Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

immunology > exam 1 > Flashcards

exam 1 Flashcards

1
Q

immunity

A

resistance to disease, being immune/insusceptible to a disease, ability of cell to react immunologically in presence of antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

mechanisms that ensure freedom from invasion

A
  • physical barriers
  • innate immunity
  • adaptive immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

cell- mediated immunity

A
  • mainly directed against viruses

- employs cells that destroy abnormal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hematopoiesis

A
  • production of immune cells, red blood cells, and platelets
  • produces 10^11 to 10^12 cells per day
  • produces three major lineages: erythroid, myeloid, lymphoid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

erythroid lineage

A

erythrocytes and platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

myeloid lineage

A

granulocytes (neutrophils, eosinophils, basophils), mast cells, monocytes, macrophages, myeloid dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

lymphoid lineage

A

lymphocytes T and B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hematopoietic growth factors

A
  • colony stimulating factors (CSF’s)- granulocyte-monocyte CSF , granulocyte CSF
  • interleukins: IL-1, IL-3, IL-4, IL-5, IL-6, IL-7
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

eosinophil production

A

-IL-5, IL-3, GM-CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

neutrophil production

A

-G-CSF, GM-CSF, IL-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

monocyte production

A

M-CSF, GM-CSF, IL-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

basophil production and mast cell differentiation

A

IL-4, IL-9, GM-CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

neutrophil function

A

-antimicrobial effectors, particularly in acute bacterial infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

eosinophil function

A

-antiparasitic effectors, particularly in helminthic infection, some antiviral action, roles in allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

basophil function

A

-mediator of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

monocyte functions

A

-precursor of macrophages and DCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

macrophage function

A

immune surveillance, moderate antimicrobial capacity, limited antigen presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

dendritic cell function

A

immune surveillance, antigen processing and presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

mast cell function

A

-immune surveillance, mediator and amplifier of inflammation and allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

NK cell function

A

destruction of virally infected or abnormal host cells (including tumor cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

lymphocytes

A
  • only cells in body capable of specifically recognizing and distinguishing different antigens
  • adaptive immune response, specificity, memory
  • different subsets, morphologically the same
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

B lymphocytes

A
  • recognize extracellular antigens
  • produce antibodies
  • differentiate in plasma cells
  • humoral immune response
  • mature in bursa of fabricius- birds
  • mammals mature in bone marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

T-lymphocytes

A
  • recognize intracellular antigens
  • do not produce antibodies
  • produce cytokines
  • differentiate into several types of lymphocytes
  • cellular immune response
  • precursors come from bone marrow
  • mature in thymus
  • thymus derived lymphocytes
  • subsets: helper T lymphocytes, cytotoxic lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

canine trapped neutrophil syndrome

A

-develop neutropenia (low number of neutrophils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Development of mature T cells

A
  • T cells mature in thymus
  • if self-reactive killed before leaving primary lymphoid organs
  • leave primary lymphoid organs to reside in secondary lymphoid organs where they encounter and respond to foreign Ags
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Development of mature B cells

A
  • B cells mature withine GI lymphoid tissues, bone marrow, or bursa of Fabricius
  • if self- reactive, killed before leaving primary lymphoid organs
  • leave primary lymphoid organs to reside in secondary lymphoid organs where they encounter and respond to foreign Ags
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

major secondary lymphoid organs

A

-lymph nodes, spleen, bone marrow, Peyer’s patches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

conduits

A
  • secondary lymphoid tissue
  • conduits consist of loosely attached fibroreticular cells surrounding collagen bundles
  • dendritic cell processes can reach into the conduits to sample their antigen content
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

mucosa-associated lymphoid tissue

A
  • gastrointestinal (GALT)
  • bronchial (BALT)
  • nasal (NALT)
  • conujunctiva (CALT)
  • skin (SALT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

innate immunity

A
  • immune response is not dependent on antigen
  • immune response immediate
  • no memory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

adaptive immunity

A
  • immune response Ag-specific
  • immune response delayed in time
  • memory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

mechanical barrier - innate immunity

A
  • physical barrier
  • skin
  • ciliary movement in epithelium of respiratory tract
  • peristaltic movement in intestinal tract
  • washing effect by tears or saliva
  • dense mucus layer in vagina, digestive tract, and respiratory tract

