unit 8 micro Flashcards
1
Q
innate immunity is:
A
initial defenses to prevent infection
non-specific: defenses act in response to all pathogens
built in mechanisms: structures/chemicals are present at birth
no memory: same response regardless of prior exposure
2
Q
adaptive immunity is:
A
response to pathogens
specific: defenses act in response to one type of bacterial strain or virus
builds up over time: requires exposure to antigens
has a memory: strong response with a second exposure to the same antigen
3
Q
first line of defense consists of
A
initial barriers to pathogens to prevent entry and colonization
4
Q
second line of defense is
A
a response to infection once the first line has been bypassed
5
Q
physical factors in first line
A
barriers that prevent entry OR processes that remove microbes from the body surface
6
Q
barriers include
A
skin: tightly packed epithelial cells that contain keratin
mucus membranes: contain epithelial cells bound by tight junctions; line nose, mouth, lungs, urinary and digestive tracts
7
Q
mucus is produced to
A
cover and protect the cell layers, and to trap debris and microbes
8
Q
endothelia is
A
tightly packed cells lining the urogenital
one well known example is blood brain barrier, which contains very tight cell junctions preventing pathogens from entering the CNS
9
Q
mechanical action is then used to
A
flush mucus-trapped microbes out of the body
mucociliary escalator in the lungs use cilia to propel mucus out of the lungs, which is then swallowed or coughed/sneezed out
shedding of skin cells
flushing action of urine, tears
10
Q
normal flora
A
through competitive inhibition, our microbiome prevents the growth of other microbes by out-competing pathogens for nutrients and by taking up spaces that can be colonized
11
Q
chemical factors (1st)
A
substances or enzymes continuously produced by body cells.
12
Q
sebum
A
produced by sebaceous glands in the dermis to seal off pores of hair follicles
13
Q
production of oleic acid by
A
normal flora to create a mildly acidic environment on the skin to inhibit pathogen colonization
14
Q
what in saliva, sweat and tears can break down bacterial cell walls
A
lysozyme
15
Q
what antibodies that protect the respiratory tract
A
IgA
16
Q
what in saliva (salivary amylase), lower digestive tract (pancreatic enzymes)
A
digestive enzymes
17
Q
name chemical defenses involved in the second line of defense
A
antimicrobial peptides (AMPs), plasma protein mediators: acute phase proteins & complement proteins & cytokines & inflammation-eliciting mediators
18
Q
AMPs are (antimicrobial peptides)
A
group of chemicals with broad-spectrum anti-microbial activity
some are produced continuously and some are produced in response to pathogen infection
some are produced by body cells and some are produced by normal flora
examples: cathelicidin, dermicidin, histatin
19
Q
plasma protein mediators are
A
proteins found in the blood that play a role in the nonspecific innate immune response
20
Q
acute phase proteins are
A
produced in the liver and secreted into the blood in response to inflammatory molecules
21
Q
examples of acute proteins
A
different examples with different methods of inhibiting or destroying microbes, such as ferritin, fibrinogen, mannose-binding lectin
22
Q
complement proteins are
A
group of proteins that circulate in inactive forms in the blood
activated in a cascade allowing for a rapid response to infection
23
Q
method 1 of complement proteins
A
classical complement activation:
- antibody binds to bacterium
- C1 protein is recruited and activated & C3 protein is recruited and activated
24
Q
method 2 of complement proteins
A
mannose-binding lectin:
- mannose-binding lectin binds to. carbohydrates on microbial surface
- C3 protein is recruited and activated
25
method 3 of complement proteins
alternative activation:
1. C3 protein is directly recruited and activated
26
upon activation, C3
splits into 2 separate proteins C3a & C3b
27
outcome 1: opsonization
C3b protein coats the microbe, which makes the microbe more easily identified by macrophages
28
outcome 2: cytolysis
1. C3b recruits and activates C5 protein
2. C5 splits into 2 separate proteins, named C5a & C5b
3. C5b recruits and combines with C6, C7, C8 & C9 proteins to form a membrane attack complex, which inserts into the cell membrane causing extracellular fluid to rush in, leading to microbial cell lysis
29
outcome 3: enhanced inflammation
C3a & C5a combine together and binds to mast cells, leading to increased production of histamine by mast cells
30
how do microbes avoid the complement system
presence of a capsule inhibits opsonisation and prevents insertion of the MAC, gram-negative cells can alter the structure of the outer membrane to prevent insertion of the MAC, gram-positive cocci can release an enzyme that breaks down C5 protein
31
cytokines are
soluble proteins that act as communication signals between cells
32
in the immune response, cytokines are
important to stimulate production of other chemical mediators or to promote cell functions
33
3 main types of cytokines
interleukins - modulate many parts of immune system
chemokines - recruit white blood cells to sites of infections, tissue damage and inflammation
interferons - important for our defenses against viral replication (can be produced in the lab and used as treatment for viral infection but have significant side effects)
34
inflammation-eliciting mediators
contributes to the inflammation response
35
examples of inflammation-eliciting mediators
histamine - produced by mast cells
leukotrienes - longer lasting effects than histamine
