14 Flashcards
(193 cards)
1
Q
pathogen
A
Any parasite
that causes disease is called a pathogen
2
Q
axenic
A
sites that are free of any microbes
3
Q
Your normal microbiota began to develop when
A
your surrounding
amniotic membrane ruptured and microorganisms
came in contact with you during birth.
4
Q
reservoirs
A
Sites where pathogens
are maintained as a source of infection are called reservoirs of
infection.
5
Q
zoonoses
A
Diseases that spread
naturally from their usual animal hosts to humans
6
Q
zoonoses most likely type to be transmitted
back to animal hosts.
A
Zoonotic diseases transmitted via the bites of bloodsucking
arthropods
7
Q
contamination
A
the mere presence of microbes
in or on the body.
8
Q
infection
A
some microbial contminannts overcome
the body’s external defenses, multiply, and become established
in the body; such a successful invasion of the body by a
pathogen is called an infection.
9
Q
portals of entry
A
skin, mucous membrane, placenta | parenteral route
10
Q
most frequently used portal of
entry.
A
respiratory tract
11
Q
adhesion
A
After entering the body, symbionts must adhere to cells if they
are to be successful in establishing colonies. The process by which
microorganisms attach themselves to cells
12
Q
adhesion factors
A
To accomplish adhesion, pathogens
use adhesion factors, which are either specialized structures or attachment proteins
13
Q
ligands
A
viruses and many bacteria
have surface lipoprotein and glycoprotein molecules called ligands
that enable them to bind to complementary receptors on host cells
(Figure 14.5). Ligands are also called adhesins on bacteria and attachment
proteins on viruses.
14
Q
ligand receptor molecules
A
Receptor molecules
on host cells are typically glycoproteins containing sugar molecules
such as mannose and galactose.
15
Q
avirulent
A
Bacterial cells and viruses that
have lost the ability to make ligands—whether as the result of
some genetic change (mutation) or exposure to certain physical
or chemical agents (as occurs in the production of some
vaccines)—become harmless, or avirulent
16
Q
biofilm
A
Some bacterial pathogens do not attach to host cells directly
but instead interact with each other to form a sticky web of bacteria
and polysaccharides called a biofilm, which adheres to a
surface within a host.
17
Q
symptoms
A
subjective characteristics of a disease that can be felt by
the patient alone
18
Q
signs
A
objective manifestations
of disease that can be observed or measured by others
19
Q
syndrome
A
a group of symptoms and signs that collectively
characterizes a particular disease or abnormal condition
20
Q
subclinical
A
asymptomatic infections
21
Q
congenital
A
diseases that are present at birth
22
Q
etiology
A
study of the cause of a disease
23
Q
Using his postulates, Koch proved that
A
Bacillus
anthracis causes anthrax and
TB
24
Q
germ theory of disease
A
Louis Pasteur,
Robert Koch, and other microbiologists proposed the germ
theory of disease, which states that disease is caused by infections
of pathogenic microorganisms
25
kochs postulates
1 The suspected agent (bacterium, virus, etc.) must be present
in every case of the disease.
2 That agent must be isolated and grown in pure culture.
3 The cultured agent must cause the disease when it is inoculated
into a healthy, susceptible experimental host.
4 The same agent mus
26
pathogenicity
The ability of a microorganism
| to cause disease is termed pathogenicity
27
virulence
degree of pathogenicity. In other
words, virulence is the relative ability of a pathogen to infect a
host and cause disease. NOT severity of disease
28
xtracellular enzymes
Many pathogens secrete enzymes that enable them to dissolve
structural chemicals in the body and thereby maintain
an infection, invade further, and avoid body defenses.
29
toxins
Toxins are chemicals that either harm tissues or trigger host
immune responses that cause damage.
30
toxemia
toxins enter the bloodstream and are carried to other parts of
the body, including sites that may be far removed from the
site of infection.
31
exotoxins
Many microorganisms secrete exotoxins that are
central to their pathogenicity in that they destroy host cells or
interfere with host metabolism. Exotoxins are of three principal
types: cyto, neuro, enterotoxins
32
antitoxins
protective
molecules called antibodies that bind to specific toxins and
neutralize them.