-defend body by mechanically removing infectious microorganisms and preventing entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

chemical barriers- innate immunity

A
  • physical barrier
  • fatty acids- inhibit bacteria growth
  • lysozyme and phospholipase- inhibit growth of infectious agents
  • low pH of sweat and gastric juices= antibacterial effect
  • surfactants in lungs enhance phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

microbiological factors- innate immunity

A
  • physical barrier
  • normal biota on the skin and digestive tract prevents infection by secretion of inhibitory agents that prevent colonization and growth of infectious microorganisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

humoral barriers of innate immunity

A
  • complement system
  • coagulative system
  • lactoferin and transferin
  • lysozyme
  • interferons
  • interleukin 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

complement system

A

-group of proteins found in serum that prevent infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

coagulative system

A
  • may be activated or not
  • leads to blood coagulation at site of damage, prevents entry of infectious agents
  • some molecules of coagulative system may act as chemotactic factors
  • beta-lysine has bactericidal effects against gram positive bacteria during coagulation process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

lactoferin/transferin

A

-bind iron so bacteria cannot grow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

lysozyme

A

-digests bacterial cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

interferons

A

-inhibit infection and replication of viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

interleukin-1

A

responsible for increase of temp during inflammation and induces acute phase proteins which are bactericidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

cellular barriers of innate immune system

A
  • neutrophils
  • macrophages
  • NK cells and LAK cells
  • eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

neutrophils

A

phagocytose microorganisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

macrophages

A
  • differentiate from monocytes and function as phagocytes
  • ingest and kill microorganisms intracellularly
  • may phagocytose and kill infected cells
  • may act as APCs
  • participate in wound healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

NK/ LAK cells

A

kill infected or tumor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

eosinophils

A

-participate in eliminating parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

neutrofile

A
  • CD66 on cell surface

- two types of granules with molecules for intracellular killing: azurophilic granules, secondary granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

azurophilic granules

A

contain:

  • defensins to kill bacteria
  • proteolytic enzymes such as elastase, catepsin G which degrade bacterial protiens
  • lysozyme- degrades bacterial cell wall
  • myeloperoxidase- generation of bactericidal substances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

secondary granules

A
  • found only in mature cells contain:
  • lysozyme
  • lactoferin
  • components of NADPH oxidase to produce toxic radicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

macrophages

A
  • identified by expression of CD14, CD11b, or F4/80
  • have lysosomes that participate in intracellular killing
  • react to danger signals (SOS) at sites of pathogen entry: N-formyl methionine, peptides, complement, cytokines which induce chemotaxis of macrophages towards site of microbe entry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Fc receptors

A
  • on macrophages
  • antibodies bound to antigens expose Fc ends
  • Fc ends of antibody used to bind Fc receptors on phagocyte
  • phagocyte binding of Fc end of antibody that is bound to surface of microorganism enhances metabolic activity of phagocyte
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

complement component receptors

A
  • posses receptors for C3b complement component

- C3b binds antigen, later it binds to its receptor on phagocyte which leads to activation of phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

phagocytosis

A

active process of capturing and ingesting foreign objects/ microorganisms by phagocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

purpose of phagocytosis

A
  • detect and destroy microbes
  • remove damaged cells and foreign objects
  • produce cytokines required for development of inflammatory reaction
  • process and present antigens required to induce immune response by lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

steps of phagocytosis

A
  1. chemotaxis- phagocytes move towards target
  2. phagocytes detect target
  3. surround captured object and engulf through endocytosis
  4. endocytosed object enclosed in phagosome
  5. phagosome fuses with lysosome- forms phagolysosome
  6. contents of lysosome released into phagolysosome
  7. digestion of endocytosed objects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

intracellular killing

A
  • in neutrophils, monocytes, macrophages

- happens through oxidative or non-oxidative pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

oxidative pathway

A
  • dependent on generation of reactive oxygen and reactive oxygen species
  • during phagocytosis use of oxygen and glucose increases- respiratory burst, leads to ROS
  • oxygen dependent intracellular killing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

