Body Defense Flashcards

1
Q

Two types of mechanisms defend the body against these tiny but mighty enemies:

A

innate and adaptive defense mechanisms

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2
Q

is a functional system rather than an organ system in an anatomical sense.

A

the immune system

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3
Q

The most important of the
immune cells are

A

lymphocytes, dendritic cells,
and macrophages.

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4
Q

play an important role in both innate and adaptive mechanisms.

A

Macrophages

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5
Q

also called the nonspecific defense system, responds immediately to protect the body from all foreign substances, whatever they are

A

innate defense system

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6
Q

Innate (nonspecific) defense mechanisms- First line of defense

A
  • Skin
  • Mucous membranes
  • Secretions of skin
    and mucous
    membranes
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7
Q

Innate (nonspecific) defense mechanisms- Second line of defense

A
  • Phagocytic cells
  • Natural killer cells
  • Antimicrobial proteins
  • The inflammatory
    response
  • Fever
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8
Q

Adaptive (specific) defense
mechanisms- Third line of defense

A
  • Lymphocytes
  • Antibodies
  • Macrophages and other
    antigen-presenting cells
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9
Q

reduce the workload of the adaptive defense mechanisms by generally preventing the entry and spread of microorganisms throughout the body.

A

innate mechanisms

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10
Q

or specific defense system, fights invaders that get past the innate defenses by mounting an attack against one or more particular foreign substances.

A

adaptive defense system

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11
Q

The resulting highly specific resistance to disease is called

A

immunity

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12
Q

Another important feature of the adaptive response is that it

A

“remembers” which invaders it has fought

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13
Q

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)

A

innate, or nonspecific, body defense

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14
Q

The body’s first line of defense against the invasion of disease-causing microorganisms includes the

A

skin and mucous membranes

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15
Q

Forms mechanical barrier that prevents entry of pathogens and other harmful substances into body.

A

Intact skin (epidermis)

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16
Q

Skin secretions make epidermal surface acidic, which inhibits
bacterial growth; sebum also contains bacteria-killing chemicals.

A

Acid mantle

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17
Q

Provides resistance against acids, alkalis, and bacterial enzymes.

A

Keratin

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18
Q

Form mechanical barrier that prevents entry of pathogens

A

Intact mucous membranes

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19
Q

Traps microorganisms in respiratory and digestive tracts.

A

Mucus

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20
Q

Filter and trap microorganisms and other airborne particles in nasal
passages.

A

Nasal hairs

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21
Q

Propel debris-laden mucus away from lower respiratory passages.

A

Cilia

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22
Q

Contains concentrated hydrochloric acid and protein-digesting
enzymes that destroy pathogens in stomach.

A

Gastric juice

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23
Q

Inhibits growth of bacteria and fungi in female reproductive tract.

A

Acid mantle of vagina

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24
Q

Continuously lubricate and cleanse eyes (tears) and oral cavity
(saliva); contain lysozyme, an enzyme that destroys microorganisms.