33
endotoxin
Gram-negative bacteria have an outer (wall) membrane
composed of lipopolysaccharide, phospholipids, and
proteins (see Figure 3.14). Endotoxin, also called lipid A, is
the lipid portion of the membrane’s lipopolysaccharide.
34
Endotoxin can be released when
Gram-negative bacteria
divide, die naturally, or are digested by phagocytic cells
such as macrophages
35
endotoxin stimulates
Many types of lipid
A stimulate the body to release chemicals that cause fever, inflammation,
diarrhea, hemorrhaging, shock, and blood coagulation.
36
capsules
The capsules of many pathogenic bacteria (see
Figure 3.5a) are effective virulence factors because many capsules
are composed of chemicals normally found in the body
(including polysaccharides); as a result, they do not stimulate
a host’s immune response.
- Additionally, capsules are often slippery, making it difficult for
phagocytes to surround and phagocytize them—their pseudopods
cannot grip the capsule
37
antiphagocytic chemicals
Some bacteria, including the cause
of gonorrhea, produce chemicals that prevent the fusion of lysosomes
with phagocytic vesicles, allowing the bacteria to survive
inside phagocytes
38
disease process
IPIDC
incubation period, a prodromal
period, illness, decline, and convalescence
39
incubation period
The incubation period is the time between infection and occurrence
of the first symptoms or signs of disease.
40
prodromal period
```
a short time of generalized,
mild symptoms (such as malaise and muscle aches) that precedes
illness. Not all infectious diseases have a prodromal stage.
```
41
illness
Illness is the most severe stage of an infectious disease. Signs
and symptoms are most evident during this time. Typically the
patient’s immune system has not yet fully responded to the pathogens, and their presence is harming the body. This stage is
usually when a physician first sees the patient.
42
decline
During the period of decline, the body gradually returns to
normal as the patient’s immune response and/or medical treatment
vanquish the pathogens. Fever and other signs and symptoms
subside. Normally the immune response and its products
(such as antibodies in the blood) peak during this stage. I
43
convalescence
```
During convalescence (kon@vaI@les´ens), the patient recovers
from the illness; tissues are repaired and returned to normal.
```
44
contact trans
Contact transmission is the spread of pathogens from one host to
another by direct contact, indirect contact, or respiratory droplets.
45
direct contact trans
Direct contact transmission, including person-to-person
spread, typically involves body contact between hosts. Touching,
kissing, and sexual intercourse, across placenta
46
indirect contact trans
when pathogens are
spread from one host to another by fomites (fom´i@tez; singular:
fomes, fo´mez), which are inanimate objects that are inadvertently
used to transfer pathogens to new hosts.
- needles, toothbrushes, paper tissues, toys, money, diapers,
drinking glasses,
47
droplet trans
Droplet transmission is a third type of contact transmission.
Pathogens can be transmitted within droplet nuclei (droplets
of mucus) that exit the body during exhaling, coughing,
and sneezing
48
vehicle trans
the spread of pathogens via air, drinking
water, and food, as well as bodily fluids being handled outside
the body.
49
airborne trans
Airborne transmission involves the spread of pathogens
farther than 1 meter to the respiratory mucous membranes of
a new host via an aerosol (ar´o@sol)—a cloud of small droplets
and solid particles suspended in the air. Aerosols may contain
pathogens either on dust or inside droplets.
50
waterborne trans
important in the spread of
| many gastrointestinal diseases
51
fecal oral infection
some waterborne pathogens r shed in feces, enter through the gastrointestinal mucous membrane or skin, and
subsequently can cause disease elsewhere in the body.
52
vectors
Vectors are animals that transmit diseases from one host to another.
Vectors can be either biological or mechanical.
53
biological vectors
Biological vectors not only transmit pathogens but also
serve as hosts for the multiplication of a pathogen during
some stage of the pathogen’s life cycle.
