Exam 4 Flashcards
1
Q
what are the components of the immune system?
A
blood (serum) and lymph (lymph system)
2
Q
what do cells, proteins, and supporting systems do?
A
- kill or inactivate invaders
- reacts to chemicals and allergens and monitor every cell in the body for cancer
3
Q
what are the advantages to the immune system?
A
- kills bacteria, viruses, fungi, and parasites
- kills human cells infected with intracellular pathogens
- neutralizes (inactivates) viruses and toxins produced by bacteria
- kills altered human cells such as tumor or cancer cells
4
Q
what are some disadvantages to the immune system?
A
- may cause hypersensitivity reactions such as allergic reactions and interferes with organ and tissue transplant
- may cause autoimmune diseases
5
Q
what are the two types of immunity?
A
- innate (natural) immunity
- acquired (adaptive) immunity
6
Q
innate immunity
A
inbuilt immunity to resist infection anatomical defenses, inflammation, fever, phagocytosis, and complement proteins
7
Q
acquired immunity
A
immunity established to adapt to infection specificity, tolerance, and memory
8
Q
primary organs and tissues of the immune system
A
bone marrow and thymus
9
Q
secondary organs and tissues of the immune system
A
lymph nodes, spleen, tonsils, and lymphoid tissues, BALT, MALT, and SALT
10
Q
SALT
A
skin-associated lymphoid tussues
11
Q
MALT
A
mucous-associated lymphoid tissue
12
Q
BALT
A
bronchial-associated lymphoid tissue
13
Q
RBC
A
no role in immune system, carry oxygen to tissues, platelets are a clotting factor
14
Q
lymphocytes
A
B, T, and K cells
15
Q
granulocytes
A
neutrophils, basophils, and eosinophils
- release and degranulate in response to allergic reactions
16
Q
neutrophils
A
essential blood phagocytes, active engulfers and killers of bacteria; phagocytic, major defense against extra-cellular infections
17
Q
basophils
A
function in inflammatory events and allergies; granulocytes
18
Q
eosinophils
A
active in worm and fungal infections, allergy, and inflammatory reactions; against parasites
19
Q
monocytes
A
blood phagocytes that rapidly leave the circulation; mature into macrophages and dendritic cells
20
Q
macrophages
A
largest phagocytes that ingest and kill foreign cells, strategic participants in certain specific immune reactions, APC, resides in tissues;
21
Q
dendritic cells
A
relatives of macrophages that reside throughout tissues, responsible for processing foreign matter and presenting it to lymphocytes; phagocytic cells, APC
22
Q
lymphocytes
A
primary cells involved in specific immune reactions to foreign matter
23
Q
T cells
A
perform a number of specific cellular immune responses such as assisting B cells and killing foreign cells (CMI)
24
Q
B cells
A
differentiate into plasma cells and form antibodies (AMI); main players in AMI
25
mast cells
granulocytes, releases inflammatory compounds
26
first line of defense
Nonspecific defense system that prevents pathogens from
entering the body
• Includes: skin and mucous membranes of the respiratory,
digestive, urogenital tracts
27
skin defenses
-Perspiration (high salt), Sebaceous glands secrete oil (low pH)
• Lysozyme- destroys cell wall of bacteria
– Epidermis, Tightly packed layer of cells, Shedding of dead cells
28
mucous membrane defenses
Line body cavities open to the outside
– Epithelium
• Thin layer composed of tightly packed live cells
• Continual shedding of cells carries attached germs
away
29
microbial antagonism
Normal flora:
– Compete with pathogens for space, nutrients
– Promote overall health by providing vitamins to host
30
mucociliary blanket
mucous secretions that traps microbes
- once trapped, microbes transported away from the lungs
- can be expelled by coughing and sneezing
- salvation washes microbes to stomach
31
what are the components of the second line of defense?
