Immune System
that cause harm to an organism.
Dr. Eduardo L. Fabella
What is Immunity?
Immunity
Immunity
The ability of the body to fight
infection and/or foreign
invaders by producing
antibodies or killing infected
cells.
Immune System
The system in the body
responsible for maintaining
homeostasis by recognizing
harmful from nonharmful
organisms and produces an
appropriate response.
Foreign Invaders
Called Pathogens
Viruses, bacteria or other living
thing that causes disease/immune
response.
Antigens
Toxins that pathogens produce
no matter what the invader may
Parts of the Immune System
1. Blood - White Blood
Cells
2. Lymph nodes
3. Thymus Gland –
Produces T Lymphocytes
4. Bone Marrow – Produces
B Lymphocytes
How does the body fight
infection/foreign invaders?
The Body’s THREE lines of
Defense
First Line of Defense – The Skin
• Provides Physical
and Chemical
barriers
Physical – hard to penetrate,
made of indigestible keratin
Chemical – tears, sweat
Second Line of Defense –
Nonspecific Immune Response
These are defenses the body uses
be. These defenses include:
Phagocytosis – done by
macrophages
Natural Cell Killers
Inflammation - caused by release
of histamine from leukocytes
Fever – caused by histamines. The
fever (high temp) kills invaders by
denaturing their proteins.
Third Line of Defense – Specific
Immune Response
This is a specific
response to a specific
pathogen/antigen
The response involves the
creation of Antibodies.
Antibodies
Y-shaped protein molecule
Made up of variable and constant
regions
Made up of Heavy and Light
chains
Produced by B-Lymphocytes
Function: Recognize antigens,
bind to and deactivate them.
Note: Variable region recognizes
the anitgens.
How an antibody operates/works?
The Pathway of Specific Immune
Response
1. Antigen infects cells.
2. Macrophage ingests
antigen and displays
portion on its surface
3. Helper T- Cell recognizes
antigen on the surface
of the macrophage and
becomes active.
4. Active Helper T-Cell
9. Memory T and Memory B
cells remain in the body
to speed up the
response if the same
antigen reappears.
10. Supressor T-Cells
stop the immune
response when all
antigens have been
destroyed.