54
mechanical vectors
Mechanical vectors are not required as hosts by the pathogens
they transmit; such vectors only passively carry pathogens
to new hosts on their feet or other body parts.
55
latent diseases
Latent diseases are those in
which a pathogen remains inactive for a long period of time before
becoming active.
56
communicable disease
When an infectious disease comes from another infected
| host, either directly or indirectly,
57
contagious disease
If a communicable disease is easily transmitted
| between hosts
58
epidemiology
the study of where and when diseases
| occur and how they are transmitted within populations.
59
incidence
Incidence is the
| number of new cases of a disease in a given area or population during a given period of time
60
prevalence
prevalence is the total number of
cases, both new and already existing, in a given area or population
during a given period of time. In other words, prevalence is
a cumulative number.
61
endemic
A disease that normally occurs continually (at
moderately regular intervals) at a relatively stable incidence
within a given population or geographical area is said to be
endemic11 to that population or region.
62
epidemic
Whenever a disease occurs at a greater
frequency than is usual for an area or population, the disease
is said to be epidemic within that area or population.
63
pandemic
If an epidemic occurs simultaneously on more than one
| continent, it is referred to as a pandemic
64
descriptive epidemiology
- earliest: snow's cholera study
- involves the careful tabulation of
data concerning a disease. Relevant information includes the
location and time of cases of the disease as well as information
about the patients, such as ages, gender, occupations, health
histories, and socioeconomic groups.
65
index case
1st case of disease in a given area/population
66
analytical epidemiolgoy
Analytical epidemiology investigates a disease in detail, including
analysis of data acquired in descriptive epidemiological
studies, to determine the probable cause, mode of transmission, and possible means of prevention of the disease.
67
experimental epidemiolgoy
Experimental epidemiology involves testing a hypothesis concerning
the cause of a disease.
68
nosocomial
acquired in healthcare settings
69
exogenous nosocomial infections
caused by pathogens acquired from
| the health care environment.
70
endogenous nosocomial infections
opportunists cause endogenous nosocomial infections
(en@doj´eI@nuI s); that is, they arise from normal microbiota within
the patient that become pathogenic because of factors within the
health care setting
71
iatrogenic infections
a subset of nosocomial infections
that ironically are the direct result of modern medical
procedures such as the use of catheters, invasive diagnostic
procedures, and surgery.
72
superinfections
may result from the use of antimicrobial
drugs that, by inhibiting some resident microbiota, allow others
to thrive in the absence of competition.
73
species resistance
Because the cells and certain basic physiological processes of
humans are incompatible with those of most plant and animal
pathogens, humans have what is termed species resistance to
these pathogens.
74
innate immunity
The first
line of defense is composed chiefly of external physical barriers
to pathogens, especially the skin and mucous membranes. The
second line of defense is internal and is composed of protective
cells, bloodborne chemicals, and processes that inactivate or
kill invaders. Together, the first two lines of defense are called
innate immunity because they are present at birth prior to contact
with infectious agents or their products.
75
adaptive immunity
the body’s ability to recognize and then
| mount a defense against distinct invaders and their products
76
epidermis
The epidermis is composed of multiple layers of tightly
packed cells. It constitutes a physical barrier to most bacteria,
fungi, and viruses. Very few pathogens can penetrate the layers
of epidermal cells unless the skin has been burned, broken, or cut.
The deepest cells of the epidermis continually divide, pushing
their daughter cells toward the surface.
77
dendritic cells
The epidermis also contains phagocytic cells called dendritic1
cells. The slender, fingerlike processes of dendritic cells
extend among the surrounding cells, forming an almost continuous
network to intercept invaders. Dendritic cells both phagocytize
pathogens nonspecifically and play a role in adaptive
immunity
78
dermis
The dermis also defends nonspecifically. It contains tough
fibers of a protein called collagen. These give the skin strength
and pliability to prevent jabs and scrapes from penetrating the
dermis and introducing microorganisms. Blood vessels in the
dermis deliver defensive cells and chemicals
79
antimicrobial peptides
```
Antimicrobial peptides (sometimes called defensins) are
positively charged chains of 20 to 50 amino acids that act against
microorganisms.
