Body Defense Flashcards
Two types of mechanisms defend the body against these tiny but mighty enemies:
innate and adaptive defense mechanisms
is a functional system rather than an organ system in an anatomical sense.
the immune system
The most important of the
immune cells are
lymphocytes, dendritic cells,
and macrophages.
play an important role in both innate and adaptive mechanisms.
Macrophages
also called the nonspecific defense system, responds immediately to protect the body from all foreign substances, whatever they are
innate defense system
Innate (nonspecific) defense mechanisms- First line of defense
- Skin
- Mucous membranes
- Secretions of skin
and mucous
membranes
Innate (nonspecific) defense mechanisms- Second line of defense
- Phagocytic cells
- Natural killer cells
- Antimicrobial proteins
- The inflammatory
response - Fever
Adaptive (specific) defense
mechanisms- Third line of defense
- Lymphocytes
- Antibodies
- Macrophages and other
antigen-presenting cells
reduce the workload of the adaptive defense mechanisms by generally preventing the entry and spread of microorganisms throughout the body.
innate mechanisms
or specific defense system, fights invaders that get past the innate defenses by mounting an attack against one or more particular foreign substances.
adaptive defense system
The resulting highly specific resistance to disease is called
immunity
Another important feature of the adaptive response is that it
“remembers” which invaders it has fought
refers to the mechanical barriers that cover body surfaces and to the cells and chemicals that act on the initial battlefronts to protect the body from invading pathogens (harmful microorganisms)
innate, or nonspecific, body defense
The body’s first line of defense against the invasion of disease-causing microorganisms includes the
skin and mucous membranes
Forms mechanical barrier that prevents entry of pathogens and other harmful substances into body.
Intact skin (epidermis)
Skin secretions make epidermal surface acidic, which inhibits
bacterial growth; sebum also contains bacteria-killing chemicals.
Acid mantle
Provides resistance against acids, alkalis, and bacterial enzymes.
Keratin
Form mechanical barrier that prevents entry of pathogens
Intact mucous membranes
Traps microorganisms in respiratory and digestive tracts.
Mucus
Filter and trap microorganisms and other airborne particles in nasal
passages.
Nasal hairs
Propel debris-laden mucus away from lower respiratory passages.
Cilia
Contains concentrated hydrochloric acid and protein-digesting
enzymes that destroy pathogens in stomach.
Gastric juice
Inhibits growth of bacteria and fungi in female reproductive tract.
Acid mantle of vagina
Continuously lubricate and cleanse eyes (tears) and oral cavity
(saliva); contain lysozyme, an enzyme that destroys microorganisms.
Lacrimal secretion (tears); saliva
Engulf and destroy pathogens that breach surface membrane
barriers; macrophages also contribute to immune response.
Phagocytes
Promote cell lysis by direct cell attack against virus-infected or
cancerous body cells; do not depend on specific antigen recognition.
Natural killer cells
Prevents spread of injurious agents to adjacent tissues, disposes of
pathogens and dead tissue cells, and promotes tissue repair; releases
chemical mediators that attract phagocytes (and immune cells) to
the area.
Inflammatory response
Group of plasma proteins that lyses microorganisms, enhances
phagocytosis by opsonization, and intensifies inflammatory response.
Complement
Proteins released by virus-infected cells that protect uninfected tissue
cells from viral takeover; mobilize immune system.
Interferons
Normally acid pH inhibits bacterial growth; urine cleanses the lower
urinary tract as it flushes from the body.
Fluids with acid pH
Systemic response triggered by pyrogens; high body temperature
inhibits multiplication of bacteria and enhances body repair
processes.
fever
The acidic pH of skin secretions
acid mantle
pH level of urine
4.5 to 6
traps many microorganisms that enter digestive and respiratory passageways.
