Immunology I Flashcards
(125 cards)
1
Q
antigens
A
anything that causes an immune response
can be a bacteria virus, fungi, parasite, or a smaller protein they express
these are also known as pathogens
2
Q
how are a pathogen’s presence announced to the immune system
A
antigens, act as name tags
3
Q
are antigens specific or general
A
they can be both, they are general ones that say danger, but there are other that tell what it is and what it will do
4
Q
what is an antibody
A
immunoglobulin or Lg is protein molecule created by our immune system to to target an antigen for destruction
5
Q
how do antibodies worl
A
the proteins bing to the foreign antigen and disable the anti, tagging it for destruction by the other immune system defenses
6
Q
cytokines
A
cell to cell communication proteins that control cell development differentiation and movement to a specific part of the body
7
Q
how are cytokines produced
A
a variety of leukocytes
8
Q
interleukins
A
(IL) are 13 cytokines that are regulators of the immune responses inflammatory reactions and hematopoiesis
9
Q
which IL’s are responsible for fever
A
1 and 6
10
Q
what causes the acute phase response
A
IL 6 causes acute phase responses
11
Q
tumor necrosis factor
A
activates neutrophils
mediates septic shock and causes tumor necrosis
12
Q
chemokine s
A
`type of cytokine released by infected and injured cells, they initiate an immune response
and signals to circulating neutrophils and macrophages
13
Q
which cells are responsible for warning neighboring cells of a threat
A
chemokine
14
Q
interferons
A
IFN block virus replication 3 types alpha beta and gamma
15
Q
gamma interferons
A
are the strongest type of interferon and are produced by the T cells
they activate macrophages natural killer cells and neutrophils
16
Q
what cells do gamma interferons activate
A
macrophages, NKC, and neutrophils
17
Q
classifying interferons
A
2 types, type one and two
type one are alpha and beta
type two is gamma
18
Q
Type I Interferons
A
function to induce viral resistance in cells, can be produced by almost any cell type in the body can at times under some circumstances suppress the T cell responses and memory T cells
19
Q
Type I cells in influenza
A
limit viral replication but create pathological inflammation in the lung
20
Q
type I cells and bacteria
A
may interfere with bactericidal mechanisms
21
Q
type II Interferons
A
secreted only by NTC and T lymphocytes
main purpose is to signal to the the immune system to respond to infectious agents or cancerous growths
22
Q
basic roles of the immune system
A
barrier, recognition of foreign none self and mutated cells, and destruction through processes such as phagocytosis
23
Q
the two branches of the immune system
A
innate and adaptive, however cross over occurs between the two functions of both of these branches
24
Q
Innate immune branch
A
considered natural and non specific
acts fast
25
adaptive immune system
considered specific, humoral, and cell mediated
| acts slow
26
hematopoiesis
the formation and development of cells that make up the blood
in an embryo and fetus this occurs mainly in the liver and spleen
birth to adult hematopoiesis occurs primarily in bone marrow small amount in lymphatic tissues
27
innate immunity characteristics
immediate, non specific response so there is no stored memory (a lot of cells will die anyways) and one response does not increase the next response, or no greater responses occur with repeated exposure
28
skin
physical barrier, protects against invasion, the acidic of sweat acts as barrier, fattry acids and enzymes form pores and follicles
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lysoymes
contain lysozyme thigh protects against gram + bacteria
30
commensal bacteria
physical barrier, out normal bacteria flora, both internal and external that will compete with potential pathogens for resources, however they can be upset by antibiotic use leading to reduced concentration greater opportunities for pathogens to use resources
31
inflammation
damaged tissues and cells release histamine, prostaglandin and leukotriene which causes vasodilation and leaky capillaries
there is also cell mediated heparin realize which decreases clotting
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heparin
reduces clotting
33
result of inflammation
Increased blood flow to area, immunologic factors leak out of capillaries into interstitial space to do their jobs
34
first step of inflammation response
damaged tissues release histamine, increasing blood flow to the area (redness)
35
second step of inflammation response
histamine = leaky capillaries releasing in the release of phagocytes and clotting factors into the wound
36
third step of inflammation response
the phagocytes engulf bacteria dead cells and cellular debris
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fourth step of inflammation response