```
80
dermicidins
Sweat glands secrete a class of antimicrobial
peptides called dermcidins. Dermcidins are broad-spectrum antimicrobials
that are active against many Gram-negative and
Gram-positive bacteria and fungi. As expected of a peptide active
on the surface of the skin, dermcidins are insensitive to low
pH and salt.
81
lysozyme
an enzyme that destroys the cell
walls of bacteria by cleaving the bonds between the sugar subunits of the walls. Bacteria without cell walls are more
susceptible to osmotic shock and digestion by other enzymes
within phagocytes
82
sebum
The skin also contains sebaceous (oil) glands, which secrete
sebum (se´buIm), an oily substance that not only helps keep the
skin pliable and less sensitive to breaking or tearing but also
contains fatty acids that lower the pH of the skin’s surface to
about pH 5, which is inhibitory to many bacteria.
83
Mucous membranes are moist and have two distinct layers:
the epithelium, in which cells form a covering, and a deeper connective
tissue layer that provides mechanical and nutritive support
for the epithelium.
84
how are microorganisms kept from invading through
| these thin mucous membranes?
Nevertheless, the epithelial cells of mucous
membranes are tightly packed to prevent the entry of many
pathogens, and the cells are continually shed and then replaced
by stem cells, which are generative cells capable of dividing to
form daughter cells of various types. One effect of mucousal
shedding is that it carries attached microorganisms away.
85
goblet cells
In the mucous membrane
of the trachea, for example, the stem cells produce both
goblet cells, which secrete an extremely sticky mucus that traps
bacteria and other pathogens
86
ciliated columnar cells
ciliated columnar cells, whose
cilia propel the mucus and its trapped particles and pathogens
up from the lungs
87
lacrimal apparatus
The lacrimal apparatus is a group of structures that produce
| and drain away tears
88
plasma
Plasma is mostly water containing electrolytes (ions), dissolved
gases, nutrients, and—most relevant to the body’s defenses—a
variety of proteins.
89
blood cotting
a defense
| mechanism that reduces both blood loss and the risk of infection.
90
serum
When clotting factors have been removed from the plasma, as
| when blood clots, the remaining liquid is called serum.
91
formed elements
Cells and cell fragments suspended in the plasma are called
| formed elements
92
erythrocytes
Erythrocytes, the most
numerous of the formed elements, carry oxygen and carbon
dioxide in the blood.
93
platelets
pieces of large cells that have split into small portions of cytoplasm
surrounded by cytoplasmic membranes, are involved in
blood clotting.
94
leukocytes
Leukocytes, the formed elements that are directly
involved in defending the body against invaders, are commonly
called white blood cells because they form a whitish layer when
the components of blood are separated within a test tube.
- Based on their appearance in stained blood smears when
viewed under the microscope, leukocytes are divided into
two groups: granulocytes n agran
95
granulocyte tyeps
baso, eosino, neutrophils
96
agranulocyte tyeps
lymphocytes, monocytes
97
basophils
stain blue with the basic dye
methylene blue
- Basophils can also leave the blood, though they are
not phagocytic; instead, they release inflammatory chemicals
98
eosinophils
stain red to orange
with the acidic dye eosin
- usually secrete antimibrobial chems
99
neutrophils
stain lilac with a
| mixture of acidic and basic dyes
100
diapedesis
Both neutrophils and eosinophils
phagocytize pathogens, and both can exit the blood to attack
invading microbes in the tissues by squeezing between the
cells lining capillaries (the smallest blood vessels). This process
is called diapedesis
101
lymphocytes
the smallest leukocytes
| and have nuclei that nearly fill the cells
102
monocytes
large agranulocytes with slightly lobed
| nuclei
103
macrophages
Monocytes
leave the blood and mature into macrophages (mak´ro@faj@eIz),
which are phagocytic cells of the second line of defense. Their
initial function is to devour foreign objects, including bacteria,
fungi, spores, and dust as well as dead body cells
104
wandering macrophages
leave the blood via diapedesis and perform
their scavenger function while traveling throughout the body,
including extracellular spaces.