Sticky mucus
secretes gastric juice containing hydrochloric acid and protein-digesting enzymes that both kill pathogens.
stomach mucosa
stomach mucosa secretes containing hydrochloric acid and protein-digesting enzymes that both kill pathogens.
gastric juice
Saliva and lacrimal secretions (tears) contain an enzyme that destroys bacteria.
lysozyme
preventing particles from entering the lungs, where the warm, moist environment provides ideal conditions for bacterial growth. (think “sticky trap”)
The cilia sweep dust- and bacteria-laden mucus
For its second line of defense, defenses rely on the destructive powers of cells called
phagocytes and natural killer cells
roam the body in blood and lymph. They are a unique group of aggressive lymphocytes.
Natural killer (NK) cells
cells can act spontaneously against any such target by recognizing certain sugars on the “intruder’s” surface as well as its lack of certain “self” cell surface molecules
Natural killer (NK) cells
not phagocytic. They attack the target cell’s membrane and release lytic chemicals
called perforin and granzymes. also release powerful inflammatory chemicals.
NK cells
NK cells attack the target cell’s membrane and release lytic chemicals called
perforin and granzymes
is a nonspecific response that is triggered whenever body tissues are injured
inflammatory response
The four most common indicators, or cardinal signs, of acute inflammation are
- redness
- heat (inflamm = set on fire)
- pain
- swelling (edema)
The inflammatory process begins with a
chemical “alarm”
When cells are damaged, they release inflammatory chemicals, including
histamine and kinins
3 phenomenon when cells are damaged
(1) cause blood vessels in the area to dilate
(2) make capillaries leaky
(3) attract phagocytes and
white blood cells to the area.
the 3rd phenomenon when cells are damaged called
positive chemotaxis
the cells are moving toward a high concentration of signaling molecules
positive chemotaxis (third phenomenon)
Increased permeability of the capillaries allows fluid to leak from the blood into the tissue spaces, causing
local edema (swelling)
Some authorities consider limitation of joint movement to be the
fifth cardinal sign of inflammation.
prevents the spread of damaging agents to nearby tissues, disposes of cell debris and pathogens, and sets the stage for repair
inflammatory response
inflammatory process
- Neutrophils enter blood from bone marrow, following the “scent.”
and roll along the vessel wall - Diapedesis- flatten out and squeeze
through the capillary walls, chemical signal is the strongest - Positive chemotaxis, the gradient of inflammatory chemicals. the neutrophils gather at the site of tissue injury
At the point where the chemical signal is the strongest, they flatten out and squeeze through the capillary walls, a process
Diapedesis
responding to a gradient of diffusing inflammatory chemicals
Neutrophils
follow neutrophils into the inflamed area, fairly poor phagocytes and after entering the tissues they become macrophages with insatiable appetites
monocytes
continue to wage the battle, replacing the short-lived neutrophils at the site of damage.
macrophages
are the central actors in the final disposal of cell debris as the inflammation subsides.
macrophages
leaked into the area from the blood, are activated and begin to wall off the damaged area with fibrin to prevent the spread of harmful agents to neighboring tissues
Clotting proteins
also forms scaffolding for permanent repair
fibrin mesh
is a mixture of dead or dying neutrophils, broken-down tissue cells, and living and dead pathogens.
Pus
If the inflammatory mechanism fails to fully clear the area of debris, the sac of pus may become walled off, forming an
abscess
Pathogens that make it through the mechanical barriers are confronted by
phagocytes
A phagocyte, engulfs a foreign particle by the process of phagocytosis, such as a
macrophage or neutrophil
enhance the innate defenses either by attacking microorganisms directly or by hindering their ability to reproduce
antimicrobial proteins
it refers to a group of at least 20 plasma proteins that circulate in the blood in an inactive state, inactive clotting proteins
complement
occurs when complement proteins bind to certain sugars or proteins (such as antibodies) on the foreign cell’s surface
complement fixation
result of complement fixation:
- the formation of membrane attack complexes (MAC) that produce holes, or pores, in the foreign cell’s surface.
