chapter 35 Flashcards
immunity
The human body has the ability to resist almost all types
of organisms or toxins that tend to damage the tissues
and organs. This capability is called immunity
acquired immunity
that does not develop
until after the body is first attacked by a bacterium,
virus, or toxin; often weeks or months are required
for the immunity to develop
This innate immunity makes the human body resistant
to
paralytic viral infections of
animals, hog cholera, cattle plague, and distemper—a viral disease that kills a large percentage of dogs that
become afflicted with it
humoral immunity or
B-cell immunity
the body develops
circulating antibodies, which are globulin molecules in
the blood plasma capable of attacking the invading agent.
This type of immunity is called humoral immunity or
B-cell immunity
cell-mediated immunity or T-cell immunity
The second type of acquired immunity is
achieved through formation of large numbers of activated
T lymphocytes that are specifically crafted in the lymph
nodes to destroy the foreign agent. This type of immunity
is called cell-mediated immunity or T-cell immunity
both type of lymphocytes are derived from
multipotent hematopoietic stem cells that form common lymphoid progenitor cells.
The Thymus Gland Preprocesses the T Lymphocytes.
The T lymphocytes, after origination in the bone marrow, first migrate to the thymus gland. Here they divide rapidly and at the same time develop extreme diversity for reacting against different specific antigens. That is, one thymic
lymphocyte develops specific reactivity against one antigen, and then the next lymphocyte develops specificity against another antigen. This process continues until there are thousands of different types of thymic lymphocytes with specific reactivities against many thousands of
different antigens
a clone
of lymphocytes.
All the different lymphocytes that are capable of
forming one specific antibody or T cell are called a clone
of lymphocytes
Role of Macrophages in the Activation
Most invading organisms are first phagocytized and partially digested by the macrophages, and the antigenic
products are liberated into the macrophage cytosol. The macrophages then pass these antigens by cell-to-cell
contact directly to the lymphocytes, thus leading to activation of the specified lymphocytic clones. The macrophages, in addition, secrete a special activating substance,
interleukin-1, that promotes still further growth and
reproduction of the specific lymphocytes.
Role of the T Cells in Activation of the B Lymphocytes
Some of the T cells that are
formed, called T-helper cells, secrete specific substances
(collectively called lymphokines) that activate the specific
B lymphocytes. Indeed, without the aid of these T-helper
cells, the quantity of antibodies formed by the B lymphocytes is usually slight.
Formation of Antibodies by Plasma Cells.
Before exposure to a specific antigen, the clones of B lymphocytes remain dormant in the lymphoid tissue. Upon entry
of a foreign antigen, macrophages in lymphoid tissue phagocytize the antigen and then present it to adjacent
B lymphocytes. In addition, the antigen is presented to T cells at the same time, and activated T-helper cells are formed. These helper cells also contribute to extreme activation of the B lymphocytes, as discussed later. The B lymphocytes specific for the antigen immediately enlarge and take on the appearance of lymphoblasts. Some of the lymphoblasts further differentiate to form
plasmablasts, which are precursors of plasma cells. In the plasmablasts, the cytoplasm expands and the rough endoplasmic reticulum vastly proliferates. The plasmablasts then begin to divide at a rate of about once every 10 hours
for about nine divisions, giving in 4 days a total population of about 500 cells for each original plasmablast. The mature plasma cell then produces gamma globulin antibodies at an extremely rapid rate—about 2000 molecules per second for each plasma cell
formation of memory cells
A few of the lymphoblasts formed by activation of a clone
of B lymphocytes do not go on to form plasma cells but
instead form moderate numbers of new B lymphocytes similar to those of the original clone. In other words, the B-cell population of the specifically activated clone becomes greatly enhanced, and the new B lymphocytes are added to the original lymphocytes of the same clone. They also circulate throughout the body to populate all the lymphoid tissue; immunologically, however, they remain dormant until activated once again by a new
quantity of the same antigen. These lymphocytes are called memory cells
what gives antigen its specificity
the structural organization of amino acids in the variable chain of antibody
5 classes of antibodies
IgM IgG IgE IgD IgE
MOST important immunoglobins of body
IgG which constitute 75% of antibodies in body are bivalent
IgE which constitute a small percentage but are involved in allergic reactions
IgM are made during primary response and have 10 binding sites so they play a major role
mechanism of action of antibody is done by two ways
direct attack
or by activation of complement system
direct attack is done by
- Agglutination, in which multiple large particles with antigens on their surfaces, such as bacteria or
red cells, are bound together into a clump - Precipitation, in which the molecular complex of soluble antigen (such as tetanus toxin) and antibody
becomes so large that it is rendered insoluble and precipitates - Neutralization, in which the antibodies cover the toxic sites of the antigenic agent
- Lysis, in which some potent antibodies are occasionally capable of directly attacking membranes of cellular agents and thereby cause rupture of
the agent
main function of compliment system
is to enhance the function of antibodies and phagocytic cells to destroy pathogens neutralize and remove damaged cells and promote inflammation
classical pathway
The classical pathway is initiated by
an antigen-antibody reaction. That is, when an antibody binds with an antigen, a specific reactive site on the “constant” portion of the antibody becomes uncovered, or “activated,” and this in turn binds directly with the C1 molecule of the complement system, setting into motion
a “cascade” of sequential reactions,
beginning with activation of the proenzyme C1. The C1 enzymes that are formed then activate successively increasing quantities of enzymes in the later stages of the
system so that from a small beginning, an extremely large “amplified” reaction occurs
t lymphocytes react to antigen only
when they are bound to specific proteins called as MHC proteins on the surface of antigen presenting cells
what are antigen presenting cells
macrophages, b lymphocytes and dendritic cells
what does MHC protein do
they bind with peptide fragments of antigen that have been degraded inside the antigen presenting cells and then transport them to the cell surface
There are two types of MHC proteins:
MHC I proteins, which present antigens to cytotoxic T cells, and
(2) MHC II proteins, which present antigens to T-helper cells.