prostaglandins - also plays role in fever
bradykinin - increases vascular permeability leading to edema
36
cellular defenses involved in the second line of defense
granulocytes & agranulocytes
37
granulocytes are
white blood cells with lobed nuclei and granules in the cytoplasm
38
mast cells
reside in tissues to produce histamine
39
basophils
produces histamine in response to allergic reactions
40
neutrophils
elimination and destruction of bacteria through direct phagocytosis or through the production of extracellular traps (NETs)
41
eosinophils
protect against protozoan and helminthic infections by releasing degradative enzymes
42
agranulocytes are
white blood cells with no granules in cytoplasm
43
agranulocytes use
nonspecific mechanisms to recognize abnormal body cells. upon recognition, NK cells will induce apoptosis in these abnormal body cells
44
apoptosis
programmed cell death
45
after movement into body tissue
monocytes will differentiate into dendritic cells and macrophages
46
phagocytosis:
| 1. extravasation (diapedesis) of leukocytes to site of infection
- site of injury leads to release of inflammation-elicitors and cytokines
- through positive chemotaxis, phagocytes leave the blood stream through capillaries and enter tissues through process called extravasation
- neutrophils usually arrive first, followed by monocytes (which differentiate into macrophages)
47
phagocytosis:
| 2. pathogen recognition
-attachment of the phagocyte's plasma membrane to the surface of the microorganism through the interaction of PAMPs on the pathogen with receptors on the phagocytes
48
PAMPs are
pathogen-associated molecular patterns
49
PRRs are
pathogen recognition receptors
50
examples of PAMPs
peptidoglycan, flagellin, lipopolysaccharides, lipopeptides
51
pathogen recognition can be enhanced by
opsonization
52
phagocytosis:
| pathogen degradation
- pseudopods form around the microbe and a phagosome is made (phagocytic vesicle)
- a lysosome containing hydrogen peroxide and several enzymes, fuse with the phagosome to form a phagolysosome
- microbe is then digested
- indigestible material (waste) are excreted by exocytosis
53
how do microbes avoid phagocytosis
- presence of capsule inhibits adherence of the phagocyte to the pathogen
- some pathogens can release molecules that leads to phagocyte death
- some pathogens use phagocytosis as a mechanism for entry into the cells, and then replication inside the phagocytes
- formation of biofilms - phagocytes are unable to detach pathogens from a biofilm
54
acute inflammation in 2nd line
- immediate response to injury is vasoconstriction, which leads to the narrowing of blood vessels to minimize blood loss
- this is followed by vasodilation and increased vascular permeability
- phagocytes are then recruited due to tissue damage and release of chemicals such as histamine
- pus is formed as damage tissue and pathogens are cleared
- eventually tissue repair begins
55
5 signs/symptoms of inflammation
swelling, heat, redness, pain, altered function
56
chronic inflammation in 2nd line
occurs when the immune system is unable to clear pathogen
when this occurs, tissue damage can occur, such as the formation of granulomas
57
body temperature is regulated by
hypothalamus
58
As a result of bacterial or viral infections
a series of chemicals are
released, eventually leading to the production of prostaglandins that
leads to elevated body temperature
59
Fever can enhance the immune system by:
inhibiting the growth of many pathogens & stimulating the release of iron-sequestering compounds from the liver
60
during fever:
vasoconstriction of the blood vessels occur, marking the skin appear pale & leads also to shivering and an increase in metabolism
61
when fever breaks:
Vasodilation is stimulated, leading to release of heat from body
62
Complications of fever in situations where the immune response is too strong:
Tissue and organ damage, tachycardia, metabolic acidosis, dehydration,
seizures, delirium, coma
63
Antigens are found on pathogens and can stimulate the immune system. Examples
include:
bacteria: cell wall, flagella, fimbriae
viruses: spikes, fibres, envelope
64
Specific regions on antigens where antibodies bind to
epitopes
65
protein antigens
are generally more potent
66
carbohydrate antigens
can only stimulate the humoral immune defense
67
lipid and DNA antigens
least antigenic
68
antibodies are also called
immunoglobulins and are produced by the immune system to target antigens
69
5 classes of antibodies
IgG, IgM, IgA, IgD, IgE
70
most abundant in the body
IgG
71
found in respiratory secretions
IgA
72
aids in allergic responses and defense against parasites
IgE
73
cellular immunity involves
T cells & main target is to kill infected body cells and to boost the overall immune response
74
humoral immunity involves
B cells & main target is to kill extracellular antigens
75
describe how a T cell library is formed
hematopoietic (stem) cells are formed in bone marrow
half of these will migrate to the thymus and eventually become naive T cells
76
naive helper T cells contain
T-cell receptor (TCR) capable of binding to a specific epitope & CD4 co-receptor
77
naive cytotoxic T cells contain
T cell receptor capable of binding to a specific epitope & CD8 co-receptor
78
activation of helper T cells
1. pathogen/antigen is phagocytosed by a
phagocyte (macrophage or dendritic cell)'
2. Inside the macrophage, a protein complex called
MHC-II combines with the antigens
3. The MHC-II combined with the antigens are then
presents on the plasma membrane
4.The macrophage is now called an antigen-presenting cell (APC)