plates move out of the capillaries to seal off the wound
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adhesion molecules in the inflammation process
membrane proteins that connect cells to other cells to the ECM
their major role is the recruitment of neutrophils to the site of inflammation
39
how do neutrophils come to the site of inflammation
are recruited by adhesion molecules and roll along the luminal surface of blood vessels towards the site of injury and then will squeeze out of leaky capillaries (between the cells of capillary walls)
40
describe chronic inflammation
cause a chronic release of cytokine and leukocyte infiltration and the release of lysozyme and free radicals which cause an overall tissue damage
41
what are possible complications of mutations in the adhesion molecules
atherosclerosis in the macular system, skin and kidney issues muscles, alzhemiers and autism (chronic inflammationP
42
basophils
granulocytes are the least common and mature in the bone marrow
circulate the blood stream
cause allergic and helmet responses
release histamine (increase blood flow) and heparin (reduce clotting)
43
eosinophils
derived from the bone marrow (1-6% CWBC)
are weakly phagocytic
and act as an APC
44
eosinophils location
in organs and bloodstream particularly the GI tract and respiratory tract
45
what do eosinophils release
release H202 and other oxygen radicals to kill microbes such as viruses and parasites
and leukotrienes
46
what may kill off a helminth
eosinophil by releasing h202 and oxygen radicals
47
what does the release of leukotrienes stimulate
cause smooth airway smooth muscle contraction
| this is a lipid signaling molecule
48
when are eosinophils active
allergic reactions
49
what cells do eosinophils stimulate
T lymphocytes
50
neutrophils
granulocytes
most abundant of the. granulocytes
circulate the bloodstream
51
when are neutrophils primary active
bacteria and fungi defense
52
neutrophil mechanism
arrive within minutes
| strongly phagocytic
53
how are neutrophils called to cite of injury
chemotaxis, respond to chemokins
| neutrophils release other cytokines to recruit monocytes and macrophages
54
what are neutrophil extracellular traps
extracellular fibers released bu neutrophils that bind bacteria
55
mast cells
release histamine and heparin causing again the inflammatory cascade
56
mast cell maturation
leave the bone marrow as immature cells and mature in tissues
mainly present in issues that lie on boundaries
57
why do mass cell degranulate (and release histamine)
if they are injured
encounters antigen or allergen
exposed to complement proteins
58
anaphylaxis
massive release of histamine by mast cells vasodilation is body wide and leads to edema and decreased blood pressure
59
how are RBCs and PLYS derives
from the myeloid stem cell
60
monocytes
agranular
give rise to dendritic cells and macrophages
first developed int the bone marrow and the half are stored in the spleen and the other half migrate to tissues and differentiate into dendritic cells and macrophages
61
Monos, Macros and Dendros 3 primary functions
phagocytosis, APC, cytokine production
62
Dendritic Cells
aganular derived from monocyte
| Antigens are captured by dendritic cells
63
what is the strongest APC
Dendritic cells best at activating helper-T lymphocytes
after finding antigen dendritic cell then migrates to the nearest lymph node & presents the antigen to T Cells and B Cells
64
langerhans cells
Specialized dendritic cells in skin
initial cellular targets in the sexual transmission of HIV,[8] and may be a target, reservoir, and vector of dissemination
65
macrophages
aganular derived from monocyte
Large phagocytes
release TNF and Interleukins (ILs)
Also act as APCs
66
macrophages location
the skin, lungs, GI tract and most other tissues
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3 stages od macrophages
1) resting = cleaning up cellular debris (scavengers)
b) primed = more active engulfing of bacteria, display fragments of bacteria for T cells (act as APCs)
c) hyper-activated = inflammatory cytokines cause macrophages to enlarge and start rapidly destroying pathogens and/or cancerous cells
68
After digesting a pathogen, a macrophage will
present the antigen to a helper T cell
this occurs because
Antigen is integrated it into the cell membrane and displayed attached to an MHC class II molecule (MHCII)
The MHCII indicates to other white blood cells that the macrophage is not a pathogen, despite having antigens on its surface
69
Kupffer cells
Specialized macrophages within the liver
| Destroy bacteria & old RBCs
70
Chronic activation of Kupffer cells
leads to overproduction of inflammatory cytokines & chronic inflammation
this happens through repeated exposure to toxins and alcohol
result is liver damage
71
macrophages and pathogens
phagocytes, macrophages may become hosts for pathogens!