105
fixed macrophages
Fixed macrophages generally phagocytize
within specific organs, such as the heart chambers, blood vessels,
and lymphatic vessels.
106
kupffer cells
found in liver
107
mononuclear phagocytic system
All macrophages, plus monocytes attached to endothelial cells, constitute the mononuclear phagocytic system
108
differential WBC count
The proportions of leukocytes, as determined
in a differential white blood cell count, can serve as a sign of
disease.
109
lab analysis of leukocytes
- Increased eosinophils can indicate allergies or parasitic worm infection
- Bacterial diseases often show increase in leukocytes and in neutrophils
- Viral infections show increase in lymphocytes
110
phagocytosis steps
CAIMKE
| chemotaxis, adherence, ingestion, maturation, killing, and elimination
111
chemotactic factors
attract phagocytic leukocytes. include
defensins, peptides derived from complement (discussed later
in this chapter), and chemicals called chemokines (ke´mo@kınz),
which are released by leukocytes already at a site of infection.
112
adherence
After arriving at the site of an infection, phagocytes attach to microorganisms
through the binding of complementary chemicals,
such as glycoproteins, found on the membranes of cells
113
opsonization
All pathogens are more readily phagocytized if they are
first covered with antimicrobial proteins, such as complement
proteins (discussed later) or the specific antimicrobial proteins
called antibodies (discussed in Chapter 16). This coating process
is called opsonization
114
opsonins
increase the number and
| kinds of binding sites on a microbe’s surface.
115
phagosome
After phagocytes adhere to pathogens, they extend pseudopods
to surround the microbe 3 . The encompassed microbe is internalized
as the pseudopods fuse to form a food vesicle called a
phagosome.
116
phagolysosome
A series of membranous organelles within the phagocyte fuse
with newly formed phagosomes to form digestive vesicles.
One organelle, the lysosome, adds digestive chemicals to the
maturing phagosome, which is now called a phagolysosome
- contain antmicrobial substances
- In the end, a phagolysosome
is known as a residual body.
117
elimination
Digestion is not always complete, and phagocytes eliminate
remnants of microorganisms via exocytosis, a process that is essentially
the reverse of ingestion
118
eiosinophilia
an
abnormally high number of eosinophils in the blood, is often indicative
of helminth infestation or allergies.
119
NK cells
Natural killer lymphocytes (or NK cells) are another type of
defensive leukocyte of innate immunity that works by secreting
toxins onto the surfaces of virally infected cells and neoplasms
(tumors). NK cells identify and spare normal body cells
because the latter express membrane proteins similar to those
on the NK cells.
120
TLRs
Toll-like receptors (TLRs)11 are integral proteins of the cytoplasmic
membranes of phagocytic cells. TLRs act as an early
warning system, triggering your body’s responses to a number
of molecules that are shared by various bacterial or viral
pathogens and are absent in humans
121
interferons
Interferons (in@ter@fer´onz) are protein molecules released
by host cells to nonspecifically inhibit the spread of viral
infections. Their lack of specificity means that interferons produced
against one viral invader protect somewhat against infection
by other types of viruses as well. However, interferons
also cause malaise, muscle aches, chills, headache, and fever,
which are typically associated with viral infections.
122
interferon types
In general,
type I interferons—also known as alpha and beta interferons—
are present early in viral infections, whereas type II (gamma)
interferon appears somewhat later in the course of infection
123
type I interferons
Interferons do not protect the cells that secrete them—these
cells are already infected with viruses. Instead, interferons activate
natural killer lymphocytes and trigger protective steps in
neighboring uninfected cells. Alpha and beta interferons bind to interferon receptors on the cytoplasmic membranes of neighboring
cells. Such binding triggers the production of antiviral
proteins (AVPs), which remain inactive within these cells until
AVPs bind to viral nucleic acids
124
type II IFN
macrophage activation factor
125
complement system
The complement system—or complement for short—is a set of
serum proteins designated numerically according to the order
of their discovery. These proteins initially act as opsonins and
chemotactic factors and indirectly trigger inflammation and fever. The end result of full complement activation is lysis of
foreign cells
126
classical pathway
antibodies activate complement.