Cellular Immunity .vs. Antibody activates Cytotoxic T- Immune Response Summary

Immunity
Cellular Immunity
Carried out by T-Cells
Infected cells are killed by
Cytotoxic T –Cells.
Antibody or Humoral
Immunity
Carried out by B-cells
Antibodies are produced and
dumped into blood stream.
Antibodies bind to antigens and
deactivate them.
Immune Response Explained
Cells and B-Cells.
Primary .vs. Secondary Immune
5. Cytotoxic T-Cells divide Response
into Active Cytotoxic T-
cells and Memory T – Primary Immune Response
Cells.
This is a response to an
Immune Response Explained invader the first time the
invader infects the body.
6. Active Cytotoxic T-Cells
kill infected cells No measurable immune
response for first few days.
7. At the same time, B-
Cells divide into Plasma Next 10 – 15 days antibody
Cells and Memory B- production grows steadily
Cells
Secondary Immune Response
8. Plasma cells produce
antibodies that A more rapid response to an
deactivate pathogen. invader the 2nd time it invades
the body.
Antibody production increases
dramatically and in a much
shorter time period.
Primary .vs. Secondary Immune
Response
Passive .vs. Active Immunity
Active Immunity
This is immunity where the body
is “actively” producing antibodies
to fight infection.
Ex:
Vaccination: An injection of
a weakened strain of an infectious
microbe (pathogen) that causes
the body to undergo active
immunity (produce antibodies).
Passive .vs. Active Immunity
Passive Immunity
This is immunity where antibodies
are given to a person from the
blood of another person or animal.
This immunity only lasts for a
short period of time.
The Immune System
Immunity: the body’s specific
protective response to invading
foreign agent or organism
Immunopathology: the study of
diseases that result from
dysfunction of the immune system
Immune disorders:
Automimmunity
Hypersensitivty
Gammopathies
Immune deficiencies: primary and
secondary
Central and Peripheral Lymphoid
Organs
Development of Cells of the
Immune System
Lymphocytes
B lymphocytes mature in the
bone marrow
T lymphocytes mature in the
thymus where they also
differentiate into cells with
various functions
Immune Function
Natural immunity: nonspecific
response to any foreign invader
White blood cell action:
release cell mediators such as
histamine, bradykinin, and
prostaglandins
engulf (phagocytize) foreign
substances
Inflammatory response
Physical barriers
Immune Function
Acquired immunity: specific
against a foreign antigen
Result of prior exposure to an
antigen
Active or passive
Stages of Immune Response
Role of Antibodies
Agglutination of antigens
Opsonization
Promote release of vasoactive
substances; activation of
complement system and
phagocytosis
Act in concert with other
components of the immune
system
Types of immunoglobulins:
IgA, IgD, IgE,IgG, and IgM
Antibody Molecule
Antigen–Antibody Binding
Cellular Immune Response
B lymphocytes: humoral
immunity
Produce antibodies or
immunoglobulins
T lymphocytes: cellular
immunity
Attack invaders directly,
secrete cytokines, and
stimulate immune system
responses
Helper T cells
Cytotoxic T cells Medications and transfusions
Memory cells Tests to Evaluate Immune
Function
Suppressor T cells (suppress
immune response) WBC count and differential
Variables That Affect Immune Bone marrow biopsy
System Function
Humoral and cellular immunity
Age and gender tests
Nutrition Phagocytic cell function test
Presence of conditions and Complement component tests
disorders:
Hypersensitivty tests
cancer/neoplasm
Specific antigen–antibody
chronic illness tests
autoimmune disorders HIV infection tests
surgery/trauma
Allergies
Variables That Affect Immune Management of Patients
System Function with
Immunodeficiency
History of infection and
immunization Immunodeficiency Disorders
Primary
Genetic factors
Lifestyle Genetic
May affect phagocytic
function, B cells and/or T cells,
or the complement system
Secondary
Acquired
HIV/AIDS
Related to underlying
disorders, diseases, toxic
substances, or medications
Primary Immunodeficiencies
Usually seen in infants and
young children
Manifestations: vary
according to type
severe or recurrent infections
failure to thrive or poor
growth
positive family history
Potential complications:
recurrent, severe, potentially
fatal infections
related blood dyscrasias
Malignancies B cells, complement defects =
bacterial infections
Primary Immunodeficiencies
Congenital (Primary)
Treatment:
B-cell Deficiency
varies by type
IgA Deficiency
treatment of infection
DiGeorge’s Syndrome
pooled plasma or
immunoglobulin Severe Combined
Immunodeficiency
thymus graft
B Cell Deficiency
stem cell
Agammaglobulinemia
bone marrow transplant
Hypogammaglobulinemia
Immunodeficiency Disease
IgA Deficiency
Patient unable to fight off
infection Most common immune deficiency
disorder
Hallmarks
Genetic condition
Repeated infections
Failure of IgA synthesis
Opportunistic infections
Patient has repeated, recurrent
Immunodeficiency Disease sinus, lung, GI infections
Most are defects in T cells or B DiGeorge’s Syndrome
cells
Thymic hypoplasia
T cells, macrophage defects =
fungal, viral infections
Severe decrease in T-cell
production, function
Defects of face, ears, heart
Severe Combined
Immunodeficiency
Thymus development arrested
at ~6-8 weeks gestation
Deficiency, defective
maturation of stem cells that
produce B and T cells
Little to no antibody
production
SCID
Two types
Autosomal recessive
X-linked disease recessive
SCID
Recurrent, frequently
overwhelming infections
Particularly respiratory,