| for example with TB, leishmaniasis and cikigunya
72
Natural Killer Cells
cytotoxic lymphocytes, but don’t need to “recognize” or remember a pathogen to kill it
killing enhanced by cytokines secreted by macrophages, can still kill in resting state
bloodstream, liver and spleen
73
Natural Killer Cells active on
cancer and viruses
| and cells that have unusual surfaces receptors
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Natural Killer Cells granules
contain destructive enzymes
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Natural Killer Cells maturation
mature in bone marrow lymph nodes spleen tonsils and thymus
76
how do Natural Killer Cells kill
releasing performs and proteases that cell cell membrane lysis or trigger apoptosis in the target cell
can also be accomplished by surface contact
77
Natural Killer Cells and viral infections
contain the viral infections while the adaptive immune response is generating antigen specific cytotoxic T cells (takes time) that will work to clear the infection
78
Major Histocompatibility Complex (MHC) Proteins/ Human Leukocyte Antigen (HLA)
Cell surface molecules which help the immune system to determine if a protein is “self” or “not-self”
Bind antigen to cell surface and display for recognition by T cells
3 sub-groups: MHC I,II & III
79
MHC key points
Determines organ donation compatibility
Autoimmune disease is a malfunction in this recognition system
Participates in T & B cell activation
80
how are Acute phase proteins produced
produced by the liver in response to inflammation induced release of IL 1 and IL6 and TNF from the T cells and macrophages
81
what are the Acute phase proteins
C-reactive protein (CRP)
mannose binding lectin (MBL)
lipopolysaccharide -binding protein
82
Acute phase proteins role
mark pathogens or injured cells for destruction
83
CRP example
CRP binds to bacterial and fungal cell walls and damaged or dead human cells, then activates complement
84
The Complement System
enhances the ability of phagocytic cells to destroy pathogens
comprised of 30 different proteins working together to signal the other cells that a pathogen is present and they have begun destroying it
85
The Complement System is activated. by
antigens
86
The Complement System are made in the
liver
87
The Complement System activation pathways
3 possible
Classical (requires triggering)
Alternative (continuously activated at low level)
Lectin Pathway (requires very specific type of triggering)
88
the most abundant complement protein in humans
c3
89
functions of complement
opsonization, chemotaxis and lysis
90
opsonization
enhancing phagocytosis of antigens by ‘marking’ them for destruction
91
Chemotaxis
attracting and activating macrophages and neutrophils; inducing mast cells & basophils to degranulate
92
Lysis
rupturing pathogen cell-membranes by forming the Membrane Attack Complex (MAC)
93
Complement Fixation
antigen combines with an antibody and its complement, causing the complement factor to become inactive or fixed exposing the patient's serum to antigen, complement, and specially sensitized red blood cells.