non-oxidative pathway

A

-depends on lysosomal toxic substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

generation of ROS

A
  1. glucose metabolized through pentose phosphate pathway leading to production of NADPH
  2. cytochrome oxidase activates NADPH
  3. activated NADPH+ uses O2 leading to production of super oxide anion
  4. superoxide anion may be reduced to peroxide and O2 by superoxide anion
  5. or superoxide anion may react with peroxide to lead to production of hydroxyl radicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

non-oxidative intracellular killing pathway

A
  • dependent on action of toxic substances in lysosomes

- cationic proteins, lysozyme, lactoferrin, proteolytic and hydrolytic enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

cationic proteins

A

damage bacterial cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

lysozyme

A

damage mucopeptides in bacterial cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

lactoferrin

A

sequesters iron and inhibits bacterial growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

proteolytic and hydrolytic enzymes

A

digest killed bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

antimicrobial action of nitric oxide

A
  • when phagocytes bind bacteria through TLR, TNF-alpha is secreted which induces expression of inducible nitric oxide synthetase (iNOS)
  • iNOS oxidizes L-arginine to yield L-citrulline and NO
  • NO highly toxic to microorganisms in vicinity of phagocytes
  • IFN-gamma also induces iNOs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

pathogen recognition by cells of innate immunity

A

-macrophages, dendritic cells, and mast cells use pattern recognition receptors to sense presence of PAMPs or DAMPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

pattern recognition receptor

A

-recognizes PAMPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Pathogen- associated molecular pattern (PAMP)

A

-repetitive motifs of molecules such as lipopolysaccharides, peptidoglycan, lipotechoic acids, mannan broadly expressed by microbial pathogens and not found on host tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

damage-associate molecular patterns (DAMPs)

A

-endogenous molecules released from damaged cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Pattern recognition receptors

A
  • toll-like receptors (TLRs)
  • NOD-like receptors (NLRs)
  • RIG-like receptors (RLRs)
  • C-type lectin receptors (CLRs)
  • peptidoglycan-recognition proteins (PRGPs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

toll-like receptors

A

major PRRs located on host cell membranes or within host cells that signal presence of invaders in innate immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

TLR3

A
  • double stranded RNA

- target viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

TLR7 and TLR8

A
  • single stranded RNA

- target viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

TLR9

A

CpG unmethylated dinucleotides, dinucleotides, herpesvirus

-targets bacterial DNA and some herpesviruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

RIG-like receptors

A
  • expressed in cytoplasm
  • detect viral RNA
  • induce production of antiviral cytokines such as IFNs and inflammatory cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

acute phase response

A
  • change in serum proteins during infections
  • acute phase response proteins- concentrations increase or decrease during infection
  • ex: complement system proteins, C-reactive proteins
  • induced by signals that travel through blood from site of injury or infection
  • most APR proteins synthesized in liver
  • synthesis induced by pro-inflammatory cytokines produced by phagocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

C-reactive proteins

A
  • pentameric proteins
  • ligands for CRP are pneumococcal polysaccharides and phosphorylcholine
  • CRP bound to surface of microbe promotes uptake by phagocytes and activates complement mediated attack
  • mannose-binding lectin is acute phase response protein that recognizes mannose on microbes and not vertebrate cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

natural killer cells

A
  • originate from bone marrow
  • found in blood, spleen, liver
  • migrate to tissues in large numbers during inflammatory response
  • do not posses receptors through gene segment rearrangement (i.e. none like TCR or BCR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

NK cell morphology

A
  • aka large granular lymphocytes because they look like lymphocytes
  • contain granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

role of NK cells in innate immunity

A
  1. kill cells that are stressed, infected with virus, or tumor cells
  2. produce cytokine and chemokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

how do NK cells recognize abnormal cells?

