IMMUNE SYSTEM

Immune System

• collection of mechanisms within an

organism that protects against infection by
identifying and killing pathogens.

• a network of cells, tissues, and organs that

work together to defend the body against
attacks by “foreign” invaders
 Major Components :
• Bone marrow = source of WBC’s
• Thymus = where T lymphocytes mature
• Lymphatic vessels = carry lymph
• Lymph nodes = where immune cells
congregate
• Spleen = compartments where immune
cells gather and work
• Tonsils, adenoids, Peyer’s patches and
appendix
 IMMUNITY

= the condition of being immune or resistant

to a particular infectious disease

= the body’s capability to repel foreign

substances and cells
NON-SPECIFIC DEFENSE
MECHANISMS
 First Line of Defense
• Skin = completely covers all other parts
of the body
• Mucous membranes = mucus entraps
invaders
• Cilia (post. nasal membranes, nasal
sinuses, bronchi and trachea
• digestive enzymes
acidity of the stomach
bile
• saliva, sweat and tears
• urine
• microbial antagonism
 Second Line of Defense
• FEVER ( T = 38◦C )
- stimulated by PYROGENS
a. external = pathogens
b. internal = interleukins
- augments host defenses by:
1. stimulates wbc’s to deploy and destroy
invaders
2. reduces available free plasma iron
3. induces production of IL-1
• IRON BALANCE
- wbc’s produce IL-1 w/c stimulates iron
storage in the liver reducing free iron
for the pathogens

• CELLULAR SECRETIONS
a. Interferons = small anti-viral proteins
produced by virus-infected cells

b. Fibronectin = epithelial tissue secretion

that blocks bacterial attachment
 c. Β lysin = polypeptide released from
pletelets during infection
d. Interleukins = polypeptides secreted by
macrophages and lymphocytes

• BLOOD PROTEINS
a. Complement = a group of 30 different
proteins in blood plasma
= constitutes the “complement system”
 Consequences of Complement Activation:
1. Initiation and amplification of inflammation
2. Chemotaxis = attraction of phagocytes
to the sites to w/c they are needed
3. Activation of leukocytes
4. Lysis of bacteria and other foreign cells
5. Opsonization = increased phagocytosis
by phagocytic cells
= phagocytosis facilitated by deposition
of opsonins on the surface
b. Prostaglandins
- membrane associated lipids acting
like local hormones
- controls platelet aggregation,
inflammation, immune response,
pain production, etc.
• PHAGOCYTOSIS
 2 most important phagocytes:

1. NEUTROPHILS (granulocytes)
= most efficient and abundant

2. MACROPHAGES
= from monocytes
a. wandering – leave the bloodstream
b. fixed – remain in tissues and organs
PHAGOCYTOSIS
 Steps in Phagocytosis:
1. CHEMOTAXIS
2. ATTACHMENT
3. INGESTION
4. DIGESTION
• INFLAMMATION
= a complex series of events as the body
responds to any local injury, irritation,
microbial invasion, or toxins

Purposes of Inflammation:
1. Localize an infection
2. Prevent spread
3. Neutralize toxins
4. Aid in repair of damaged tissue
THIRD LINE OF DEFENSE

“Immune response to disease”

 Properties of an Ideal VACCINE

• With enough antigens

• With antigens from all strains of a

pathogen

• Not too toxic

• Doesn’t cause disease

 Types of Vaccines
A. Artificial Active

Live (attenuated) viruses

• Ex. Measles, OPV, MMR

Dead (inactivated) viruses

• Ex. Hepa B, influenza, rabies

Live (attenuated) bacteria

• Ex. BCG
• Dead (inactivated) bacteria
Ex. Anthrax, cholera

• Bacterial capsular antigens

Ex. Hib (H. influenza type B)

• Bacterial toxoids
Ex. tetanus
B. Artificial Passive

Human gamma globulins/ pooled immune

serum globulins

Ex. HBIg (Hepatitis B)

TIg (Tetanus)
Rig (Rabies)
 IMMUNOLOGY

= scientific study of immune

responses
ANTIGENS
- foreign organic substance large enough to

stimulate production of antibodies

“should be foreign to the human body”

ex. microorganisms
ANTIBODIES
- glycoproteins produced by lymphocytes
in response to the presence of an antigen
- formed by B lymphocytes
- “immunoglobulins”

Factors affecting Antibody production:

1. Nature of antigen
2. Site of antigenic stimulus
3. Amount of antigen
4. Frequency of exposure
 Five classes of Immunoglobulins:
• IgA
- 15-20% of Igs in human serum
- in tears, saliva, colostrom etc

• IgD
- less than 1% on serum Igs
- large amounts on B cell surfaces

• IgE
- less than 1% in serum but in large amounts
in basohils and mast cells (allergy)
• IgG
- 70 to 75% of the total Ig pool
- smallest and can cross the placenta

• IgM
- 10% of the serum Ig pool
- largest Ig and the first to be formed in
the primary response to antigens
- most efficient complement fixing Ig
• Agammaglobulinemia
= inability to produce antibodies

• Hupogammaglobulinemia
= produce insufficient amounts of Abs

• Immunosuppressed
= unable to make Abs following
chemotherapy or immunosuppressive drug
injection
IMMUNE RESPONSES
 Humoral Immunity
= “antibody-mediated immunity”
= involves antibody production
 Cell-mediated Immunity
= complex system of interactions between
many types of cells and cellular
secretions
 HYPERSENSITIVITY

• Defensive immune responses becomes

overly sensitive

Types of Hypersensitivity Reactions:

A. Immediate ( Type I, II, III)
= few minutes to 24 hours

B. Delayed (Type IV)

= after 24 hours
• Type I HR (anaphylactic reaction)
- involves IgE
Ex. Asthma, hives, food allergies

• Type II HR (cytotoxic reaction)

- involves IgG or IgM
Ex. Transfusion reactions
Rh incompatibility

• Type III HR ( immune complex reaction)

- involves IgG and IgM
Ex. Serum sickness
autoimmune diseases (SLE)
• Type IV HR (delayed type hypersensitivity)
Ex. Tuberculin test
transplant rejection
 Immunodeficiency
• ACQUIRED
= caused by drugs and certain infections

• INHERITED
= treated with bone marrow transplant
Ex. Chediak-Higashi synd.
Wiskott-Aldrich synd.
 Med. Tech

IMMUNOLOGY
&
SEROLOGY
 LYMPHOCYTE EFFECTOR
FUNCTION
antigen – antibody complexes
Humoral Immunity
1. Precipitation
2. Agglutination
3. Neutralization
4. Opsonization
5. Antibody dependent cytotoxicity
6. Complement activation
7. Immediate hypersensitivity

Cell Mediated Immunity

1. Delayed hypersensitivity
2. Cell mediated lysis
 IMMUNOLOGIC MEMORY
primary immune response
secondary immune espose

memory cells – greater number and thus

shorter response time
(isotype switch)

vaccination
 Regulation of Immune Response
- immune system goes awry
autoimmunity

Mechanism that deal with potentially self

reactive lymphoytes(B and T cells)
 SELECTIVE NONRESPONSIVENESS
OR TOLERANCE
 REGULATORY T CELLS
 REGULATING CYTOKINES