vocab
 Tonsillitis
 Mucosa-associated lymphatic
tissue (MALT)
 Pathogen
 Complement fixation
 Pyrogens
 Chemotaxis
 Immunocompetant
 Autograft
 Isograft
 Allograft
 Xenograft
 Hapten
 Allergy/hypersensitiviy
 Immediate/acute
hypersensitivity
 Anaphylactic shock
 Delayed hypersensitivity
 Immunodeficiency
 Severe combined
immunodeficiency disease
 Acquired immune deficiency
syndrome
 Autoimmune diseases
 Multiple sclerosis
 Myasthenia gravis
 Graves’ disease
 Type 1 diabeties
 Systemic lupus erythematosus
 Glomerulonephritis
 Rheumatoid arthritis
Lymphatic and
Immune System
Inflammatory response
 Blood vessels dilate creating the heat and redness and
directing more blood to the area.
 Within the first hour neutrophils move out of the capillaries
to the injured tissue and begin engulfing damaged/dead
cells and pathogens.
 Monocytes that follow the neutrophils begin as poor
phagocytes but after 8-12 hrs they become macrophages
and replace the short lived neutrophils.
 This process occurs concurrently with the blood clotting
process discussed in the previous unit.
 If pathogens have invaded the tissues the third line of
defense is the immune response.
Specific body defense
 Aka immune response aka third line of defense attacks
particular foreign substances.
 Recognizes foreign molecules (antigens) and acts to inactivate
or destroy them.
 3 important aspects of immunity:
 It recognizes and acts against particular pathogens and
foreign substances
 It is not restricted to the initial infection site
 The initial exposure to an antigen “primes” the body or
creates a “memory” to react more vigorously next time.
 There are two overlapping branches of immunity. Humoral
immunity is based on antibodies located in the “humors” or
fluids. Cellular immunity where living cells attack cells either
directly by lysing them or indirectly by releasing chemicals.
Structures involved in specific body
defenses
 Antigen: any substance capable
of exciting our immune system
and creating an immune
response. All types of
macromolecules can act as
antigens but proteins are the
strongest. Our cells have
antigens but as the immune
system develops it takes an
inventory of the “self-antigens”
so it can identify the nonself
antigens. However, a person’s
“self-antigens” would be foreign if
placed in another person’s body.
Structures involved in specific body
defenses
 T Lymphocytes: do not
produce antibodies. Involved
in cell mediated immunity.
Arise from lymphocytes that
migrate to the thymus and
mature in 2-3 days. Their
maturation is controlled by
the hormones of the thymus
like thymosin. These cells
divide rapidly but only the
ones best able to identify
foreign antigens and ignore
self antigens survive.
Structures involved in specific body
defenses
 B Lymphocytes: produce antibodies
and supervise humoral immunity.
These cells develop fully in the bone
marrow. Both type of WBCs become
immunocompetent (able to identify
and fight one particular antigen) as
they mature before they are released
to fight infection. This means that our
genes determine our immunity. After
fully developing both T and B cells
migrate to the spleen and lymph
nodes and circulate throughout the
body where they will meet the antigen
they are specific to. When they bind
with the foreign antigen their
differentiation is complete.
Structures involved in specific body
defenses
 Macrophages: arise from
monocytes in the bone marrow
and migrate to lymph organs
where they remain. These cells
engulf foreign particles and
present fragments of the
antigens on their own surface
as red flags for T cells. They
also secrete proteins called
monokines that are important
to the immune response. T
cells can release chemicals
which make macrophages
even more active to speed up
the immune process.
Humoral immune response:
 An immunocompetent B cell will not
reach full maturity until an antigen
binds to its surface receptors to
“sensitize or activate” it.
 The B cell then undergoes clonal
selection where is grows and multiplies
rapidly creating exact replicas of itself
or clones. This process is the primary
humoral response.
 These clones will mostly become
plasma cells that are antibody
producing factories producing 2000
antibodies per second. This activity will
last 4-5 days and then the plasma cells
begin to die. The antibody levels in the
blood peak about day 10 and then
slowly decline.
Humoral immune response:
 The clones that don’t become
plasma cells develop into longlived memory cells which will
respond to the antigen if it ever
enters the body again.
 This interaction would be
secondary response which is
much faster and more
prolonged and effective. Within
hours of the antigen entering
the body new plasma cells are
made and in 2-3 days antibody
levels in the blood peak and
remain high for weeks to
months.
Humoral immune response:
 Antibodies/immunoglobulins (Igs) are soluble blood proteins that
bind with a specific antigen. Their basic structure includes
 Heavy chain: longer amino acid chains that are identical to
each other
 Light chain: shorter amino acid chains that are identical to
each other
 Disulfide bonds: connect the four amino acid chains together
into a T or Y shape
 Variable region: region of amino acid chain that is different
between antibodies, variable region of the light and heavy
chain combine to form an antigen-binding site to “fit” the
antigen
 Constant region: form the stem of the antibody
 There are five basic classifications based on the antibodies
structure and function (MADGE).
Humoral immune response:
 Active humoral immunity:
when your B cells encounter
an antigen and create
antibodies against them.
Naturally acquired immunity
occurs when an active
pathogen enters the body
prompting the humoral
response. Artificial acquired
immunity occurs when a
vaccine containing dead or
attenuated pathogens is used
to prompt a response.
Regardless the response
from the body is the same.
Humoral immune response:
 Passive humoral immunity: when antibodies are removed from
a donor and placed into your body. This means your B cells
are not challenged by the antigen and will not create
immunological memory. The protection of these antibodies
ends as they are naturally degraded and removed. This occurs
naturally when antibodies are passed from mother to fetus
through the placenta. This can be artificially performed when a
person receives immune serum or gamma globulin after an
exposure. These include hepatitis, antivenum for snake bites,
botulism, rabies, and tetanus. These things would normally kill
a person before active immunity could be established so the
antibodies offer immediate protection for 2-3 weeks.
Cellular Immune Response:
 Macrophages must engulf
foreign antigens, digest them,
and present pieces of them
along with pieces of selfproteins in order for a T cell to
recognize the antigen and
bind with it.
 At this point the T cell
becomes fully mature and
activated to make clones.
 Cytotoxic (killer) T cells bind
with virus infected,
cancerous, or foreign graft
cells and injects a toxin called
perforin which causes the cell
to ruptures.
Cellular Immune Response:
 Helper T cells circulate throughout
the body recruiting other cells to
fight invaders such as interacting
with activated B cells and
encouraging them to divide faster
and signaling for antibody creation
to begin.
 Helper T cells also release
cytokine chemicals called
lymphokines that stimulate killer T
and B cells, attract other WBCs to
the area and stimulate
macrophages to become even
more phagocytic.
Cellular Immune Response:
 Suppressor T cells
suppress the activity
of T and B cells once
and antigen has been
destroyed to prevent
unnecessary immune
system activity.
Memory T cells remain
to provide immunity to
the antigens in the
future.