Body Defenses
What is the immune system?
 body’s defense against disease causing organisms, malfunctioning cells,
and foreign particles
 immunocompetence: intact immune system - functioning
Lines of Defense
First Line of Defense
 nonspecific
 distinguishes self from non-self
 does NOT distinguish between pathogens
First Line of Defense - Skin
 The dead, outer layer of skin, known as the epidermis, forms a shield
against invaders and secretes chemicals that kill potential invaders
 shed between 40 – 50 thousand skin cells every day!
First Line of Defense - Mucus & Cilia
 as you breathe in, foreign particles and bacteria bump into mucus
throughout your respiratory system and become stuck
 hair-like structures called cilia sweep this mucus into the throat for
coughing or swallowing
Other First Line Defenses
Second Line of Defense
 responds to antigens that penetrate the first line
 includes
− WBC (phagocytes)
− Inflammatory response
− Pyrogens
− Interferons
− Complement proteins
Second Line of Defense - WBCs
 if invaders actually get within the body, then your white blood cells
(WBCs) begin their attack
 WBCs normally circulate throughout the blood, but will enter the body’s
tissues if invaders are detected
Second Line of Defense
 Cellular Components of Inflammation – WBCs
− Neutrophils
 Phagocytes
 Short life span
− Monocytes and Macrophages
 Monocytes mature into macrophages
 Longer lifespan
− Eosinophils
 Allergic reaction
 Parasites
Inflammatory Response
 injured body cells release chemicals called cytokines (histamine), which
begin inflammatory response
− Capillaries dilate
− Pyrogens released, reach hypothalamus, and temperature rises
− Pain receptors activated
− WBCs flock to infected area like sharks to blood
Inflammatory Response
 Key Characteristics
− rapid
− non-specific
− includes cellular and chemical activity
− triggered by mast cells – histamine release
Inflammatory Response
 provides immediate protection against the effects of tissue injury and
“invaders”
 ability of the body to mount an inflammatory response is critical to health
and well-being
 causes visible symptoms and can rid the body of harmful organisms
 tissue damage may result from excessive inflammatory response
Sequence of Inflammatory Responses
 Stage I (vascular)—change in blood vessels:
− Phase I—constriction
− Phase II—hyperemia and edema
 Stage II (cellular exudate)—neutrophils, pus
 Stage III (tissue repair and replacement)
Second Line of Defense
 Vascular Phase
− arterioles spasm and constrict
− vasodilation
− increased capillary permeability
− white blood cell adhere to the inner walls of vessels
Cardinal Signs of Inflammation
 Erythema
 Heat
 Edema
 Pain
 Altered function
Second Line of Defense
 Benefits of Inflammation
− Limit and control tissue damage by preventing the spread of
inflammation to healthy tissues
− Prevent and limit infection and further damage
− Initiate adaptive immune response
− Initiate healing
Second Line of Defense
 Pyrogens
− released by macrophages
− stimulates the hypothalamus
− results in an increase in body temperature
Second Line of Defense
 Interferons
− Proteins released from cells infected by viruses
− Bind to receptors on the plasma membranes of uninfected cells
− These uninfected cells produce an enzyme that inhibits viral replication
− When virus enter the uninfected cell it can not replicate and spread
− Do not protect cells already infected – they stop the spread
Second Line of Defense
 Complement Proteins - Major functions:
− embed in the plasma membrane of the bacterial cells and causes cells
to swell, burst, and die.
− stimulate vasodilatation in the infected area
− increase permeability of vessels
− chemotaxis – attracting macrophages, monocytes, and neutrophils to
the infected area
− bind to microbes and form a rough outer coat that promotes
phagocytosis.
Third Line of Defense - Antibodies
 most infections never make it past the first and second levels of defense
 those that do trigger the production and release of antibodies
− proteins that latch onto, damage, clump, and slow foreign particles
− each antibody binds only to one specific binding site, known as an
antigen
Third Line of Defense – Immune System
 Specific
 Develops over time
 Uses memory system
 Distinguishes self from non- self AND between pathogens
 Includes
− T cells-cell mediated immunity
− B cells-humoral immunity
Third Line of Defense – Immune System
 Self-regulated
 Self-limiting
 Essential for survival
 Must be able to distinguish self from non-self
 Antigens
Third Line of Defense – Adaptive
 B and T cells
− B cell
 Bone Marrow
 Produce antibodies
− T cell
 Thymus
 Attack antigen directly
Third Line of Defense – Humoral
 Immunoglobulins
− IgG
 80-85% of plasma antibodies
 Main defense against bacteria
 Major antibody found in fetal blood – crosses the placenta to give
passive immunity
Third Line of Defense – Humoral
 Immunoglobulins
− IgM
 Largest immunoglobulin
 First Ig produced during the initial response to an antigen
 Eliminates pathogens in the early stages of B cell mediated
immunity before there is sufficient IgG
Third Line of Defense – Humoral
 Immunoglobulins
− IgA
 Found in mucosal areas, such as the gut, respiratory tract and
urogenital tract
 Prevents colonization by pathogens
 Also found in saliva, tears, and breast milk
Third Line of Defense – Humoral
 Immunoglobulins
− IgE
 Binds to allergens and triggers histamine release from mast cells
and basophils
 Involved in allergy
 Also protects against parasitic worms
Third Line of Defense – Humoral
 Immunoglobulins
− IgD
 Functions mainly as an antigen receptor on B cells that have not
been exposed to antigens
 Shown to activate basophils and mast cells to produce antimicrobial
factors
Third Line of Defense – Cell - Mediated
 Different T cell classifications
− Cytotoxic T cells (Tc)
− Helper T cells (Th) – CD4
− Suppressor T Cells
− Memory T Cells
Overview of the Immune Response
What is immunity?
 resistance to a disease - causing organism or harmful substance
 two types
− Active Immunity
− Passive Immunity
Active Immunity
 You produce the antibodies
− Your body has been exposed to the antigen in the past either through:
− exposure to the actual disease causing antigen – The body fought,
won, and remembers
− planned exposure to a form of the antigen that has been killed or
weakened –body detects, eliminates, and remembers
 Vaccines
− antigens are deliberately introduced into the immune system to
produce immunity
− because the bacteria has been killed or weakened, minimal symptoms
occur
− have eradicated or severely limited several diseases, such as polio
and smallpox
 How long does active immunity last?