127
alternative pathway
pathogens or pathogenic products
(such as bacterial endotoxins and glycoproteins) activate
complement.
128
lectin pathway
microbial polysaccharides bind to activating
| molecules.
129
inflammation
Inflammation is a general, nonspecific response to tissue damage
resulting from a variety of causes, including heat, chemicals, ultraviolet
light (sunburn), abrasions, cuts, and pathogens.
130
acute inflammation
is an important part of the second line of defense because it
results in
(1) dilation and increased permeability of blood vessels,
| (2) migration of phagocytes, and (3) tissue repair.
131
fever
Fever is a body temperature above 37°C. Fever augments the
beneficial effects of inflammation, but like inflammation it also
has unpleasant side effects, including malaise, body aches, and
tiredness.
132
__ controls the body’s internal (core) temperature
hypothalamus
133
fever results when
the presence of chemicals called pyrogens trigger the hypothalamic “thermostat” to reset at
a higher temperature. Pyrogens include bacterial toxins, cytoplasmic
contents of bacteria that are released upon lysis,
134
langerhans cells
epidermal dendritic cells
135
adaptive immunity involve the activities of
lymphocytes (lim´fo@sıtz), which are a type of leukocyte (WBC) that acts against specific pathogens
136
lymphocytes
Lymphocytes in
their resting state are the smallest white blood cells, and each is
characterized by a large, round, central nucleus surrounded by
a thin rim of cytoplasm (Figure 16.1). Initially, lymphocytes of
humans form in the red bone marrow
137
B cells
B lymphocytes,
which are also called B cells, arise and mature in
the red bone marrow of adults
138
T cells
T lymphocytes, also known as
T cells, begin in bone marrow as well but do not mature there.
Instead, T cells travel to and mature in the thymus, located in
the chest near the heart in humans
139
T cells
T lymphocytes, also known as
T cells, begin in bone marrow as well but do not mature there.
Instead, T cells travel to and mature in the thymus, located in
the chest near the heart in humans
140
lymphatic vessels
Lymphatic vessels form a one-way system that conducts lymph
(pronounced “limf”) from local tissues and returns it to the
circulatory system.
141
lymph
lymph carries toxins and pathogens to areas where lymphocytes
are concentrated.
Lymph is a colorless, watery liquid similar in composition
to blood plasma; indeed, lymph arises from fluid that has
leaked out of blood vessels into the surrounding intercellular
spaces
142
aff, eff
Each lymph node receives
lymph from numerous afferent (inbound) lymphatic vessels and
drains lymph into just one or two efferent (outbound) lymphatic
vessels
143
lymph nodes
The
hundreds of lymph nodes are located throughout the body but
concentrated in the cervical (neck), inguinal (groin), axillary
(armpit), and abdominal regions. Essentially, lymph nodes are sites to facilitate
interactions among immune cells and between immune cells
and material in the lymph arriving from throughout the body.
144
malt
The lymphatic system contains additional secondary lymphoid
tissues and organs, including the spleen, the tonsils, and
mucosa-associated lymphoid tissue (MALT).
145
spleen
The spleen is similar
in structure and function to lymph nodes, except that it filters
blood instead of lymph. The spleen removes bacteria, viruses,
toxins, and other foreign matter from the blood. It also cleanses
the blood of old and damaged blood cells
146
malt
The tonsils and MALT lack the tough outer capsules of
lymph nodes and the spleen, but they function in the same
way by physically trapping foreign particles and microbes.
MALT includes the appendix; lymphoid tissue of the respiratory
tract, vagina, urinary bladder, and mammary glands; and
discrete bits of lymphoid tissue called Peyer’s patches in the
wall of the small intestine. MALT contains most of the body’s
lymphocytes.