A
  • abnormal cells alter expression of cell surface markers
  • normal (nucleated) cells express Major Histocompatability Complex class I (MHC I) molecule on surface
  • in abnormal cells expression of MHC I is supressed
  • proteins such as MICA and others highly expressed on surface of stressed cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

receptors on NK cells

A
  • activating and inhibitory receptors
  • high level of activating signals leads to killing of target cells
  • strong inhibitory signal preserves target cell
  • generally activating signals blocked by inhibitory signals to prevent killing of normal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

KIRS (killer cell immunoglobin-like receptors)

A
  • humans, cattle, cats, dogs, pigs

- NK receptors that recognize class 1 molecule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

KLRs (killer cell lectin-like receptors)

A
  • mice, rats, horses
  • NK cells that recognize MHC class I
  • possess NKG2D which recognizes stress proteins like MICA, MICB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Activating receptors on NK cells

A

-binds to ligands expressed on stressed, infected, or transformed cells
-NKp46
-CD16
NKG2D

86
Q

inhibitory receptors on NK cells

A
  • recognize MHC class I on normal cells
  • prevent killing of cells by NK cells
  • CD94/NKG2A
87
Q

effector functions of NK cells

A
  • lysis of infected, stressed, or transformed cells (abnormal)
  • activation of macrophages through secretion of cytokines
88
Q

perforin dependent cytotoxicity method

A
  • once triggered, NK cell releases perforin from granules
  • perforin creates lesions (perforin channels) in cell membrane
  • granulysin, NK-lysin (granzymes) and fragmentin (protease) released from cytotoxic channels and passed into perforin channels
  • granzymes and protease induce apoptosis of target cell
89
Q

CD16 killing pathway (cytotoxicity method)

Antibody dependent cellular cytotoxicity

A
  • NK cells recognize target cells using CD16 (Fc receptor on NK cells)
  • antibodies bind to antigen on infected cell, NK cells bind to antibodies through CD16 leading to NK cell cytotoxicity (apoptosis)
  • only occurs when antibodies are present
90
Q

Regulation of NK cell activity

A
  • regulated by cytokines such as IL-1, IL-1, IL-12, IL-15, IL-18, IL-21, and type 1 and 2 IFNs
  • treatment of NK cells with cytokines turn them into LAK
91
Q

lymphokine activated killer cells

A
  • activated NK cells
  • activated by cytokines
  • increased cytotoxic capacity
92
Q

inflammation

A

-defense reaction of living tissue against damage, aimed at removing the cause of injury and repairing the tissue

93
Q

biological agents that cause inflammation

A
  • bacteria, viruses, parasites, fungi

- exogenous

94
Q

calor

A

heat

95
Q

rubor

A

redness

96
Q

tumor

A

swelling

97
Q

dolor

A

pain

98
Q

functio laesa

A

loss of function

99
Q

signs of inflammation

A
  • vasodilation occurs, rise in blood flow and heat
  • large volume of blood causes hyperaemia (redness)
  • vascular permeability
  • edema
  • leukocytes lead to extravasation (cells from blood into tissue)
  • leukocytes phagocytose invading pathogens and release mediators
  • some mediators cause pain
  • injured tissue eliminated from normal function
100
Q

pro-inflammatory cytokines

A
  • TNF-alpha, IL-1 induce fever, stress hormone production (norepinephrine, vasopressin, activation of RAAS)
  • TNF-alpha and IL-1 induce synthesis of IL-6, IL-8, and IFN-y
  • IL-6 stimulates release of C-reactive protein
  • proinflammatory cytokines activate coagulation cascade, release of NO, platelet activating factor, prostaglandins, and leukotrienes
  • IL-1, IL-6, IL-8 promote chemotaxis, induce extravasation of granulocytes, and degranulation of neutrophils
101
Q

complement proteins

A
  • C3a, C5a increase vascular permeablity

- stimulate chemotaxis of neutrophils, eosinophils, and monocytes

102
Q

prostaglandins

A
  • contribute to vasodilation, capillary permeability, pain, and fever during inflammation
  • stable prostaglandins potentiate effects of histamine and other inflammatory mediators
  • thromboxane A2 promotes platelet aggregation and vasoconstriction
103
Q

leukotrienes

A
  • induce smooth muscle contraction

- LTB4 is potent chemoattractant of neutrophils

104
Q

vasoactive amines (histamine, serotonin)