t helper cells serves as a major regulator how
they release lymphokines which are protein mediators which act on other cells of immune system and bone marrow
HIV affects what cells
helper T cells
B-cell stimulating factor are
interleukin 4, 5, 6 which have a affect on b cell response
helper t cells affect on macrophages
First, they slow orstop the migration of the macrophages after they have been chemotactically attracted into the inflamed tissue area, thus causing great accumulation of macrophages. Second, they activate the macrophages to cause far more efficient phagocytosis, allowing them to attack and destroy
increasing numbers of invading bacteria or other tissue destroying agents.
what lymphokine has a direct positive feedback on stimulating activation t helper cells
interleukin 2
cytotoxic c cells
The receptor proteins on the surfaces of the cytotoxic cells cause them to bind tightly to the organisms or cells that contain the appropriate binding-specific
antigen. After binding, the cytotoxic T cell
secretes hole-forming proteins, called perforins, that literally punch round holes in the membrane of the attacked
cell. Then fluid flows rapidly into the cell from the interstitial space. In addition, the cytotoxic T cell releases cytotoxic substances directly into the attacked cell. Almost
immediately, the attacked cell becomes greatly swollen,
and it usually dissolves shortly thereafter.
autoimmune disease
(1) rheumatic fever, in which the body becomes immunized against tissues in the joints and heart, especially the heart valves, after exposure to a specific type of
streptococcal toxin that has an epitope in its molecular structure similar to the structure of some of the body’s
own self-antigens; (2) one type of glomerulonephritis, in which the person becomes immunized against the basement membranes of glomeruli; (3) myasthenia gravis, in which immunity develops against the acetylcholine receptor proteins of the neuromuscular junction, causing paralysis; and (4) systemic lupus erythematosus (SLE), in which the person becomes immunized against many different
body tissues at the same time, a disease that causes extensive damage and even death when SLE is severe.
first type of immunization
is done by injecting the body with a dead organism that is no longer capable of causing disease ( typhoid fever, whooping cough, diphtheria, and other bacterial diseases)
2nd type of immunization
injecting toxins that have been treated by chemicals so their toxicity is destroyed but still have the antigens on them for immunization
( tetanus, botulism, similar toxic disease)
3rd type of immunization
And, finally, a person can be immunized by being infected with live organisms that have been “attenuated.” That is, these organisms either have been grown in special culture media or have been passed through a series of animals until they have mutated enough that they will not cause disease but do still carry specific antigens required for immunization. This procedure is used to protect against smallpox, yellow fever, poliomyelitis, measles, and many other viral diseases.
passive immunity
transfusion of antibody or t cells from another human or animal for immunity is called as passive immunity
delayed reaction allergy is caused by
T cells
Anaphylaxis.
When a specific allergen is injected
directly into the circulation, the allergen can react with
basophils of the blood and mast cells in the tissues located
immediately outside the small blood vessels if the basophils and mast cells have been sensitized by attachment
of IgE reagins. Therefore, a widespread allergic reaction
occurs throughout the vascular system and closely associated tissues. This reaction is called anaphylaxis. Histamine
is released into the circulation and causes body-wide
vasodilation, as well as increased permeability of the
capillaries with resultant marked loss of plasma from the
circulation. Occasionally, a person who experiences this
reaction dies of circulatory shock within a few minutes
unless treated with epinephrine to oppose the effects of
the histamine.
Also released from the activated basophils and mast
cells is a mixture of leukotrienes called slow-reacting
substance of anaphylaxis. These leukotrienes can cause
spasm of the smooth muscle of the bronchioles, eliciting
an asthma-like attack, sometimes causing death by
suffocation.
Urticaria.
Urticaria results from antigen entering specific skin areas and causing localized anaphylactoid reactions. Histamine released locally causes (1) vasodilation
that induces an immediate red flare and (2) increased
local permeability of the capillaries that leads to local
circumscribed areas of swelling of the skin within another
few minutes. The swellings are commonly called hives.
Administration of antihistamine drugs to a person before
exposure will prevent the hives.
Hay Fever
In hay fever, the allergen-reagin reaction
occurs in the nose. Histamine released in response to the
reaction causes local intranasal vascular dilation, with
resultant increased capillary pressure and increased capillary permeability. Both these effects cause rapid fluid
leakage into the nasal cavities and into associated deeper
tissues of the nose, and the nasal linings become swollen
and secretory. Here again, use of antihistamine drugs can
prevent this swelling reaction. However, other products
of the allergen-reagin reaction can still cause irritation of
the nose, eliciting the typical sneezing syndrome.