- These pores allow water to rush into the cell
- causing it to burst, or lyse.
produce holes, or pores, in the foreign cell’s surface.
membrane attack complexes (MAC)
Some of the molecules released during the activation process are
vasodilators, and some are chemotaxis chemicals
attract neutrophils and macrophages into
the region
chemotaxis chemicals
this effect cause the cell membranes of the foreign cells to become sticky so they are easier to phagocytize
opsonization
is a nonspecific defensive mechanism that “complements,” or enhances, the effectiveness of both innate and adaptive defenses
Complement
Complement proteins must be activated in a particular sequence, which insures that complement is not accidentally activated, is called
cascade
acellular particles—essentially nucleic acids surrounded by a protein coat—that lack the cellular machinery required to generate ATP or make proteins.
viruses
does “dirty work” in the body by taking over target cells
viruses
viruses uses to reproduce themselves
cellular machinery and nutrients
virus-infected cells defend cells that have not yet been infected by secreting small proteins called
interferons
diffuse to nearby cells and bind to their
membrane receptors
interferon molecules
abnormally high body temperature, is a systemic response to invading microorganisms.
Fever
Body temperature is regulated by the body’s “thermostat.”
hypothalamus
a group of chemically diverse substances that cause fever and shock in severe cases
pyrogens
stalks and eliminates with nearly equal precision almost any type of pathogen that intrudes into the body.
specific defense system
response to a threat involves tremendously increased internal nonspecific defenses
immune response
the adaptive, or specific, defense mechanism is a functional system that recognizes foreign molecules called antigens and acts to inactivate or destroy them.
antigens
animals surviving a serious bacterial infection have “factors” in their blood that protect them from future attacks by the same pathogen
antibodies
These landmark experiments revealed three important aspects of adaptive defense:
- It is antigen specific
- It is systemic
- It has “memory”
important aspects of adaptive defense, immunity is not restricted to the initial infection site.
It is systemic
important aspects of adaptive defense, it recognizes and actsagainst particular pathogens or foreign substances.
It is antigen specific
important aspects of adaptive defense, it recognizes and mounts even stronger attacks on previously encountered pathogens.
It has “memory”
also called antibody-mediated immunity, is provided by antibodies (immune proteins) present in the body’s “humors,” or fluids
Humoral immunity
When lymphocytes themselves defend the body, the immunity is called
cellular immunity or cell-mediated immunity
act against such targets either directly, by lysing the foreign cells, or indirectly, by releasing chemicals that enhance the inflammatory response or activate other immune cells
lymphocytes
is any substance capable of provoking an immune response
antigen
are large, complex molecules that are not normally present in our bodies, non-self.
Foreign antigen
As a rule, small molecules are not antigenic, but when they link up with our own proteins,
hapten or incomplete antigen
The crucial cells of the adaptive system are
lymphocytes and antigen-presenting cells (APCs)
Lymphocytes exist in twoother major “flavors.”
B lymphocytes or B cells and T lymphocytes or T cells
produce antibodies and oversee humoral
immunity
B lymphocytes or B cells
constitute the cell-mediated arm of the adaptive defenses and do not make antibodies
T lymphocytes, or T cells
can recognize and eliminate specific virus-infected or tumor cells
T lymphocytes, or T cells
can target specific extracellular antigens
B lymphocytes, or B cells
do not respond to specific antigens but instead play an essential role in activating the lymphocytes that do
APCs
immature lymphocytes, released from the marrow are essentially identical
naive
migrate (in blood) to the thymus and develop immunocompetence there
T cells
develop immunocompetence in red bone marrow
B cells
sites of development of immunocompetence as B or T cells
Primary lymphoid organs
site of lymphocyte origin
Red bone marrow
sites of antigen encounter, and activation to become effector and memory B or T cells
Secondary lymphoid organs
arise from lymphocytes that migrate to the thymus
t cells
development of self-tolerance for the body’s own cells is an essential part of a
lymphocyte’s “education.”