A
  • in platelets, basophils, mast cells

- cause dilation and increased permeability of capillaries

105
Q

platelet activating factor

A
  • induces platelet aggregation
  • activates neutrophils, eosinophil chemoattractant
  • exflux of plasma proteins leading to edema
106
Q

phase one of vascular response

A
  • vasoconstriction

- momentary constriction of small blood vessels in area

107
Q

phase 2 of vascular response

A
  • active vasodilation
  • increased blood flow, dilation of arterioles and capillaries
  • increased cellular metabolism and higher local temp
108
Q

phase 3 of vascular response

A
  • passive vasodilation

- tumor, pain, impaired function

109
Q

cellular response to inflammation

A
  • movement of leukocytes into area of injury

- mainly granulocytes and monocytes

110
Q

sequence of events of cellular response to inflammation

A

-chemotaxis, rolling, migration, phagocytosis

111
Q

chemotaxis

A

leukocytes migrate in response to chemical signal

112
Q

rolling

A

leukocytes slow down and increase expression of adhesion molecules

113
Q

migration

A

migrate into the tissue spaces

114
Q

phagocytosis

A

neutrophils and macrophages engulf and degrade bacteria and cellular debris

115
Q

4 types of CAM proteins

A
  • selectins
  • mucins
  • integrins
  • Ig-superfamily CAM
116
Q

selectins

A
  • bind CHO moieties
  • most important selectins are selectin E, L, and P (CD62E, CD62L, and CD62P)
  • responsible for leukocyte interaction with the endothelium during initial phase of inflammation
117
Q

selectin L

A

on leukocytes

118
Q

selectin P and E

A

-expressed on endothelium during inflammation

119
Q

mucins

A

-heavily glycosylated, serine- and thereonine rich proteins that bind to selectins

120
Q

integrins

A
  • heterodimeric proteins with alpha and beta chains covalently joined at cell surface
  • leukocytes express integrins with B2 chain (CD18)
  • deficiency in B12 leads to leukocyte adhesion deficiency, autosomal recessive disease
  • in LAD neutrophils are unable to extravasate
121
Q

CAM of Ig-superfamily

A
  • contain fibronectin domains
  • Ig superfamily CAMs bind to integrins
  • expressed on endothelial cells
122
Q

leukocyte extravasation

A

-divided into 4 steps which allow leukocytes to exit blood vessels into inflamed tissue

123
Q

phase I leukocyte extravasation (rolling)

A

-leukocytes loosley bind to selectin E and P on endothelial cells, begin to roll on endothelium

124
Q

phase 2 leukocyte extravasation (activation)

A

-increase in cytokine, cytokine secreton, and chemokine receptor expression

125
Q

phase 3 leukocyte extravasation (adhesion)

A
  • conformational change in cells

- integrins on leukocytes bind firmly to endothelium

126
Q

phase 4 leukocyte extravasation (transendothelial migration)

A
  • leukocytes squeeze in between neighboring endothelial cells
  • use homotypic binding of platelet- endothelial-cell adhesion molecule 1 (PECAM-1) (CD131) on endothlium (cell to cell binding)
127
Q

complement activation pathways

A
  1. classical pathway
  2. lectin pathway
  3. alternative pathway
128
Q

initiation of classical pathway

A

antigen: antibody complexes

129
Q

initiation of lectin pathway

A

lectin binding to pathogen surfaces

130
Q

initiation of alternative pathway

A

pathogen surfaces

131
Q

what do three complement pathways generate?

A

C3

132
Q

ways complement system protects against pathogens

A
  1. recruitment of inflammatory and immunocompetent cells
  2. opsonization of pathogens
  3. killing of pathogens
133
Q

chemoattractants

A

-components of the complement that recruit phagocytic cells to sites of complement activation

134
Q

opsonization by complement

A

-large amounts of activated complement bind covalently to pathogens opsonizing them for phagocytosis

135
Q

MAC (membrane attack complex)