* Phagocytosis
* Extracellular killing (NK cells)
* Inflammation
* Fever
* Complement System
32
phagocytosis
process by which monocytes, macrophages, neutrophils, and dendritic cells recognize, ingest, and digest extracellular microbes
• Binds to microbe. Internalize it. Fuse it with lysosome. Digest the microbe
33
hydrolytic enzymes
Lipase, Nuclease, Protease, lysozyme
34
respiratory burst
reactions occur as soon as phagosome is formed
| – toxic oxygen products are produced which can kill invading microbe
35
phagocytic failure
Bacteria may survive the killing. Bacteria may prevent fusion of lysosome with phagosome. Or, Bacteria may produce chemicals that kills or inhibit phagocytic cells
36
anti-phagocytic factors
* Capsule (hard to engulf)
* Carotenoid (antioxidant that neutralizes oxygen)
* Leukocidine (kills phagocytic cells)
37
inflammation
The release of inflammatory mediators from injured tissue cells initiates
a cascade of events which result in the signs of inflammation
• nonspecific response to tissue injury due to infection or physical means
• cardinal signs, redness, warmth, pain, swelling, and altered function
38
acute inflammatory response
involves chemical mediators
• Quickly developed, beneficial, promotes healing
– events which result in elimination of invading pathogens
• capillary dilation and increased blood flow
• temperature rise stimulates inflammatory response
• restrict pathogen movement
• Recruit phagocytes to the area
39
chronic inflammation
slow process
| • Slow and causes permanent tissue damage
40
fever
Pyrogens (chemicals) trigger the hypothalamus to increase the body’s core temperature, temperature over
37C (98.6 F)
41
what are the types of pyrogens
Bacterial toxins
– Cytoplasmic contents of bacteria released by lysis
– Antibody-antigen complexes (inflammation)
– Interleukins-1 (IL-1)
- Muscle contractions, increased metabolic activity, and constriction of blood vessels/reduced blood flow, raises the temperature
42
pyrogen
fever inducing
43
pyogen
puss forming
44
serum proteins
- destroy extracellular bacteria and viruses
-function as chemotactic signals that recruit phagocytes
-puncture cell membranes causing cell lysis
-many complement activities unite the nonspecific and specific arms of
the immune system to destroy and remove invading pathogens
45
complement proteins
- group of 20 or more proteins that bind and destroy infection
- normally not active, bind to the surface of bacteria and accumulate and poke a hole and kill it
46
antibody
identifies bacteria and complement binds
47
MAC
membrane attack complex that pokes holes in bacteria to kill it, attracts phagocytes to the area, and aid phagocytes in doing their job
48
classical complement pathway
dependent on antigen-antibody interaction
49
lectin complement pathway
nonspecific defense against intravascular invasion by bacteria and fungi
50
opsonization
coating of microbes by serum proteins, which assist with recognition/ingestion by phagocytic cells
– molecules that carry out above are called opsonins, such as antibody and complement proteins
– bind to microbial cells, coating them for phagocyte recognition
51
acute phase proteins
macrophage activation by bacteria cytokine release liver stimulation Produce acute phase protein
– includes C-reactive protein (CRP), mannan-binding lectin (MBL)
• can bind bacterial surfaces and act as opsonins
52
antigens
* elicit an immune response and B cells and T cells are activated in response to each specific antigen
* most are large, complex molecules Size restriction
* can have several antigenic determinant sites (epitopes)
53
how do antigens enter into the body?
– Breaks in the skin and mucous membranes
– Via bite or needle (injection)
– Via grafts and organ transplant
– Autoimmunity
54
what can antigens be?
– Cell wall, capsule, pili, flagella, and proteins of viruses, fungi,
and protozoa
– Food and dust can also contain antigenic particles
55
haptens
small organic molecules
not antigenic by themselves but may become antigenic when bound
to larger carrier molecule e.g., penicillin
56
adjuvents
added to vaccine (inactivated microbes) to make them
| more antigenic
57
IgG
major circulating antibody
58
IgM
first to appear after infection
59
IgA
major antibody in secretions
60
IgE
involved in allergic reactions
61
what are the components of the third line of defense?
antibodies
62
what are the consequences of antigen-antibody binding?
opsonization, angulation, complement reaction, neutralization, and precipitation
63
cytokines
Soluble proteins or glycoproteins that act as mediators
– released by one cell population that act as intercellular mediators or signaling molecules
• Autocrine Function, self
• Paracrine function, nearby
• Endocrine function, systemic
64
what are the classes of cytokines?