B cells develop immunocompetence in
bone marrow
capable of responding to a specific antigen by binding to it with antigen specific receptors that appear on the lymphocyte’s surface
immunocompetent
There they undergo a maturation process lasting 2 to 3 days, directed by thymic hormones
T cell in Thymus
acting against body
cells
self-antigens
Thus, it is our genes, not antigens, that determine what foreign substances our immune system will be able to recognize and resist
TRUE
in immunity is to engulf antigens and then present fragments of them, like signal flags, on their own surfaces, where they can be recognized by T cells
antigen-presenting cells
(APCs)
present antigens to the cells that will actually deal with the antigens
antigen-presenting cells
(APCs)
The major types of cells acting as APCs are
dendritic cells, macrophages, and B lymphocytes.
also called Langerhans cells, are present in connective tissues and in the epidermis
Dendritic cells
are widely distributed throughout the lymphoid organs and connective tissues, where they act as phagocytes in the innate defense system
Macrophages
true “killers” that are insatiable phagocytes and secrete bactericidal (bacteria killing) chemicals
activated macrophages
are the most effective antigen presenters
known—it’s their only job. Key link between innate and adaptive immunity.
dendritic cells
In this process, the lymphocyte begins to grow and then multiplies rapidly to form an army of cells exactly like itself and bearing the same antigen-specific receptors
clonal selection
The resulting family of identical cells descended from the same ancestor cell are called
clones
to that antigen, clone formation is the
primary humoral response
Most of the B cell clone members, or descendants, become
plasma cells
B cell clone members that do not become
plasma cells become long-lived
memory cells
Memory cells are responsible for the
immunological memory
are produced much faster, are more prolonged, and are more effective than the events of the primary response because all the preparations for this attack have already been made
secondary humoral responses
the ability of the immune system to respond more rapidly and effectively to pathogens that have been encountered
immunological memory
When your B cells encounter antigens and produce antibodies against them, you are exhibiting
active immunity
which may intensify the immune
response at later meetings with the same antigen,
are also available
booster shots
a phenomenon in which
a population of people are generally protected
because most of a given population is immune to a
disease or infection
herd immunity
the antibodies are obtained from the serum of an immune human or animal donor
Passive immunity
is conferred naturally on a fetus when the mother’s antibodies cross the placenta and enter the fetal circulation, and after birth during breastfeeding
Passive immunity
artificially conferred when a person receives immune serum or gamma globulin (donated antibodies)
Passive immunity
is commonly administered after exposure to hepatitis.
Gamma globulin
used for such purposes are descendants of a single cell and are pure antibody preparations that exhibit specificity for one, and only one, antigen
Monoclonal antibodies
used for early cancer diagnosis and to track cancers hidden deep within the body
Monoclonal antibodies
Humoral Immunity- Infection; contact with pathogen
Active- Naturally acquired
Humoral Immunity- Vaccine; dead or attenuated pathogens
Active- Artificially acquired
Humoral Immunity- Antibodies passed from mother to fetus via placenta; or to infant in her milk
Passive- Naturally acquired
Humoral Immunity- Injection of donated antibodies (gamma globulin)
Active- Artificially acquired
also referred to as immunoglobulins (Igs), constitute the gamma globulin part of blood proteins
Antibodies
are soluble proteins secreted by activated B cells or by their plasma-cell offspring in response to an antigen, they are capable of binding specifically with that antigen.
Antibodies
When the four chains are combined, the antibody molecule formed has two identical halves, each consisting of a heavy and a light chain, and the molecule as a whole is commonly described as being
Y-shaped
Each of the four chains forming an antibody had a
variable (V) region and constant
(C) region
uniquely shaped to “fit” a specific antigen
antigen-binding site
Y-shaped structured, monomers
IgD, IgG, IgE
IgM antibodies are called
pentamers
IgA antibodies occur in both
monomer and dimers
is the most abundant antibody
in blood plasma and is the only type that can cross the placental barrier
IgG
only can fix complement
IgM and IgG
dimers, is found mainly in secretions
that bathe body surfaces, such as mucus and tears.