A

Lacrimal secretion (tears); saliva

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25
Engulf and destroy pathogens that breach surface membrane barriers; macrophages also contribute to immune response.
Phagocytes
26
Promote cell lysis by direct cell attack against virus-infected or cancerous body cells; do not depend on specific antigen recognition.
Natural killer cells
27
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
28
Group of plasma proteins that lyses microorganisms, enhances phagocytosis by opsonization, and intensifies inflammatory response.
Complement
29
Proteins released by virus-infected cells that protect uninfected tissue cells from viral takeover; mobilize immune system.
Interferons
30
Normally acid pH inhibits bacterial growth; urine cleanses the lower urinary tract as it flushes from the body.
Fluids with acid pH
31
Systemic response triggered by pyrogens; high body temperature inhibits multiplication of bacteria and enhances body repair processes.
fever
32
The acidic pH of skin secretions
acid mantle
33
pH level of urine
4.5 to 6
34
traps many microorganisms that enter digestive and respiratory passageways.
Sticky mucus
35
secretes gastric juice containing hydrochloric acid and protein-digesting enzymes that both kill pathogens.
stomach mucosa
36
stomach mucosa secretes containing hydrochloric acid and protein-digesting enzymes that both kill pathogens.
gastric juice
37
Saliva and lacrimal secretions (tears) contain an enzyme that destroys bacteria.
lysozyme
38
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
39
For its second line of defense, defenses rely on the destructive powers of cells called
phagocytes and natural killer cells
40
roam the body in blood and lymph. They are a unique group of aggressive lymphocytes.
Natural killer (NK) cells
41
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
42
not phagocytic. They attack the target  cell’s membrane and release lytic chemicals called perforin and granzymes. also release powerful inflammatory chemicals.
NK cells
43
NK cells attack the target  cell’s membrane and release lytic chemicals called
perforin and granzymes
44
is a nonspecific response that is triggered whenever body tissues are injured
inflammatory response
45
The four most common indicators, or cardinal signs, of acute inflammation are
1. redness 2. heat (inflamm = set on fire) 3. pain 4. swelling (edema)
46
The inflammatory process begins with a
chemical "alarm"
47
When cells are damaged, they release inflammatory chemicals, including
histamine and kinins
48
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.
49
the 3rd phenomenon when cells are damaged called
positive chemotaxis
50
the cells are moving toward a high concentration of signaling molecules
positive chemotaxis (third phenomenon)
51
Increased permeability of the capillaries allows fluid to leak from the blood into the tissue spaces, causing
local edema (swelling)
52
Some authorities consider limitation of joint movement to be the
fifth cardinal sign of inflammation.
53
prevents the spread of damaging agents to nearby tissues, disposes of cell debris and pathogens, and sets the stage for repair
inflammatory response
54
inflammatory process
1. Neutrophils enter blood from bone marrow, following the “scent.” and roll along the vessel wall 2. Diapedesis- flatten out and squeeze through the capillary walls, chemical signal is the strongest 3. Positive chemotaxis, the gradient of inflammatory chemicals. the neutrophils gather at the site of tissue injury
55
At the point where the chemical signal is the strongest, they flatten out and squeeze through the capillary walls, a process
Diapedesis
56
responding to a gradient of diffusing inflammatory chemicals
Neutrophils
57
follow neutrophils into the inflamed area, fairly poor phagocytes and after entering the tissues they become macrophages with insatiable appetites
monocytes
58
continue to wage the battle, replacing the short-lived neutrophils at the site of damage.
macrophages
59
are the central actors in the final disposal of cell debris as the inflammation subsides.
macrophages
60
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
61
also forms scaffolding for permanent repair
fibrin mesh
62
is a mixture of dead or dying neutrophils, broken-down tissue cells, and living and dead pathogens.
Pus
63
If the inflammatory mechanism fails to fully clear the  area of debris, the sac of pus may become walled off, forming an
abscess
64
Pathogens that make it through the mechanical barriers are confronted by
phagocytes
65
A phagocyte, engulfs a foreign particle by the process of phagocytosis, such as a
macrophage or neutrophil
66
enhance the innate defenses either by attacking microorganisms directly or by hindering their ability to reproduce
antimicrobial proteins
67
it refers to a group of at least 20 plasma proteins that circulate in the blood in an inactive state, inactive clotting proteins
complement
68
occurs when complement proteins bind to certain sugars or proteins (such as antibodies) on the foreign cell’s surface
complement fixation
69
result of complement fixation:
1. the formation of membrane attack complexes (MAC) that produce holes, or pores, in the foreign cell’s surface. 2. These pores allow water to rush into the cell 3. causing it to burst, or lyse.
70
produce holes, or pores, in the foreign cell’s surface.
membrane attack complexes (MAC)
71
Some of the molecules released during the activation process are
vasodilators, and some are chemotaxis chemicals
72
attract neutrophils and macrophages into the region
chemotaxis chemicals
73
this effect cause the cell membranes of the foreign cells to become sticky so they are easier to phagocytize
opsonization
74
is a nonspecific defensive mechanism that “complements,” or enhances, the effectiveness of both innate and adaptive defenses
Complement
75
Complement proteins must be activated in a particular sequence, which insures that complement is not accidentally activated, is called
cascade
76
acellular particles—essentially nucleic acids surrounded by a protein coat—that lack the cellular machinery required to generate ATP or make proteins.
viruses
77
does “dirty work” in the body by taking over target cells
viruses
78
viruses uses to reproduce themselves
cellular machinery and nutrients
79
virus-infected cells defend cells that have not yet been infected by secreting small proteins called
interferons
80
diffuse to nearby cells and bind to their membrane receptors
interferon molecules
81
abnormally high body temperature, is a systemic response to invading microorganisms.
Fever
82
Body temperature is regulated by the body’s “thermostat.”
hypothalamus
83
a group of chemically diverse substances that cause fever and shock in severe cases
pyrogens
84
stalks and eliminates with nearly equal precision almost any type of pathogen that intrudes into the body.
specific defense system
85
response to a threat involves tremendously increased internal nonspecific defenses
immune response
86
the adaptive, or specific, defense mechanism is a functional system that recognizes foreign molecules called antigens and acts to inactivate or destroy them.
antigens
87
animals surviving a serious bacterial infection have “factors” in their blood that protect them from future attacks by the same pathogen
antibodies
88
These landmark experiments revealed three important aspects of adaptive defense:
1. It is antigen specific 2. It is systemic 3. It has “memory”
89
important aspects of adaptive defense, immunity is not restricted to the initial infection site.
It is systemic
90
important aspects of adaptive defense, it recognizes and acts against particular pathogens or foreign substances.
It is antigen specific
91
important aspects of adaptive defense, it recognizes and mounts even stronger attacks on previously encountered pathogens.
It has “memory”
92
also called antibody-mediated immunity, is provided by antibodies (immune proteins) present in the body’s “humors,” or fluids
Humoral immunity
93
When lymphocytes themselves defend the body, the immunity is called
cellular immunity or cell-mediated immunity
94
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
95
is any substance capable of provoking an immune response
antigen
96
are large, complex molecules that are not normally present in our bodies, non-self.
Foreign antigen
97
As a rule, small molecules are not antigenic, but when they link up with our own proteins,
hapten or incomplete antigen
98
The crucial cells of the adaptive system are
lymphocytes and antigen-presenting cells (APCs)
99
Lymphocytes exist in two other major “flavors.”
B lymphocytes or B cells and T lymphocytes or T cells
100
produce antibodies and oversee humoral immunity
B lymphocytes or B cells
101
constitute the cell-mediated arm of the adaptive defenses and do not make antibodies
T lymphocytes, or T cells
102
can recognize and eliminate specific virus-infected or tumor cells
T lymphocytes, or T cells
103
can target specific extracellular antigens
B lymphocytes, or B cells
104
do not respond to specific antigens but instead play an essential role in activating the lymphocytes that do
APCs
105
immature lymphocytes, released from the  marrow are essentially identical
naive
106
migrate (in blood) to the thymus and develop immunocompetence there
T cells
107
develop immunocompetence in red bone marrow
B cells
108
sites of development of immunocompetence as B or T cells
Primary lymphoid organs
109
site of lymphocyte origin
Red bone marrow
110
sites of antigen encounter, and activation to become effector and memory B or T cells
Secondary lymphoid organs
111
arise from lymphocytes that migrate to the thymus
t cells
112
development of self-tolerance for the body’s own cells is an essential part of a
lymphocyte’s “education.”
113
B cells develop immunocompetence in
bone marrow
114
capable of responding to a specific antigen by binding to it with antigen specific receptors that appear on the lymphocyte’s surface
immunocompetent
115
There they undergo a maturation process lasting 2 to 3 days, directed by thymic hormones
T cell in Thymus
116
acting against body cells
self-antigens
117
Thus, it is our genes, not antigens, that determine what foreign substances our immune system will be able to recognize and resist
TRUE
118
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)
119