gastrointestinal
Most die in first few years of
life, usually by one year of age
Death usually due to
opportunistic infection
Acquired Immunodeficiency
Nutritional deficiency
Iatrogenic (drugs, radiation)
Trauma (prolonged hypo-
perfusion)
Stress
Infection (HIV)
Immune Deficiency Therapies
B-cell deficiency: Gamma globulin
SCID: Bone marrow transplants,
enzyme replacement
DiGeorge’s Syndrome: Fetal
thymus transplants
Gene therapy
Nursing Management
Monitor for signs and
symptoms of infections
Symptoms of inflammatory
response may be blunted
Monitor lab values
Promote good nutrition
Address anxiety, stress, and
coping
Nursing Management
Strategies to reduce risk of
infection
Hand washing and strict
aseptic technique
Patient protection and
hygiene measures:
skin care
promote normal bowel and
bladder function
pulmonary hygiene
Patient Teaching
Signs and symptoms of
infection
Medication teaching
Prevention of infection
Handwashing
Avoid crowds and persons
with infections
Hygiene and cleaning
Nutrition and diet
Lifestyle modifications to
reduce risk
Follow-up care
Allergic Disorders
Allergic Reactions
Allergy
An inappropriate, often
harmful response of the
immune system to normally
harmless substances
Hypersensitive reaction to an
allergen initiated by
immunological mechanisms
that is usually mediated by
IgE antibodies
Allergic Reactions
Allergen
the substance that causes the
allergic response
Atopy
allergic reactions
characterized by IgE antibody
action and a genetic
predisposition
Immunoglobulins and Allergic
Response
Antibodies (IgE, IgD, IgG, IgM,
and IgA) react with specific
effector cells and molecules,
and function to protect the
body
IgE antibodies are involved in
allergic disorders
IgE molecules bind to an
allergen and trigger mast cells
or basophils
Immunoglobulins and Allergic
Response
These cells then release
chemical mediators such as:
Histamine
Serotonin
Kinins
SRS-A
neutrophil factor
These chemical substances
cause the reactions seen in
allergic response
Immunoglobulins and Allergic
Response (cont.)
Allergen triggers the B cell to
make IgE antibody, which
attaches to the mast cell; when
that allergen reappears, it binds
to the IgE and triggers the mast
cell to release its chemicals
Hypersensitivity
Exaggerated Immune Response
Hypersensitivity
A reflection of excessive or
aberrant immune response
Sensitization: initiates the
buildup of antibodies
Types of hypersensitivity
reactions
Anaphylactic: type I (IgE
mediated)
Cytotoxic: type II (tissue
specific)
Immune complex: type III
Delayed type: type IV (cell-
mediated)
Type I—Anaphylactic Reaction
Type I
Immediate hypersensitivity
IgE mediated
Exogenous antigen
Type I: Signs/Symptoms
Clinical signs, symptoms =
response to histamine release
GI, skin, respiratory system
High mast cells numbers
Most sensitive
Type I: Signs/Symptoms
Histamine effects Severe, generalized Type I
reaction
Vasodilatation
Life-threatening
Increased capillary permeability
Loss of airway
Non-vascular smooth muscle
spasm Ventilatory failure
Type I: Signs/Symptoms Hypoperfusion
Skin: flushing, itching, edema, Type II
urticaria, hives
Tissue specific
Respiratory: bronchospasm,
laryngospasm, laryngeal edema Reaction to tissue-specific
antigens
Cardiovascular: tachycardia,
hypotension Causes target cell destruction,
dysfunction
GI: nausea, vomiting, cramping,
diarrhea Exogenous or endogenous antigen
Type I: Atopia Type II
“Allergy prone” individuals Most commonly affected cells
Genetic predisposition Red blood cells
More IgE Thyroid cells
More mast cell receptors for Type II: Mechanisms
antibodies than normal Antibody binds to cell membrane,
Type I: Anaphylaxis triggers compliment-mediated
lysis
Examples
Reaction to transfused blood
Hemolytic disease of newborn
Type II: Mechanisms
Antibodies promote target cell
clearance by macrophages
Type II: Mechanisms
Antibodies bind to target cells and
cytotoxic T-cells
Trigger release of toxins to
destroy target cells
Type II: Mechanisms
Antibody binds to cell
membrane, causes alterations
in target cell function
Example: Graves' disease
Antibody binds to thyroid cell
membrane
Mimics Thyroid Stimulating
Hormone action
Causes production of
excessive amounts of thyroid
hormone
Results in common form of
hyperthyroidism
Type III—Immune Complex
Reaction
Type III
Mediated by antigen/ antibody
complex deposition in tissues
Exogenous or endogenous antigen
Type III: Mechanism
Ag-Ab complex deposited in
tissues
Especially sensitive tissues
are blood vessels, GI,
respiratory system
Causes complement
activation, increased
neutrophil activity
Neutrophils have trouble
digesting complexes, release
lysosomes causing damage
Type III
Immune complex quantity varies
over time
Symptomatic periods alternate
with periods of remission
Type III: Serum Sickness
Repeated intravenous antigen
injections
Immune complexes deposited in
tissues
Fever, rash, pain,
lymphadenopathy
Type III: Raynaud’s Phenomenon
Temperature governs immune
complex deposition in peripheral
circulation
Exposure to cold causes redness,
pain of fingers, toes followed by
numbness, cyanosis, gangrene
Type III: Arthus Reaction
Occurs after repeated LOCAL
exposure to exogenous antigen
Immune complexes in vessel walls
Examples
Celiac disease from wheat protein
Hemorrhagic alveolitis from moldy
hay inhalation
Type IV—Delayed or Cellular
Reaction
Hapten binds to protein molecule Total serum IgE
Changes its antigenicity Skin tests: note precautions
Causes it to become an allergen Screening procedures