IgA
antibodies are the
“troublemaker” antibodies involved in allergies.
IgE
Attached to B cell; free in
plasma, When bound to B cell membrane,
serves as antigen receptor; first
Ig class released by plasma
cells during primary response;
potent agglutinating agent; fixes
complement.
IgM
Almost always attached to
B cell, Believed to be cell surface receptor
of immunocompetent B cell;
important in activation of B cell.
IgD
Most abundant antibody in
plasma; represents 75–85%
of circulating antibodies,
Main antibody of both primary
and secondary responses;
crosses placenta and provides
passive immunity to fetus; fixes
complement.
IgG
Secreted by plasma
cells in skin, mucosae
of gastrointestinal and
respiratory tracts, and tonsils,
Binds to mast cells and basophils
and triggers release of histamine
and other chemical mediators of
inflammation and some allergic
responses.
IgE
Antibodies inactivate antigens in a number of ways
by complement fixation, neutralization, agglutination, opsonization,
and precipitation
chief antibody ammunition used against cellular antigens, such as bacteria or mismatched red blood cells
Complement
occurs when antibodies bind to specific sites (usually at or close to the site where a cell would bind) on bacterial exotoxins (toxic chemicals secreted by bacteria) or on viruses that can cause cell injury
Neutralization
can be cross-linked into large lattices
antigen-antibody complexes
When the cross-linking involves cell-bound antigens, the process causes clumping of the foreign cells, a process called
agglutination
This type of antigen-antibody reaction occurs when mismatched blood is transfused
agglutination
When the cross-linking process involves soluble antigenic molecules, the resulting antigen antibody complexes are so large that they become insoluble and settle out of solution.
precipitation
antigen molecules are much more
easily captured and engulfed by the body’s phagocytes than are freely moving antigens.
agglutinated bacteria and immobilized
(precipitated)
cells secrete their anti body “weapons,”
B cells
cells fight their anti gens directly
T cells
are activated to form a clone by binding
with a “recognized” antigen
T cells
are not able to bind with free antigens. Instead, the antigens must be “presented” by a macrophage.
T cells
Two types that are involved in the
activation process are called
helper T cells and cytotoxic T cells
T cell must recognize the antigen fragment presented by the APC
“nonself,”
T cell must recognize this by coupling with a specific glycoprotein on the APC’s surface at the same time
“self,”
is now known to be essential for the activation and clonal selection of T cells
antigen presentation
chemicals released by macrophages and dendritic cells also play important roles in the immune response
Cytokine
specialize in killing virus-infected, cancer, or foreign graft cells directly
Cytotoxic T cells
enters the foreign cell’s plasma membrane, delivering the so-called lethal hit
perforin
pores appear in the target cell’s membrane, allowing to enter and kill the foreign cell
granzymes
are the T cells that act as the “directors” or “managers” of the adaptive immune response
Helper T cells
A proposed mechanism by which cytotoxic T cells kill target cells.
- Cytotoxic T cell binds tightly to the foreign target cell.
- Cytotoxic T cell releases perforin and granzyme molecules from its granules by exocytosis
- Perforin molecules insert into the target cell membrane and form pores similar to those produced by complement activation.
- Granzymes enter the target cell via the pores and degrade cellular contents.
- The cytotoxic T cell detaches and searches for another prey.
The helper T cells also release a
variety of cytokines that act indirectly to rid the body of antigens by
- stimulating cytotoxic T cells and B cells to grow and divide
- attracting other types of protective white blood cells, such as neutrophils, into the area; and
- enhancing the ability of macrophages to engulf and destroy microorganisms
(formerly called suppressor T cells), release chemicals that suppress the activity of both T and B cells
regulatory T cells
are vital for winding down and stopping the immune response after an antigen has been successfully inactivated or destroyed.
regulatory T cells
are tissue grafts transplanted from
one site to another in the same person.
