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CHAPTER 43
THE BODY’S DEFENSES
Nonspecific mechanisms and general
barriers
Skin-water proof and impenetrable if unbroken;
acidity of sweat and normal bacteria flora inhibit
pathogens
Lysozymes in perspiration, tears and saliva attacks
cell walls of many bacteria
Stomach acid kill most bacteria in food
Hair and
cilia in
respiratory
tracts
traps
bacteria
and
viruses
Neutrophils-most numerous, attracted by chemical signals,
become amoeboid, phagocytic, living only a few days
Monocytes-macrophages-larger, longer lived, wander
through interstitial fluid, found in connective tissue, lymph
nodes, and spleen, interact with T-cells
Eosinophils-enzymes against parasitic worms
Natural killer cells-lyse infected or abnormal cells,
similar to cytotoxic T’s but less discriminatory
Basophils (circulating)-and mast cells (in connective
tissue) degranulate releasing histamines that
cause vasodilation of local capillaries and makes
them leakier
Dendritic cells-are a type of blood cell that have the
ability to stimulate an immune response against
specific targets and are being widely pursued as a
new treatment for cancer and viral diseases.
Phagocytic, and interact with T & B cells
Cytotoxic T cells killing
a cancerous cell
Inflammatory Response
Injured tissue releases prostaglandins and histamines that
causes basophils and mast cells to release more
histamines causing:
– Vasodilation of capillaries and increased blood flow
– Capillaries to become leakier
– Increased metabolic rate and local temperature rises
– Neutrophils become amoeboid and leave capillaries and
begin to phagocytize
– Monocytes become macrophages and move into the
area and begin phagocytizing then become antigen
presenting cells and release interleukin 1 to attract T
cells
-- Dendritic cells phagocytize and present antigens to
T & B cells
Inflammatory Response
• Toxins and pyrogens cause fever
• Various chemicals released cause pluripotent stem cells to
divide more rapidly
• Natural killers in area check locals cell’s MHC I’s for
antigens
• Viral infected cells release interferon
• Complements stick to pathogens and lyse or induce
opsonization
• T lymphocytes and B lymphocytes are alerted and move
into the area
Phagocytosis by a
macrophage
Clonal Selection-the
antibodies of each
B cell only recognize
certain antibodies but
collectively they should
recognize any antigen
B lymphocyte
Cytotoxic T
perforating a
cell
Specific defense mechanisms
IMMUNE RESPONSE
1. Macrophages phagocytize pathogen; attach a piece to
their MHC-II’s and release interleukin I to attract
Helper T’s
2. Helper T's confirm antigen and divide forming memory
and active helper T’s
3. Active Helper T’s also secrete interleukin II that
causes:
a. macrophages to go and attack more pathogens
b. Cytotoxic T's check cells in the area for antigens on
their MHC-I's When they find one they divide
forming memory and active cells which:
1. release lymphokines to attract more macrophages
2. release perforins-kill infected cells
3. release interferon
Specific defense mechanisms
c. Meanwhile; the interleukin II also alerts B-cells to
check antigens on activated helper T’s antigen
receptors for fit with their preformed antibodies
1. B cell which fits checks with Helper T
2. Helper T secretes interleukins which causes B
cell to proliferate
3. B cell divides to form plasma cells and memory
cells
4. rearrangement of the antibody DNA for perfect
fit antibody
Specific defense mechanisms
4. Antibody Functions
a. Agglutination–stick to antigens, clump pathogens
together
b. Neutralization–interfere with life functions of
pathogens
c. Precipitation of soluble
d. Activation–join with complement to lyse pathogen
e. Opsonization–attract macrophages to phagocytize
pathogens
5. suppressor T's release interleukin 10; slow down the
immune system after the infection is killed off
Some people overreact to
specific allergens and
produce IgE antibodies that
stick to the membranes of
mast cells. Then when the
allergen attaches to the IgE it
causes the mast cell to
degranulate and release
histamines.
Arthritis
T cell infected with HIV
Close-up of T cell
infected with HIV
HIV budding
Neutrophil phagocytizing a bacteria
Mold that
is a
common
allergen
• Monoclonal
Antibodies
Myeloma
cells
Rh factor
• When an Rh+ fetus is carried by an Rh- mother, during
birth or the last few days before birth, some Rh+ blood
can go into the mother’s body and she will make
antibodies against it. That child will not have a
problem because it is born before the antibodies are
produced. However any subsequent Rh+ fetus will get
antibodies form the mother that will attack its blood
resulting in hemolytic anemia and death.
• To prevent this problem, Rh- mothers are given an
injection of Rhogan that contains small amounts of
Rh+ antibodies two or three times during their
pregnancies.
• Anaphylactic shock-a severe systemic allergic
reaction to an antigen; causes rapid drop in
blood pressure and often death
• Cyclosporine-the best antirejection drug; only
affects cytotoxic T cells
T cells contribute to the immune defenses in two major ways.
Regulatory T cells are vital to orchestrating the elaborate system.
(B cells, for instance, cannot make antibody against most
substances without T cell help). Cytotoxic T cells, on the other
hand, directly attack body cells that are infected or malignant.
Chief among the regulatory T cells are "helper/inducer" cells.
Typically identifiable by the T4 cell marker, helper T cells are
essential for activating B cells and other T cells as well as natural
killer cells and macrophages. Another subset of T cells acts to turn
off or "suppress" these cells.
Cytotoxic T cells, which usually carry the T8 marker, are
killer cells. In addition to ridding the body of cells that have
been infected by viruses or transformed by cancer, they are
responsible for the rejection of tissue and organ grafts.
(Although suppressor/ cytotoxic T cells are often called T8
cells, in reality the two are not always synonymous. The T8
molecule, like the T4 molecule, determines which MHC
molecule-class I or class II-the T cell will recognize, but not
how the T cell will behave.)
T cells work primarily by secreting substances known as
cytokines or, more specifically, lymphokines. Lymphokines
(which are also secreted by B cells) and their relatives, the
monokines produced by monocytes and macrophages, are
diverse and potent chemical messengers. Binding to specific
receptors on target cells, lymphokines call into play many
other cells and substances, including the elements of the
inflammatory response. They encourage cell growth,
promote cell activation, direct cellular traffic, destroy target
cells, and incite macrophages.
A single cytokine may have
many functions; conversely,
several different cytokines
may be able to produce the
same effect.
One of the first cytokines to be discovered was
interferon. Produced by T cells and macrophages (as
well as by cells outside the immune system), interferons
are a family of proteins with antiviral properties.
Interferon from immune cells, known as immune
interferon or gamma interferon, activates macrophages.
Two other cytokines, closely related to one another, are
lymphotoxin (from lymphocytes) and tumor necrosis
factor (from macrophages). Both kill tumor cells; tumor
necrosis factor (TNF) also inhibits parasites and viruses.
Many cytokines are initially given descriptive names but, as their
basic structure is identified, they are renamed as "interleukins"messengers between leukocytes, or white cells. Interleukin-1, or
IL-1, is a product of macrophages (and many other cells) that
helps to activate B cells and T cells. IL-2, originally known as T
cell growth factor, or TCGF, is produced by antigen-activated T
cells and promotes the rapid growth or differentiation of mature T
cells and B cells. IL-3 is a T-cell derived member of the family of
protein mediators known as colony-stimulating factors (CSF); one
of its many functions is to nurture the development of immature
precursor cells into a variety of mature blood cells. IL-4, IL-5, and
IL-6 help B cells grow and differentiate; IL-4 also affects T cells,
macrophages, mast cells, and granulocytes.