− depends on the antigen
− some disease-causing bacteria multiply into new forms that our body
doesn’t recognize, requiring annual vaccinations, like the flu shot
− booster shot - reminds the immune system of the antigen
− others last for a lifetime, such as chicken pox
Passive Immunity
 You don’t produce the antibodies
− A mother will pass immunities on to her baby during pregnancy through what organ?
− These antibodies will protect the baby for a short period of time
following birth while the immune system develops. What endocrine
gland is responsible for this?
− Lasts until antibodies die
Active vs. Passive Immunity
Naturally Acquired
Artificially acquired
Hypersensitivity
 Typically, inflammatory responses rid the body of antigens and resolve
the infection within days
 In some cases, the inflammatory response can have harmful effects –
even result in death!
-this type of immune response (IR) is called ‘hypersensitivity’ or ‘allergy’
Hypersensitivity
 Allergy
− Exaggerated response to environmental agents
 Autoimmunity
− Response directed at one’s own cells
 Alloimmunity
− Response directed against beneficial foreign tissues (transplant
reactions)
Hypersensitivity – Immediate vs Delayed
 Immediate hypersensitivity reaction
− Occurs within minutes or hours
− Reactions initiated by Ab or Ab-Ag complexes
− Anaphlaxis-severe immediate reaction
 Delayed hypersensitivity reaction
− May take several hours
− Initiated by cell-mediated response
− Contact dermatitis & graft rejection
Hypersensitivity
 Type I: Rapid Hypersensitivity Reaction
− Introduction
− Results from an increase in the production of IgE antibodies
− Vary in severity & manner of exposure
− Local vs. widespread systemic reaction
− Examples: reactions to specific allergens such as latex, insect
sting/bite, iodine, shellfish, nuts, drugs, etc.
Hypersensitivity
 Anaphylactic Shock Symptoms
− Neuro: sensation of impending doom, anxiety, restlessness,
drowsiness, seizures
− Respiratory: hoarse voice, wheezing, stridor
− CV: hypotension, dysrhythmias, angioedema
− GI: severe cramps, nausea, diarrhea
− Can result in cardiac arrest & death without immediate intervention
Hypersensitivity
 Type II
− Tissue specific reactions
− Immediate type reaction
− IgG and IgM antibodies
− Lysis of blood cells occurs because of the activation of the complement
system
− Examples: Blood transfusion reaction and erythroblastosis fetalis
(hemolytic disease of the newborn)
Hypersensitivity
Hypersensitivity
 Type III Overview
− Excess antigens produce immune complexes in the blood which may
lodge is small vessels (kidney, skin, joints)
− Circulating antigen-antibody complexes accumulate and are deposited
in the tissue
− Triggers the complement system and inflammation
Hypersensitivity
 Type III Reaction
− Results in an inflammatory response that damages tissues &/or blood
vessels
− Examples: Systemic Lupus Erythematosus (SLE), Rheumatoid
Arthritis (RA)
− Raynaud phenomenon – form of serum sickness – circulation to
fingers/toes is blocked by immune complexes
 localized pallor, numbness, cyanosis
 trigger: temperature extremes
Hypersensitivity
 Type IV
− Delayed reaction
− Cell mediated tissue reactions rather than antibody mediated
− Examples: transplant reactions, tuberculin reactions, contact
dermatitis
Hypersensitivity
Autoimmune Disorders
 Immune system losses the ability to recognize self
 Defenses are directed against host
 Can affect any tissue
 Mechanism that triggers this response is not clear
Autoimmune Disorders
 Known characteristics
− genetics play a role
− more prevalent in females
− onset is frequently associated with an abnormal stressor, either
physical or psychological
− frequently progressive, relapsing-remitting disorders characterized by
periods of exacerbation and remission
Systemic Lupus Erythematosus






Chronic inflammatory condition
Remission and exacerbations-stressors tend to trigger
May affect connective tissue of any body organ
Disease progression varies from mild to severe
More common in women
Cause is unclear, but thought that B cells are activated to produce
autoantibodies and autoantigens that combine to form immune
complexes, which attack the body’s own tissues
Systemic Lupus Erythematosus
 Signs & Symptoms
− mimics Rheumatoid Arthritis
− photosensitivity
− butterfly rash
− alopecia
− renal, hematologic, CV, pulmonary, neurologic, ocular, GI
Immunodeficiency
 Impaired function of one or more components of immune or inflammatory
response
 Renders the person susceptible to disease normally prevented
 Opportunistic infections
 Hallmark: Tendency to develop unusual or recurrent, severe infections
HIV/AIDS
 Caused by HIV (human immunodeficiency virus)
 Destroys the helper T cells (CD4) that regulate normal immune response
 Transmission
− Blood and bodily fluids
ABO & Rh
ABO System
ABO System
Rh System
 DD or Dd genotype are Rh-positive
 dd genotype are Rh-negative
Erythroblastosis Fetalis