147
antigens
lymphocytes bind to antigens. Adaptive immune responses are directed not against whole bacteria,
fungi, protozoa, or viruses but instead against portions of
cells, viruses, and even parts of single molecules that the body
recognizes as foreign and worthy of attack. Immunologists call
these biochemical shapes antigens
148
epitopes
The body recognizes antigens by the three-dimensional shapes
of regions called epitopes, which are also known as antigenic
determinants because they are the actual part of an antigen that
determines an immune response
149
Among the properties
that make certain molecules more effective at provoking
adaptive immunity are a molecule’s shape, size, and complexity
larger molecules r better antigens than smaller ones (small evade detection), complex better than simple (more eipitopes)
150
Exogenous3
| antigens
include toxins and other secretions and
components of microbial cell walls, membranes, flagella,
and pili.
151
endogenous antigens
Protozoa, fungi,
bacteria, and viruses that reproduce inside a body’s cells
produce endogenous antigens. The immune system cannot
assess the health of the body’s cells; it responds to endogenous
antigens only if the body’s cells incorporate such
antigens into their cytoplasmic membranes, leading to their
external display
152
autoantigens
Antigenic molecules derived
| from normal cellular processes are autoantigens
153
autoantigens
Antigenic molecules derived
| from normal cellular processes are autoantigens
154
B cells found primarily in
Found primarily in the spleen, lymph nodes, and MALT
| Small percentage of B cells circulate in the blood
155
BCR
The surface of each B lymphocyte is covered with about 500,000
identical copies of a protein called the B cell receptor (BCR). A BCR
is a type of immunoglobulin
156
antigen binding sites
Together the two
variable regions form antigen-binding sites (see Figure 16.4).
Antigen-binding sites are complementary in shape to the threedimensional
shape of an epitope and bind precisely to it. Exact
binding between antigen-binding site and epitope accounts for
the specificity of an antibody immune response.
157
antigen binding sites
Together the two
variable regions form antigen-binding sites (see Figure 16.4).
Antigen-binding sites are complementary in shape to the threedimensional
shape of an epitope and bind precisely to it. Exact
binding between antigen-binding site and epitope accounts for
the specificity of an antibody immune response.
158
plasma cells
Activated, immunoglobulin-secreting B lymphocytes are called
| plasma cells.
159
how are B cells stimulated to divide
When an antigenic epitope stimulates a specific B cell via
| the B cell’s unique BCR
160
antibodies
Antibodies are free immunoglobulins—not attached to a
membrane—and similar to BCRs in shape. Antibodies are secreted
and lack most of the transmembrane portions of BCRs
(Figure 16.5). Thus, a basic antibody molecule is Y-shaped with
two identical heavy chains and two identical light chains
161
fab regions
Because the arms of an antibody molecule contain antigenbinding
sites, they are also known as the Fab regions (fragment,
antigen-binding).
162
neutralization
IgA antibodies can neutralize a toxin by binding
to a critical portion of the toxin so that it can no longer
harm the body.
163
opsonins
Antibodies act as opsonins6
—molecules that
stimulate phagocytosis. Changing the surface of an antigen so as to enhance
phagocytosis is called opsonization
164
agglutination
Because each basic antibody has two antigenbinding
sites, each can attach to two epitopes at once. Numerous
antibodies can aggregate antigens together—a state called
agglutination. Agglutination
of soluble molecules typically causes them to become insoluble
and precipitate.
165
TCR
T lymphocytes are like B cells in their specificity. Each T cell
has about half a million copies of a T cell receptor (TCR) on its
cytoplasmic membrane. Each T cell randomly chooses and combines
segments of DNA from TCR genes to create a novel gene
that codes for that cell’s unique and specific TCR.
166
cytotoxic T cell
Every cytotoxic T cell (Tc or CD8
cell) is distinguished by copies of its own unique TCR as well as the presence of CD8 cell-surface glycoprotein.
- directly kill other cells
167
helper T cells
Immunologists distinguish helper T
cells (Th or CD4 cells) by the presence of the CD4 glycoproteins.
