulinemia
B, T cells (decreased
immunoglobulins)
Frequent viral and bacterial infections
second most common immune
deficiency, affecting about 1 in 70,000
inherited

hypogammaglobulinemia

Reticular dysgenesis
B, T. and stem cells (a combined
immunodeficiency: deficiencies in
Band T cells and neutrophils)
Usually fatal in early infancy:
inherited

Reticular dysgenesis

Severe combined
immunodeficiency
B. T. and stem cells(deficiency of
both Band T cells)
Affects about 1 in 100,000: allows
severe infections:
Inherited

Thymic aplasia
(DiGeorge syndrome)
T cells (defective thymus causes
deficiency of T cells)
Absence of cell-mediated immunity;
usually fatal in infancy
from Pneumocyslis pneumonia or viral
or fungal infections: due to failure of the
thymus to develop in embryo

DiGeorge syndrome

Wiskott-Aldrich syndrome
B, T cells (few platelets in blood,
abnormal T cel ls)
Frequent infections by viruses, fungi,
protozoa: eczema,
defective blood clotting; usually causes
death in childhood:
inherited on X chromosome

Wiskott-Aldrich
syndrome

X-linked infantile (Bruton's)

agammaglobulinemia
B cells (decreased immunoglobulins)
Frequent extracellular bacterial
infections; affects about 1 in
200,000: the first immunodeficiency
disorder recognized (1952):
inherited on X chromosome

HIV (Human
Immunodeficiency
Virus) Infection
HIV(human immunodeficiency
virus) is a virus that attacks the
immune system.
HIV infects and destroys certain
whitebloodcells called CD4+ cells.

AIDS(acquired
immunodeficiency
syndrome)
The last stage of HIV infection .
People with AIDS have a low number of
CD4+ cells and get infections or cancers
that rarely occur in healthy people. These
can be deadly.

 But having HIV doesn't mean you have

AIDS. Even without treatment, it takes a
long time for HIV to progress to AIDS
usually 10 to 12 years.
With treatment, many people with HIV are
able to live long and active lives.

aids

two types of HIV

HIV-1-which causes almost all the
cases of AIDS worldwide
HIV-2-which causes an AIDS-like
illness. HIV-2 infection is uncommon
in North America.

Signs and symptoms

Symptoms may appear from a few days to
several weeks after a person is first
infected. The early symptoms usually go
away within 2 to 3 weeks.

After the early symptoms go away, an infected

person may not have symptoms again for many
years. After a certain point, symptoms reappear
and then remain. These symptoms usually
include:
Swollen lymph nodes.
Extreme tiredness.
Weightloss.
Fever.
Night sweats.

Risk factors
contact with infected blood, semen, or
vaginal fluids.
unprotectedsexwith someone who has HIV.
sharing drug needles with someone who is
infected with HIV.
duringpregnancy, birth, orbreast-feeding.
casual contact like kissing or sharing
drinking glasses with an infected person.

Diagnostic examination
A doctor may suspect HIV if symptoms last and
no other cause can be found.
If you have been exposed to HIV, your immune
system will make antibodies to try to destroy
the virus. Doctors use tests to find these
antibodies in urine,saliva or blood.
Viral load which shows the amount of virus in
your blood.
CD4+ cell count,which shows how well your
immune system is working.

Most doctors use two blood tests, called the

ELISA and the Western blot. If the ELISA is
positive (meaning that HIV antibodies are found),
a Western blot or other test will be done to be
sure.
It may take as long as 6 months for HIV
antibodies to show up in your blood. If you think
you have been exposed to HIV but you test
negative for it:
Get tested again. Tests at 6, 12, and 24 weeks
can be done to be sure you are not infected.

 You can getHIV testingin most doctors'

offices, public health clinics, hospitals,
and PlannedParenthoodclinics.
You can also buy a home HIV testkit in
a drugstore or by mail order. Make sure
it's one that is approved by the Food
and Drug Administration (FDA). If a
home test is positive, see a doctor to
have the result confirmed and to find
out what to do next.

treatment

The standard treatment for HIV is a

combination of medicines called antiretroviral
therapy, or ART. Antiretroviral medicines slow
the rate at which the virus multiplies.
Taking these medicines can reduce the
amount of virus in your body and help you
stay healthy.
Medical experts recommend that people
begin treatment for HIV as soon as they know
that they are infected.

 After you start treatment, it's important to

take your medicines exactly as directed
by your doctor. When treatment doesn't
work, it is often because HIV has
becomeresistant to the medicine. This
can happen if you don't take your
medicines correctly.

prevention
HIV is often spread by people who don't know they
have it. So it's always important to protect yourself
and others by taking these steps:
Practice safersex.Use acondomevery time you
have sex (including oral sex) until you are sure that
you and your partner aren't infected with HIV or
other sexually transmitted infection (STI).
Don't have more than one sex partnerat a
time. The safest sex is with one partner who has
sex only with you.
Talk to your partnerbefore you have sex the first
time. Find out if he or she is at risk for HIV. Get
tested together. Getting tested again at 6, 12, and
24 weeks after the first test can be done to be sure
neither of you is infected. Use condoms in the
meantime.

 Don't drink a lot of alcohol or use illegal

drugsbefore sex.You might let down your
guard and not practice safer sex.
Don't share personal items, such as
toothbrushesor razors.
Never share needles or syringeswith anyone.
You also can take antiretroviral medicine to help
protect yourself from HIV infection. But to keep
your risk low, you still need to practice safer sex
even while you are taking the medicine.

The Stages of HIV

Infection

Phase I
The number of viral RNA molecules per
milliliter of
blood plasma may reach more than 10
million in the first week. Billions of CD4 + T
cells may be infected within a couple of
weeks.

 Immune responses and fewer uninfected

cells to target
deplete viral numbers in blood plasma
sharply within a few
weeks.
The infection may be asymptomatic or
cause lymphadenopathy (swollen lymph
nodes).

Phase 2
The numbers of CD4 + T cells decline steadily.
HIV replication continues but at a relatively low
level, probably controlled by CDS+ T cells
mainly in lymphatic tissue.
Other early HIV symptoms include slight fever,
headaches, fatigue, and muscle aches. These
symptoms may last for only a few weeks. Then
there are usually no HIV symptoms for many
years. That is why it can be hard to know if you
have HIV.

Phase 3
-Clinical AIDS emerges, usually within 10 years of
infection.
CD4 + T cell counts are below 350 cells/f.ll (200
cells/f.ll
defines AIDS).
Important AIDS indicator conditions appear,such as
C. albicaus infections of bronchi, trachea, or lungs;
cytomegalovirus eye infections; tuberculosis;
Puel/moeys/is
pneumonia; toxoplasmosis of the brain; and Kaposi's
sarcoma.