94
Complement-fixation tests can be used to detect
antibodies for infectious diseases, especially syphilis and viral illnesses
95
MAC
Membrane Attack Complex
C5b forms a complex with c6 c7 c8 and c9 to form MAC
causes lysis of cell by disturbing osmotic balance
more concentrated within the cell so microbe will swell and burst
96
antibodies
recognizes only one nation and bind to a specific site on the invader
97
how do antibodies function
directly blocking binding of invader to the cell
inactivate viruses and neutralize the toxin
mark the pathogen for destruction by phagocytes called opsonization
98
antibody structure
2 light chain 2 heavy changes
antigen binding site
fab legion and fc region
99
Fab region
antigen specific variable
100
Fc region
constance class effect
101
IgM
big first class to be produced
half life 10 days
increase Igm is a recent exposure to antigen
102
IgM location
because it is Large molecule- usually confined to intravascular space but inflammations opens capillaries and also entrance of Igm to interstitial space
103
igG
```
4 subclass
only class that crosses the placenta
longest half life 23 days
use it for passive immunity in rabies and hepatitis
```
104
IgG location
blood lymph CSF and peritoneal fluid
| evenly distributed in the intra and extra vascular space
105
IgG placenta
passes mothers immunity to child
bad if the mom forms IgG against fetal antigens
difficult to use IgG as an indicator of infection in the baby
106
IgG functions
helps natural killer cells find their targets through opsonization
immobilizes bacteria by binding to cilia
activates complement
neutralizes toxins and viruses through binding
107
polyclonal antibodes
Prepared from immunized animals
| Each Ab can interact/bind with multiple sites on an antigen (human antigens can only interact with one )
108
monoclonal antibodies
Produced in the lab
| Bind only to one site on an antigen
109
IgA locaion
external secretions
| mucus tears salvia gastric fluids colostrum (first breast milk) and sweat
110
IgA function
protect of infants through breast milk
prevents viruses from entering the cells
prevent pathogens from attaching to and penetrating epithelial surfaces
high function in respiratory and GI tracts
111
IgE
present in low amounts
2 day half life
bind to mast cells and basophils when it discovers and antigen and trigger degranulation which releases mistime and leukotriene
and heparin from granulocytes
112
when is IgE increased
atopic (hyper allergic) individuals and in the presence of parasites
113
IgD location
surface of naive B cells
| present in low amounts in the serum
114
IgD function
unknown
115
components of adaptive immune system cell mediated
T-cells
| B-cells
116
components of adaptive immune system
```
T-cells
B-cells
Antibodies
Complement
APCs
```
117
adaptive immune system
requires days to develop
specific to an antigen
response is enhanced through repeated exposure
develops a memory that is more rapid and intense in its immune response
118
primary Lymphoid Organs
where the lympocycces grow up and proliferate
thymus (T cell in children)
and bone marrow
119
Secondary Lymphoid Organs
Where antigens are presented to mature (but naïve) B & T lymphocytes to initiate the adaptive immune response
spleen lymph nodes tonsils and adenoids and appendix
120
B-Cells (B-lymphocytes)
eliminate extracelular pathgens
is an APC with MHC
will produce antibodies
Has membrane-bound antibodies
Recognition of antigen by the B-cell receptor coupled with a signal from “Helper” T-cells (CD-4), prompts the B-cell to divide into “clones”
some of these are effector cells produce antibodies
others are memory B cells
121
T-Cells (T-lymphocytes)
destroy the intracellular patens viruses and intracellular bacteria
has subtypes
122
Killer” T-cells (CD-8)
T-Cell T-lymphocytes)
cytotoxic
specialize in identifying and killing cells infected with virus
123
Helper T cells (CD4)
Does not directly kill pathogens- raises the “alarm” via cytokines
Assists in the activation of “killer” T-cells
Signal B cells to begin secreting antibodies (Ig)
Activated cell differentiates into effector cells & memory cells
124
acquired immunodeficiencies
medications (steroids, chemotherapy), malnutrition, splenectomy (or functional asplenia), some cancers, AIDS
125
congenital or primary immunodeficiencies
autosomal recessive or X-linked, impaired or absent granulocyte, complement or lymphocyte production. May be an immunoproliferative disorder