These cells are called “helpers” because their function
is to assist in regulating the activity of B cells and cytotoxic
T cells during immune responses
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Th1
type 1 helper T
cells (Th1 cells), which assist cytotoxic T cells and stimulate and
regulate innate immunity
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Th2
type 2 helper T cells (Th2 cells),
| which function in conjunction with B cells
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regulatory T cells
Tr cells :
repress adaptive immune responses
and prevent autoimmune diseases.
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clonal deletion
The body eliminates self-reactive lymphocytes via clonal
deletion, so named because elimination of a cell deletes its potential
offspring (clones). In this process, lymphocytes are exposed to
autoantigens, and those lymphocytes that react to autoantigens undergo
apoptosis (programmed cell suicide) and are thereby deleted
from the repertoire of lymphocytes.
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cytokines
soluble regulatory proteins that act
as intercellular messages when released by certain body cells,
including those of the kidney, skin, and immune system. Here
we are concerned with cytokines that signal among various immune
leukocytes.
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ILs
interleukins. signal among leukocytes
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IFNs
interferons. proteins that inhibit the spread of viral infections
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growth factors
These proteins stimulate leukocyte stem
cells to divide, ensuring that the body is supplied with
sufficient white blood cells of all types.
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TNF
tumor necrosis factor : Macrophages and T cells
secrete TNF to kill tumor cells and to regulate immune
responses and inflammation.
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chemokines
Chemokines are chemotactic
cytokines; that is, they signal leukocytes to move—for
example, to rush to a site of inflammation or infection or
to move within tissues
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chemokines
Chemokines are chemotactic
cytokines; that is, they signal leukocytes to move—for
example, to rush to a site of inflammation or infection or
to move within tissues
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major histocompatibility antigens
- 1st identified in graft patients
- glycoproteins
found in the membranes of most cells of vertebrate
animals
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MHC
Major histocompatibility antigens are coded by a cluster
of genes called the major histocompatibility complex (MHC)
- MHC proteins in cytoplasmic membranes
function to hold and position epitopes for presentation to
T cells.
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class I MHC
Class I MHC
molecules are found on the cytoplasmic membranes of all cells except
red blood cells.
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The body initiates adaptive immune responses where
not at the
site of an infection but rather in lymphoid organs, usually
lymph nodes
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T independent
A few large antigens have many identical, repeating epitopes.
These antigens can induce an antibody immune response without
the assistance of a helper T cell (Th cell); therefore, these antigens
are called T-independent antigens, and they trigger response
of T-independent antibody immunity
- B cells can bind these directly without being processed
- Stimulates B cells to differentiate into a plasma cell and produce
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T dependent
T-dependent antigens lack the numerous, repetitive, and identical
epitopes and the large size of T-independent antigens, and immunity against them requires the assistance of helper T cells.
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memory B cells
A small percentage of the cells produced during B cell proliferation
do not secrete antibodies but survive as memory B cells—
that is, long-lived cells with BCRs complementary to the specific
epitope that triggered their production (Figure 16.18 4 ). In contrast
to plasma cells, memory cells retain their BCRs and persist
in lymphoid tissues
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primary response
relatively small amounts of antibodies are produced,
and it may take days before sufficient antibodies are
made to completely eliminate the toxoid from the body. ends when the plasma cells
have lived out their normal life spans.
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2ndary immune response
Thus,
tetanus toxin produced during the course of a bacterial infection
will restimulate a population of memory cells, which proliferate
and differentiate rapidly into plasma cells. The newly differentiated
plasma cells produce large amounts of antibody within a
few days (Figure 16.19b), and the tetanus toxin is neutralized before
it can cause disease.
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artificial immunity
response to antigens introduced via a vaccine
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active immunity
active response to antigens via humoral or cell-mediated responses
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passive immunity
passively receive antibodies from another individual
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naturally acquired passive
a mother provides her
| baby with antibodies
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artifically acquired active
immunization
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art acquired passive immunotherapy
medical personnel routinely harvest
antibodies specific for toxins and pathogens that are so deadly
or so fast acting that an individual’s active immune response
is inadequate. then these aBs are injected into infected patients
