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foundations. exam 2 > Immunology I > Flashcards

Immunology I Flashcards

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

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2
Q

how are a pathogen’s presence announced to the immune system

A

antigens, act as name tags

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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

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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

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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

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6
Q

cytokines

A

cell to cell communication proteins that control cell development differentiation and movement to a specific part of the body

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7
Q

how are cytokines produced

A

a variety of leukocytes

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8
Q

interleukins

A

(IL) are 13 cytokines that are regulators of the immune responses inflammatory reactions and hematopoiesis

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9
Q

which IL’s are responsible for fever

A

1 and 6

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10
Q

what causes the acute phase response

A

IL 6 causes acute phase responses

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11
Q

tumor necrosis factor

A

activates neutrophils

mediates septic shock and causes tumor necrosis

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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

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13
Q

which cells are responsible for warning neighboring cells of a threat

A

chemokine

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14
Q

interferons

A

IFN block virus replication 3 types alpha beta and gamma

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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

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16
Q

what cells do gamma interferons activate

A

macrophages, NKC, and neutrophils

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17
Q

classifying interferons

A

2 types, type one and two
type one are alpha and beta
type two is gamma

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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
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19
Q

Type I cells in influenza

A

limit viral replication but create pathological inflammation in the lung

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20
Q

type I cells and bacteria

A

may interfere with bactericidal mechanisms

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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

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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

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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

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24
Q

Innate immune branch

A

considered natural and non specific

acts fast

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25
Q

adaptive immune system

A

considered specific, humoral, and cell mediated

acts slow

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26
Q

hematopoiesis

A

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

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27
Q

innate immunity characteristics

A

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

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28
Q

skin

A

physical barrier, protects against invasion, the acidic of sweat acts as barrier, fattry acids and enzymes form pores and follicles

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29
Q

lysoymes

A

contain lysozyme thigh protects against gram + bacteria

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30
Q

commensal bacteria

A

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

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31
Q

inflammation

A

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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32
Q

heparin

A

reduces clotting

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33
Q

result of inflammation

A

Increased blood flow to area, immunologic factors leak out of capillaries into interstitial space to do their jobs

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34
Q

first step of inflammation response

A

damaged tissues release histamine, increasing blood flow to the area (redness)

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35
Q

second step of inflammation response

A

histamine = leaky capillaries releasing in the release of phagocytes and clotting factors into the wound

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36
Q

third step of inflammation response

A

the phagocytes engulf bacteria dead cells and cellular debris

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37
Q

fourth step of inflammation response

A

plates move out of the capillaries to seal off the wound

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38
Q

adhesion molecules in the inflammation process

A

membrane proteins that connect cells to other cells to the ECM
their major role is the recruitment of neutrophils to the site of inflammation

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39
Q

how do neutrophils come to the site of inflammation

A

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)

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40
Q

describe chronic inflammation

A

cause a chronic release of cytokine and leukocyte infiltration and the release of lysozyme and free radicals which cause an overall tissue damage

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41
Q

what are possible complications of mutations in the adhesion molecules

A

atherosclerosis in the macular system, skin and kidney issues muscles, alzhemiers and autism (chronic inflammationP

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42
Q

basophils

A

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)

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43
Q

eosinophils

A

derived from the bone marrow (1-6% CWBC)
are weakly phagocytic
and act as an APC

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44
Q

eosinophils location

A

in organs and bloodstream particularly the GI tract and respiratory tract

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45
Q

what do eosinophils release

A

release H202 and other oxygen radicals to kill microbes such as viruses and parasites
and leukotrienes

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46
Q

what may kill off a helminth

A

eosinophil by releasing h202 and oxygen radicals

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47
Q

what does the release of leukotrienes stimulate

A

cause smooth airway smooth muscle contraction

this is a lipid signaling molecule

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48
Q

when are eosinophils active

A

allergic reactions

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49
Q

what cells do eosinophils stimulate

A

T lymphocytes

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50
Q

neutrophils

A

granulocytes
most abundant of the. granulocytes
circulate the bloodstream

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51
Q

when are neutrophils primary active

A

bacteria and fungi defense

52
Q

neutrophil mechanism

A

arrive within minutes

strongly phagocytic

53
Q

how are neutrophils called to cite of injury

A

chemotaxis, respond to chemokins

neutrophils release other cytokines to recruit monocytes and macrophages

54
Q

what are neutrophil extracellular traps

A

extracellular fibers released bu neutrophils that bind bacteria

55
Q

mast cells

A

release histamine and heparin causing again the inflammatory cascade

56
Q

mast cell maturation

A

leave the bone marrow as immature cells and mature in tissues
mainly present in issues that lie on boundaries

57
Q

why do mass cell degranulate (and release histamine)

A

if they are injured
encounters antigen or allergen
exposed to complement proteins

58
Q

anaphylaxis

A

massive release of histamine by mast cells vasodilation is body wide and leads to edema and decreased blood pressure

59
Q

how are RBCs and PLYS derives

A

from the myeloid stem cell

60
Q

monocytes

A

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
Q

Monos, Macros and Dendros 3 primary functions

A

phagocytosis, APC, cytokine production

62
Q

Dendritic Cells

A

aganular derived from monocyte

Antigens are captured by dendritic cells

63
Q

what is the strongest APC

A

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
Q

langerhans cells

A

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
Q

macrophages

A

aganular derived from monocyte
Large phagocytes
release TNF and Interleukins (ILs)
Also act as APCs

66
Q

macrophages location

A

the skin, lungs, GI tract and most other tissues

67
Q

3 stages od macrophages

A

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
Q

After digesting a pathogen, a macrophage will

A

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
Q

Kupffer cells

A

Specialized macrophages within the liver

Destroy bacteria & old RBCs

70
Q

Chronic activation of Kupffer cells

A

leads to overproduction of inflammatory cytokines & chronic inflammation
this happens through repeated exposure to toxins and alcohol
result is liver damage