present antigens to the cells that will actually deal with the antigens
antigen-presenting cells (APCs)
120
The major types of cells acting as APCs are
dendritic cells, macrophages, and B lymphocytes.
121
also called Langerhans cells, are present in connective tissues and in the epidermis
Dendritic cells
122
are widely distributed throughout the lymphoid organs and connective tissues, where they act as phagocytes in the innate defense system
Macrophages
123
true “killers” that are insatiable phagocytes and secrete bactericidal (bacteria killing) chemicals
activated macrophages
124
are the most effective antigen presenters known—it’s their only job. Key link between innate and adaptive immunity.
dendritic cells
125
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
126
The resulting family of identical cells descended from the same ancestor cell are called
clones
127
to that antigen, clone formation is the
primary humoral response
128
Most of the B cell clone members, or descendants, become
plasma cells
129
B cell clone members that do not become plasma cells become long-lived
memory cells
130
Memory cells are responsible for the
immunological memory
131
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
132
the ability of the immune system to respond more rapidly and effectively to pathogens that have been encountered
immunological memory
133
When your B cells encounter antigens and produce antibodies against them, you are exhibiting
active immunity
134
which may intensify the immune response at later meetings with the same antigen, are also available
booster shots
135
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
136
the antibodies are obtained from the serum of an immune human or animal donor
Passive immunity
137
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
138
artificially conferred when a person receives immune serum or gamma globulin (donated antibodies)
Passive immunity
139
is commonly administered after exposure to hepatitis.
Gamma globulin
140
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
141
used for early cancer diagnosis and to track cancers hidden deep within the body
Monoclonal antibodies
142
Humoral Immunity- Infection; contact with pathogen
Active- Naturally acquired
143
Humoral Immunity- Vaccine; dead or attenuated pathogens
Active- Artificially acquired
144
Humoral Immunity- Antibodies passed from mother to fetus via placenta; or to infant in her milk
Passive- Naturally acquired
145
Humoral Immunity- Injection of donated antibodies (gamma globulin)
Active- Artificially acquired
146
also referred to as immunoglobulins (Igs), constitute the gamma globulin part of blood proteins
Antibodies
147
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
148
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
149
Each of the four chains forming an antibody had a
variable (V) region and constant (C) region
150
uniquely shaped to “fit” a specific antigen
antigen-binding site
151
Y-shaped structured, monomers
IgD, IgG, IgE
152
IgM antibodies are called
pentamers
153
IgA antibodies occur in both
monomer and dimers
154
is the most abundant antibody in blood plasma and is the only type that can cross the placental barrier
IgG
155
only can fix complement
IgM and IgG
156
dimers, is found mainly in secretions that bathe body surfaces, such as mucus and tears.
IgA
157
antibodies are the “troublemaker” antibodies involved in allergies.
IgE
158
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
159
Almost always attached to B cell, Believed to be cell surface receptor of immunocompetent B cell; important in activation of B cell.
IgD
160
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
161
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
162
Antibodies inactivate antigens in a number of ways
by complement fixation, neutralization, agglutination, opsonization, and precipitation
163
chief antibody ammunition used against cellular antigens, such as bacteria or mismatched red blood cells
Complement
164
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
165
can be cross-linked into large lattices
antigen-antibody complexes
166
When the cross-linking involves cell-bound antigens, the process causes clumping of the foreign cells, a process called
agglutination
167
This type of antigen-antibody reaction occurs when mismatched blood is transfused
agglutination
168
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
169
antigen molecules are much more easily captured and engulfed by the body’s phagocytes than are freely moving antigens.
agglutinated bacteria and immobilized (precipitated)
170
cells secrete their anti body “weapons,”
B cells
171
cells fight their anti gens directly
T cells
172
are activated to form a clone by binding with a “recognized” antigen
T cells
173
are not able to bind with free antigens. Instead, the antigens must be “presented” by a macrophage.
T cells
174
Two types that are involved in the activation process are called
helper T cells and cytotoxic T cells
175
T cell must recognize the antigen fragment presented by the APC
“nonself,”
176
T cell must recognize this by coupling with a specific glycoprotein on the APC’s surface at the same time
“self,”
177