5. The corresponding TCR on a naïve helper
T cell binds to the displayed antigen,
partially activating the naïve helper T cell
6. The CD4 co-receptor on the naïve helper T
cell also binds to the displayed antigen to
anchor the TCR-antigen complex
7. The APC releases cytokines which further
activates the naïve helper T cell
8. Once activated, the naïve helper T cell will
proliferate through mitosis and then differentiate into different types of cells (3)
79
memory T cells
```
function to remember the antigen. Should the antigen be
encountered again, these cells will rapidly switch to cytotoxic T cells
```
80
T helper 1 (TH1)
stimulate other cells in the immune response
81
T helper 2 (TH2)
function to stimulate the humoral immunity
82
Cytotoxic T cells are activated
in the same way as helper T cells, with a few key
differences:
o Recognition of antigens are presented on MHC-I, not MHC-II
Anchoring is done by a CD8
co-receptor
Naïve cytotoxic T cells differentiate
into effector cytotoxic T cells
o Assistance from cytokines secreted
by TH1 cells leads to
longer-lasting effects
83
Once activated, effector cytotoxic T cells will release:
o perforin to create pores in the target cell
o granzymes, which are proteases, which will enter the
pores and induce programmed cell death (apoptosis)
84
describe how a B cell library is formed
• Hematopoietic (stem) cells are formed in the bone marrow
• Half of these cells remain in the bone marrow and eventually become B cells
o Each B cell is coated with IgM antibodies, capable of binding to a single epitope
85
T-dependent B cell activation
1. The IgM antibodies of an
inactive B cell binds to a
foreign antigen
2. The IgM-antigen complex is
then internalized into the
inactive B cell
3. Inside the B cell, the antigen is combined with MHC-II and the antigen is then presented onto the B cell plasma membrane
4. The B cell becomes an antigen-presenting cell (APC)
5. A corresponding TH2 cell
(previously activated in cellular
immunity) binds to the presented antigen
6. After binding, the TH2 cell releases cytokines which activates the B cell
7. Once activated, the B cell will proliferate through mitosis and then differentiate into
different types of cells (2)
86
plasma cells . . .
which secrete IgM antibodies initially, and later secrete
| the longer-lasting IgG antibodies
87
memory B cells
which remember the antigen. Should the antigen be
| encountered again, these cells will rapidly switch to plasma cells to secrete antibodies
88
T-dependent B cell activation is a
longer-lasting and leads to memory
89
T-independent B cell activation
1. This usually occurs with T-independent antigens (e.g.
carbohydrate) which are sufficient to provide the first signal for activation
2. The B cell is directly activated through binding of
the IgM antibody to the foreign antigen
3. Once activated, the B cell will proliferate through mitosis, and then differentiate into plasma cells, which secrete IgM antibodies; no memory cells are made
• This response is short -lived and requires boosting from
innate immunity pathways such as the complement pathway
90
neutralization
the binding of antibodies to epitopes to prevent attachment to cells
91
opsonization
the coating of a pathogen to enhance phagocytosis
92
agglutination
the cross-linking of antigens to create large clumps
93
complement
activation of the complement cascade
94
antibody-dependent cell-mediated cytotoxicity
enhanced killing of pathogens that are too large to be phagocytosed
95
active, natural immunity
immunity gained from illness and recovery
96
active, artificial immunity
vaccination
97
passive, natural immunity
antibodies passed through breast milk or placenta
98
passive, artificial immunity
transfer of antibodies harvested from an individual or animal
99
describe the function of vaccinations
The deliberate exposure of a person to an antigen to trigger a primary response without the person feeling the effects of the pathogen
• Therefore, when they actually encounter the pathogen, a secondary response occurs
100
herd immunity is
when there are too few susceptible individuals for a disease to spread effectively
• This can be done by vaccination programs to reduce the number of susceptible individuals
• Susceptible individuals cannot be vaccinated for a variety of reasons, such as too young or allergic to a vaccine
ingredient
101
live, but attenuated (weakened) organisms vaccine
* Can still replicate, meaning boosters are not needed
* Increased challenges for storage and transport
* Example: chickenpox
102
inactivated, dead organisms vaccine
• No risk of severe infections, but boosters are often needed
• Useful for vaccination programs for developing countries (easy to store and
administer)
• Example: influenza, hepatitis A vaccine
103
subunit vaccines
contains only the key antigens of a pathogen
* Produced through genetic engineering or isolation from a degraded pathogen
* No protection against antigenic variation
* Example: hepatitis B, HPV
104
toxoid vaccines
contains inactivated toxins; pathogens themselves are not included
* Least amount of side effects, but does not prevent infection by pathogen
* Example: botulism, tetanus, pertussis
105
conjugate vaccines
synthetic vaccines that combine carbohydrate antigens with larger
proteins to stimulate both cellular and humoral immunity
* More expensive to produce
* Example: meningitis
106
nucleic acid vaccines
nucleic acid is injected; cells take up the nucleic acid and
use it as a template to make protein antigens
example: west nile vaccine (horses), covid-19 (pfizer, moderna)