71
Q

macrophages and pathogens

A

phagocytes, macrophages may become hosts for pathogens!

for example with TB, leishmaniasis and cikigunya

72
Q

Natural Killer Cells

A

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
Q

Natural Killer Cells active on

A

cancer and viruses

and cells that have unusual surfaces receptors

74
Q

Natural Killer Cells granules

A

contain destructive enzymes

75
Q

Natural Killer Cells maturation

A

mature in bone marrow lymph nodes spleen tonsils and thymus

76
Q

how do Natural Killer Cells kill

A

releasing performs and proteases that cell cell membrane lysis or trigger apoptosis in the target cell
can also be accomplished by surface contact

77
Q

Natural Killer Cells and viral infections

A

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
Q

Major Histocompatibility Complex (MHC) Proteins/ Human Leukocyte Antigen (HLA)

A

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
Q

MHC key points

A

Determines organ donation compatibility
Autoimmune disease is a malfunction in this recognition system
Participates in T & B cell activation

80
Q

how are Acute phase proteins produced

A

produced by the liver in response to inflammation induced release of IL 1 and IL6 and TNF from the T cells and macrophages

81
Q

what are the Acute phase proteins

A

C-reactive protein (CRP)
mannose binding lectin (MBL)
lipopolysaccharide -binding protein

82
Q

Acute phase proteins role

A

mark pathogens or injured cells for destruction

83
Q

CRP example

A

CRP binds to bacterial and fungal cell walls and damaged or dead human cells, then activates complement

84
Q

The Complement System

A

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
Q

The Complement System is activated. by

A

antigens

86
Q

The Complement System are made in the

A

liver

87
Q

The Complement System activation pathways

A

3 possible
Classical (requires triggering)
Alternative (continuously activated at low level)
Lectin Pathway (requires very specific type of triggering)

88
Q

the most abundant complement protein in humans

A

c3

89
Q

functions of complement

A

opsonization, chemotaxis and lysis

90
Q

opsonization

A

enhancing phagocytosis of antigens by ‘marking’ them for destruction

91
Q

Chemotaxis

A

attracting and activating macrophages and neutrophils; inducing mast cells & basophils to degranulate

92
Q

Lysis

A

rupturing pathogen cell-membranes by forming the Membrane Attack Complex (MAC)

93
Q

Complement Fixation

A

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
Q

Complement-fixation tests can be used to detect

A

antibodies for infectious diseases, especially syphilis and viral illnesses

95
Q

MAC

A

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
Q

antibodies

A

recognizes only one nation and bind to a specific site on the invader

97
Q

how do antibodies function

A

directly blocking binding of invader to the cell
inactivate viruses and neutralize the toxin
mark the pathogen for destruction by phagocytes called opsonization

98
Q

antibody structure

A

2 light chain 2 heavy changes
antigen binding site
fab legion and fc region

99
Q

Fab region

A

antigen specific variable

100
Q

Fc region

A

constance class effect

101
Q

IgM

A

big first class to be produced
half life 10 days
increase Igm is a recent exposure to antigen

102
Q

IgM location

A

because it is Large molecule- usually confined to intravascular space but inflammations opens capillaries and also entrance of Igm to interstitial space

103
Q

igG

A 
4 subclass 
only class that crosses the placenta 
longest half life 23 days 
use it for passive immunity in rabies and hepatitis
104
Q

IgG location

A

blood lymph CSF and peritoneal fluid

evenly distributed in the intra and extra vascular space

105
Q

IgG placenta

A

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
Q

IgG functions

A

helps natural killer cells find their targets through opsonization
immobilizes bacteria by binding to cilia
activates complement
neutralizes toxins and viruses through binding

107
Q

polyclonal antibodes

A

Prepared from immunized animals

Each Ab can interact/bind with multiple sites on an antigen (human antigens can only interact with one )

108
Q

monoclonal antibodies

A

Produced in the lab

Bind only to one site on an antigen

109
Q

IgA locaion

A

external secretions

mucus tears salvia gastric fluids colostrum (first breast milk) and sweat

110
Q

IgA function

A

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
Q

IgE

A

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
Q

when is IgE increased

A

atopic (hyper allergic) individuals and in the presence of parasites

113
Q

IgD location

A

surface of naive B cells

present in low amounts in the serum

114
Q

IgD function

A

unknown

115
Q

components of adaptive immune system cell mediated

A

T-cells

B-cells

116
Q

components of adaptive immune system

A 
T-cells
B-cells
Antibodies
Complement
APCs
117
Q

adaptive immune system

A

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
Q

primary Lymphoid Organs

A

where the lympocycces grow up and proliferate
thymus (T cell in children)
and bone marrow

119
Q

Secondary Lymphoid Organs

A

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
Q

B-Cells (B-lymphocytes)

A

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
Q

T-Cells (T-lymphocytes)

A

destroy the intracellular patens viruses and intracellular bacteria
has subtypes

122
Q

Killer” T-cells (CD-8)

A

T-Cell T-lymphocytes)
cytotoxic
specialize in identifying and killing cells infected with virus

123
Q

Helper T cells (CD4)

A

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
Q

acquired immunodeficiencies

A

medications (steroids, chemotherapy), malnutrition, splenectomy (or functional asplenia), some cancers, AIDS

125
Q

congenital or primary immunodeficiencies

A

autosomal recessive or X-linked, impaired or absent granulocyte, complement or lymphocyte production. May be an immunoproliferative disorder

foundations. exam 2 (10 decks)

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