Autografts
are tissue grafts donated by a genetically identical person, the only example being
an identical twin.
Isografts
are tissue grafts taken from a person other than an identical twin.
Allografts
are tissue grafts harvested from a different animal species, such as a porcine (pig) heart valve transplanted into a human.
Xenografts
Treatment that lowers the activity of the body’s immune system. This reduces its ability to fight infections and other diseases, such as cancer
immunosuppressive therapy
is the most frequent cause of death in these patients
Explosive infection
are abnormally vigorous immune responses in which the immune system causes tissue damage as it fights off a perceived “threat” that would otherwise be harmless to the body
Allergies, or hypersensitivities
Sensitization stage
- Antigen (allergen) invades body.
- Plasma cells produce large amounts of class IgE antibodies against allergen.
- IgE antibodies attach to mast cells in body tissues (and to circulating basophils).
secondary response
- More of same allergen invades body.
- Allergen binding to IgE on mast cells triggers release of histamine (and other chemicals).
- Histamine causes blood vessels to dilate and become leaky, which promotes edema; stimulates release of large amounts of mucus; and causes smooth
muscles to contract.
starts with the release of a flood of histamine when IgE antibodies bind to mast cells.
secondary response
causes small blood vessels in the area
to become dilated and leaky and is largely to blame for the best-recognized symptoms of allergy
Histamine
Over-the-counter (OTC) anti-allergy drugs contain
antihistamines
most common type of allergy
immediate hypersensitivity, or acute hypersensitivity
is fairly rare, the bodywide, or systemic, acute allergic response known as
anaphylactic shock
occurs when the allergen directly enters the blood and circulates rapidly through the body, as might happen with certain bee stings, spider bites, or an injection of a foreign substance (such as horse serum, penicillin, or other drugs that act as hap tens) into susceptible individuals
anaphylactic shock
Food allergies (peanut or wheat allergies) may also trigger
anaphylaxis
found in emergency EpiPen® shots,
is the drug of choice to reverse these histamine mediated effects.
Epinephrine
mediated mainly by a special subgroup of helper T cells, cytotoxic T cells, and macrophages, take much longer to appear (1 to 3 days) than any of the acute reactions produced by antibodies.
Delayed hypersensitivities
The most familiar examples of delayed hypersensitivity reactions are those classed as
allergic contact dermatitis,
happens when the body’s natural defense system can’t tell the difference between your own cells and foreign cells, causing the body to mistakenly attack normal cells.
autoimmune disease
which systematically destroys joints
Rheumatoid arthritis (RA)
which impairs communication between nerves and skeletal muscles
Myasthenia gravis
which destroys the white matter (myelin sheaths) of the brain and spinal cord
Multiple sclerosis (MS)
in which the thyroid gland produces excessive amounts of thyroxine in response to autoantibodies thatmimic TSH
Graves’ disease
which destroys pancreatic beta cells, resulting in deficient production of insulin
Type 1 diabetes mellitus
a systemic disease that occurs mainly in young women and particularly affects the kidneys, heart, lungs, and skin
Systemic lupus erythematosus (SLE)
a severe impairment of kidney function due to acute inflammation
Glomerulonephritis
may appear as a result of gene mutations that change the structure of self-proteins or as a result of alterations in self-proteins by hapten attachment or by bacterial or viral damage.
“new” self-antigens
causing damage to both the heart muscle and its valves, as well as to the joints and kidneys
rheumatic fever
The most devastating congenital condition in which there is a marked deficit
of both B and T cells.
severe combined immunodeficiency
disease (SCID)
include both congenital and acquired conditions in which the production or function of immune cells or complement is
abnormal.
immunodeficiencies
the most important and most devastating of the acquired immunodeficiencies, cripples the immune system by interferingwith the activity of helper T cells
acquired immune deficiency syndrome (AIDS).
fungal brain infection
cryptococcal meningitis
an eye infection
cytomegalovirus retinitis