– Tumor necrosis factor (TNF)
– Interleukins
– colony-stimulating factors (CSFs)
– Interferons (INFs)
65
MHC
- major histocompatibility complex
- receptor molecules are like fingerprints
- on all cells except RBC
66
T-independent antigen
- antigen processing
- Large molecules/Bind to B cells.
resulted in B cell activation and Ab production, No need to
APC
67
T-dependent antigens
Small molecules, APC
needed to process them and present them to T
helper cells
68
CMI
- cellular mediated immunity
| - T cells to memory T cells and effector T cell, the Effector T cell turns into cytokines
69
AMI
- antibody-mediated immunity
| - B cells turn into memory B cell and plasma cell, and plasma cell turns into antibody
70
consequences of antigen-antibody binding
neutralize toxins
- neutralize viruses
- marks invaders for attack by immune system components
- Activate complement system
- aids phagocytosis (opsonization)
- Stimulate inflammation
71
natural immunity
acquired through the normal life experiences of a human and is not induced through medical means
- active (infection) and passive(breastmilk) forms
72
artificial immunity
- produced purposefully through medical procedures - immunizations
- active (vaccination) and passive (immune globulin therapy) forms
73
attenuated vaccines
Live/weakened strains/reducing virulence
• Mild infections/no disease, strong immune response/ triggers CMI
• Viral vaccines trigger a cell-mediated immune response
• Results in herd immunity
• Problems: with reversion, with immunosuppressed, with pregnant
74
inactivated vaccines
Dead microbes or their fragments
• Problems: May causes inflammatory response and no herd immunity
• Antigenically weak, and needs high or multiple doses, or the incorporation of an
adjuvant, to make the vaccine more effective, (also may produce allergic reactions)
75
toxoid vaccines
Chemically or thermally modified toxins
• Useful for some bacterial diseases/ Stimulate antibody-mediated immunity/ Require
multiple doses
76
vaccine safety
• Mild toxicity is the most common problem, or may cause disease or allergic reactions
• Anaphylactic shock
• Allegations that certain vaccines against childhood diseases cause or trigger autism,
diabetes, and asthma, Research has not substantiated these allegations
77
donor-recipient matching
MHC compatibility between donor and recipient is hard to achieve due
to a high degree of MHC variability among individuals
• Host T helper cells recognizes foreign MHC molecules on the transplanted tissue (graft),
which aid cytotoxic T cells in destroying the graft, OR T-helper cells releases cytokines
which stimulate destruction of graft by macrophages
78
graft-versus-host disease
Graft cells attack the recipient tissues
• e.g., in bone marrow transplants
– disease prevented by treating donor with immunosuppressive drugs to deplete marrow of
mature T cells
79
why are fetuses not rejected?
– The fetus is not a privileged site but is not rejected
– Rejection is prevented by the many different immunosuppressive mechanisms
• Early embryos do not express MHC class I and II molecules on the placental layer that is in contact with maternal
tissues
• Cytokines that enhance MHC expression have no effect on placental cells
• T cells are prevented from functioning in the placenta to reject the fetus
80
autoimmunity
– presence of serum antibodies against self antigens (autoantibodies)
– often benign/natural consequence of aging/induced by infectious organisms, drugs...
81
autoimmune disease
– results from activation of self-reactive T and B cells/leads to tissue damage
82
immunodeficiency
* Conditions resulting from defective immune mechanisms
* failure to recognize and/or respond properly to foreign antigens
* Opportunistic infections can play an important part of these diseases
83
primary immunodeficiency
* Result from some genetic or developmental defect
| * Develop in infants and young children
84
acquired immunodeficiency
* Develop as a direct consequence of some other recognized cause
* Develop in later life
* Sever Stress: Excess production of corticosteroids suppresses CMI
* Malnutrition: Inhibit B cells and T cells development
85
clinical immunology:
Serology; study and diagnostic
| use of antigen-antibody interactions in serum