is now known to be essential for the activation and clonal selection of T cells
antigen presentation
178
chemicals released by macrophages and dendritic cells also play important roles in the immune response
Cytokine
179
specialize in killing virus-infected, cancer, or foreign graft cells directly
Cytotoxic T cells
180
enters the foreign cell’s plasma membrane, delivering the so-called lethal hit
perforin
181
pores appear in the target cell’s membrane, allowing to enter and kill the foreign cell
granzymes
182
are the T cells that act as the “directors” or “managers” of the adaptive immune response
Helper T cells
183
A proposed mechanism by which cytotoxic T cells kill target cells.
1. Cytotoxic T cell binds tightly to the foreign target cell. 2. Cytotoxic T cell releases perforin and granzyme molecules from its granules by exocytosis 3. Perforin molecules insert into the target cell membrane and form pores similar to those produced by complement activation. 4. Granzymes enter the target cell via the pores and degrade cellular contents. 5. The cytotoxic T cell detaches and searches for another prey.
184
The helper T cells also release a variety of cytokines that act indirectly to rid the body of antigens by
1. stimulating cytotoxic T cells and B cells to grow and divide 2. attracting other types of protective white blood cells, such as neutrophils, into the area; and 3. enhancing the ability of macrophages to engulf and destroy microorganisms
185
(formerly called suppressor T cells), release chemicals that suppress the activity of both T and B cells
regulatory T cells
186
are vital for winding down and stopping the immune response after an antigen has been successfully inactivated or destroyed.
regulatory T cells
187
are tissue grafts transplanted from one site to another in the same person.
Autografts
188
are tissue grafts donated by a genetically identical person, the only example being an identical twin.
Isografts
189
are tissue grafts taken from a person other than an identical twin.
Allografts
190
are tissue grafts harvested from a different animal species, such as a porcine (pig) heart valve transplanted into a human.
Xenografts
191
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
192
is the most frequent cause of death in these patients
Explosive infection
193
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
194
Sensitization stage
1. Antigen (allergen) invades body. 2. Plasma cells produce large amounts of class IgE antibodies against allergen. 3. IgE antibodies attach to mast cells in body tissues (and to circulating basophils).
195
secondary response
4. More of same allergen invades body. 5. Allergen binding to IgE on mast cells triggers release of histamine (and other chemicals). 6. 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.
196
starts with the release of a flood of histamine when IgE antibodies bind to mast cells.
secondary response
197
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
198
Over-the-counter (OTC) anti-allergy drugs contain
antihistamines
199
most common type of allergy
immediate hypersensitivity, or acute hypersensitivity
200
is fairly rare, the bodywide, or systemic, acute allergic response known as
anaphylactic shock
201
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
202
Food allergies (peanut or wheat allergies) may also trigger
anaphylaxis
203
found in emergency EpiPen® shots, is the drug of choice to reverse these histamine mediated effects.
Epinephrine
204
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
205
The most familiar examples of delayed hypersensitivity reactions are those classed as
allergic contact dermatitis,
206
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
207
which systematically destroys joints
Rheumatoid arthritis (RA)
208
which impairs communication between nerves and skeletal muscles
Myasthenia gravis
209
which destroys the white matter (myelin sheaths) of the brain and spinal cord
Multiple sclerosis (MS)
210
in which the thyroid gland produces excessive amounts of thyroxine in response to autoantibodies that mimic TSH
Graves’ disease
211
which destroys pancreatic beta cells, resulting in deficient production of insulin
Type 1 diabetes mellitus
212
a systemic disease that occurs mainly in young women and particularly affects the kidneys, heart, lungs, and skin
Systemic lupus erythematosus (SLE)
213
a severe impairment of kidney function due to acute inflammation
Glomerulonephritis
214
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
215
causing damage to both the heart muscle and its valves, as well as to the joints and kidneys
rheumatic fever
216
The most devastating congenital condition in which there is a marked deficit of both B and T cells.
severe combined immunodeficiency disease (SCID)
217
include both congenital and acquired conditions in which the production or function of immune cells or complement is abnormal.
immunodeficiencies
218
the most important and most devastating of the acquired immunodeficiencies, cripples the immune system by interfering with the activity of helper T cells
acquired immune deficiency syndrome (AIDS).
219
fungal brain infection
cryptococcal meningitis
220
an eye infection
cytomegalovirus retinitis