Type IV Hypersensitivity Targets Medication

Delayed Autoantigens Oxygen, if respiratory

assistance needed
Mediated by Td (lymphokine- Sequestered cells (cornea, testes)
producing) or Tc (cytotoxic) cells Epinephrine for anaphylactic
Foreign antigen triggered reactions
No antibody involved (infection)
Histamines
Type IV Suppressor T-cell malfunction
Corticosteroids
Examples Genetic causes
Prevention and Treatment of
Graft rejection Hypersensitivity Targets Anaphylaxis

Contact allergic reactions (poison Isoantigens Screen and prevent

ivy) Tissue grafts, transplants Treat respiratory problems;
Hypersensitivity Targets Rh negative sensitivity provide oxygen, intubation,
and cardiopulmonary
Allergens Management of Patients With resuscitation as needed
Pollen (hay fever) Allergic Disorders
Epinephrine: 1:1,000 SQ
Drug reactions History and manifestations;
comprehensive allergy history Auto injection system: EpiPen
Foods May follow with IV
Diagnostic tests
Hypersensitivity Targets epinephrine
CBC-eosinophil count
Neoantigens IV fluids
Self-Administration of
Epinephrine
Allergic Rhinitis
Also called hay fever and
seasonal allergic rhinitis
Allergic rhinitis is a common
respiratory allergy presumed
to be mediated by a type I
hypersensitivity
Affects 10% to 25% of the
population
Allergic Rhinitis
Symptoms include:
sneezing and nasal congestion
clear, watery discharge
nasal itching
itching of throat and soft
palate
dry cough
Hoarseness
Headache
May affect the quality of life:
Fatigue
loss of sleep
poor concentration
Assessment of the Patient
With Allergic Rhinitis
Assess health history
Include personal and family
history
Perform an allergy
assessment
Subjective data includes
symptoms and how the
patient feels before symptoms
become obvious
Note the relationship between
symptoms and seasonal
changes, emotional problems,
and stress
Identify nature of antigens,
seasonal changes in
symptoms, and medication
history
Diagnosis of the Patient With
Allergic Rhinitis
Ineffective breathing pattern
related to allergic reaction
Deficient knowledge about
allergy and the recommended
modifications in lifestyle and
self-care practices
Ineffective individual coping
with the chronicity of the
condition and the need for
environmental modifications
Collaborative
Problems/Potential
Complications
Anaphylaxis
Impaired breathing
Nonadherence to therapeutic
regimen
Planning the Care of the
Patient With Allergic Rhinitis
Goals may include:
Restoration of normal
breathing pattern
Increased knowledge about
the causes and control of
allergic symptoms
Improved coping with
alterations and modifications
Absence of complications
Improved Breathing Pattern
Modify the environment to
reduce allergens
Reduce exposure to people
with upper respiratory
infection
Take deep breaths and cough
frequently
Promoting
Understanding/Patient
Teaching
Instruction to minimize
allergens
Use of medications
Desensitization procedures
Other Allergic Disorders
Contact dermatitis
Atopic dermatitis
Drug reactions (dermatitis
medicamentosa)
Urticaria and angioneurotic
edema
Food allergy
Serum sickness
Latex allergy
Pathophysiology Rheumatoid
Arthritis
Autoimmune Disease
Clinical disorder produced by
immune response to normal tissue
component of patient’s body
Rheumatoid Arthritis
Antibody reaction to collagen in
joints
Causes inflammation, destruction
of joints
Myasthenia Gravis
Antibodies destroy acetylcholine
receptors on skeletal muscle
Produce episodes of severe
weakness
Antibodies can cross placenta,
affect newborn
Immune Thrombocytopenic
Purpura
Antibodies destroy platelets
Produces clotting disorders,
hemorrhaging
Antibodies can cross placenta,
affect newborn
Other Autoimmune Diseases
Type I diabetes mellitus
Primary myxedema
Rheumatic fever
Crohn’s disease
Ulcerative colitis
Systemic Lupus Erythematosis
(SLE)
SLE
Chronic, multi-system auto-
immune disease
Highest incidence
Women, 20-40 years of age
Black, Hispanic women
Mortality after diagnosis averages CNS involvement with
5% per year seizures/psychosis

SLE Peripheral vasculitis/gangrene

Antibody against nucleic acid Hemolytic anemia

components (ANA, anti-nuclear
antibody) SLE: Chronic management

Immune complex precipitates in Anti-inflammatory drugs

tissues, causes widespread Aspirin
destruction
Ibuprofen
Especially affected are renal
system, blood vessels, heart Corticosteroids

SLE Avoidance of emotional stress,

physical fatigue, excessive sun
Signs/Symptoms exposure
Facial rash/skin rash triggered by
sunlight exposure

Oral/nasopharyngeal ulcers

Fever

Arthritis

SLE

Signs/Symptoms

Serositis (pleurisy, pericarditis)

Renal injury/failure