A

-final components of complement create pores in microbe’s membrane

136
Q

complement function in adaptive immunity

A
  • opsonization by complement components allows uptake of microbes by APCs
  • B cells have complement receptors which enhance B cell response to microbes
137
Q

initiation of classical pathway

A
  • initiated by binding of C1q to surface of pathogen either:
    1. directly to surface of bacterial components (proteins, lipoteichoic acid)
    2. binds to C-reactive protein that binds to phosphocholine on bacterial polysaccharides
    3. *binds to antigen-antibody complex on pathogen surface- most effective
138
Q

initiation of lectin pathway

A

-initiated by binding of carbohydrate- binding proteins to carbohydrates on surface of pathways including: mannose binding lectin (MBL), ficolins

139
Q

initiation of alternative pathway

A

-initiated by binding of spontaneously derived plasma C3b to pathogen surfaces

140
Q

activation of complement through classical pathway

A
  • IgM, IgG

- when Ig bind to antigen, Fc portion of antibody binds complement component C1

141
Q

C1

A
  • backbone is C1q
  • six globular heads
  • associated with tails of C1q are two copies C1r, two copies C1sd
142
Q

Classical pathway C3 convertase

A

C4b2a

143
Q

activation of complement through lectin pathway

A
  • independent innate immune response
  • lectins bind CHO residues
  • MBL and ficolins can recognize microbial-specific CHO on surface of microbes
144
Q

Mannose binding lectin molecule

A
  • C type lectin family with similarities to C1q

- recognizes mannose, fucose, N-acetylglucosamine presnet in walls of bacteria, fungi, and some protozoa and viruses

145
Q

action of MBL

A
  • when it binds to microbial cell wall, it activates confirmational changes which promote activation of MBL-associated serine proteases (causing cleavage of C4 and C2 to C4a, C4b, C2a, C2b)
  • C4b complexes with C2a to create C3 convertase (C4b2a)
  • C4b2a complexes with C3b to create C4b2a3b (C5 convertase)
146
Q

activation of complement through alternative pathway

A

-uses non-specific, low level hydrolysis of C3

147
Q

importance of C3

A

-abundant complement protein and key player in ALL complement pathways

148
Q

alternative pathway

A
  • spontaneous cleavage of C3 produces C3a and C3b

- C3b binds to microbial surface or is degraded if binds to healthy host

149
Q

C3b bound to microbial surface

A
  • not degraded by factor H and I
  • binds factor B to form C3bB complex
  • C3bB is cleaved by factor D
  • Ba relesed then C3bBb
  • C3bBb is alternative C3 convertase
  • alternative C3 convertase unstable but stabilized by factor P (properdin)
  • alternative C3 convertase cleaves C3 into C3a and C3b
  • C3b complexes with C3bBb to form C3bBb3b which is alternative C5 convertase
150
Q

MAC

A
  • initiated by C5 convertase
  • C4b2a3b by classical and lectin
  • C3bBb3b by alternative
151
Q

regulation of complement activation

A
  • prevent complement from acting on inappropriate targets
  • C1 inhibitor
  • Factor H &I
  • Decay accelerating factor (CD55)
  • Protectin (CD59)
152
Q

role of MHC in graft rejection

A

-major histocompatability complex contains genes for survival or rejection of graft

153
Q

Which animals do not have histocompatability molecules?

A

none, they all have them with at least 3 classes of gene loci

154
Q

Class I MHC molecules

A
  • on all nucleated cells

- highly polymorphic loci (class Ia, Ib, Ic)

155
Q

Class II MHC molecules

A

-found only on antigen presenting cells

156
Q

Class III MHC molecules

A
  • do not function as antigen presenting molecules

- function in innate immunity

157
Q

Why do most MHC names end with LA?

A
  • because they were originally found on white blood cells

- LA stands for leukocyte antigen

158
Q

Which MHC genes are more dominantly expressed? Mother’s or fathers?

A

-co-dominantly expressed

159
Q

What is a haplotype?

A

-set of MHC alleles present on chromosome

160
Q

Role of MHC in adaptive immunity

A

-MHC class I & II are main antigen presenting molecules

161
Q

What do MHC class I molecules present peptide antigens to?

A

CD8+ T lymphocytes

162
Q

What are MHC class II molecules expressed on? What do they present?

A
  • expressed on APCs: dendritic cells, macrophages, B cells

- present antigens to CD4+ T lymphocytes (helper T lymphocytes)

163
Q

structure of MHC class I molecule

A
  • heterodimer with alpha and beta chains
  • has extracellular domain and antigen binding groove
  • binding groove is most variable part of MHC molecule
  • co-receptor CD8 binds to a3
164
Q

structure of MHC class II molecule

A
  • consists of alpha and beta chains
  • peptide binding groove is made up a1 and b1
  • stable expression requires 2 chains and bound peptide
165
Q

regulation of MHC expression

A
  • IFNa, IFNB, IFNy increase expression of MHC class I
  • IFNy increases expression MHC class II on macrophages and dendritic cells
  • recognition of pathogens through toll like receptors increase expression MHC class II
  • cytokines secreted by CD4 cells increase expression MHC class II
166
Q

MHC molecules and disease

A
  • foreign antigenic peptide that does not fit MHC will not stimulate immune response
  • heterozygous animals=more alleles
  • homozygous animals=less alleles
167
Q

antigens

A

= antibody, generator

  • bind to antibodies, MHC or TCRs
  • induce immune response
168
Q

immunogens

A

-substances that stimulate immune response

169
Q

haptens

A
  • will not stimulate immune response alone but will when complexed with larger molecule such as host protein
  • ex. penicilloyl from penicillin
170
Q

two main features of antigens

A

-immunogenicity, antigenicity

171
Q

immunogenicity

A

-antigens capable of inducing immune response

172
Q

antigenicity

A

-antigens can bind with products of immune response they induced

173
Q

epitope

A
  • antigenic determinant

- induces immune response and binds to products of immune response

174
Q

sources of antigens

A
  • infectious agents- bacteria, fungi, parasites, viruses

- altered self antigens- tumors

175
Q

factors affecting immunogenicity of antigens

A
  • foreigness
  • size (larger more immunogenic)
  • chemical composition
  • physical properties
  • degradability
  • genetic factors (species or individual)
  • age (young or old)
176
Q

chemical nature of antigens

A
  • proteins- largest group
  • polysaccharides
  • nucleic acids
  • lipids
177
Q

adjuvants

A

substance that enhances body’s immune system to antigen

178
Q

T-independent antigen

A
  • directly stimulate B lymphocytes
  • do not need helper T cells
  • lipoplisaccharides
179
Q

properties of T-independent antigens

A
  • polymeric structure
  • same antigenic determinant repeats
  • may activate lymphocytes polyclonally
  • resistant to degradation
180
Q

T-dependent antigens

A
  • indirectly stimulate B-lymphocytes
  • need helper T-cells
  • mostly proteins
  • contain few copies each of various antigenic depterminants
181
Q

superantigens

A
  • can activate large number of lymphocytes at one time
  • mostly from bacteria or viruses
  • bind to variable domain of beta chain in TCR of CD4+ T cells and alpha chain of MHC class II
  • induces strong signal that activates T cells
  • polyclonal activation leads to excessive production of interleukins, and TNFs
182
Q

antigen processing and presentation

A

-antigen presenting cells digest antigens and display via MHC molecules for recognition by T-lymphocytes

183
Q

Antigen presenting cells

A

-digest (process) and display (present)

184
Q

T-lymphocytes

A

-recognize presented antigens and are activated to initiate cellular immune response

185
Q

dendritic cells

A
  • professional APC
  • present antigen to naive CD4+ and CD8+ T lymphocytes
  • initiate T-cell responses
186
Q

macrophages

A
  • professional APC

- present antigens to differentiated CD4+ T lymphocytes in effector phase of cell-mediated immunity

187
Q

B-lymphocytes

A

-present antigens to helper T-cells (CD4+) during humoral immune response

188
Q

MHC II expression

A
  • macrophages- low levels, induced by PAMPs, DAMPs, cytokines
  • DC- always expressed
  • B cell- always expressed
189
Q

antigen type and presentation by MHC

A
  • macrophages- extracellular antigens- MHC II
  • DC- intra and extracellular antigens- MHC I and II
  • B-cell- MHC II
190
Q

macrophage location

A
  • lymphoid tissue
  • connective tissue
  • body cavities
191
Q

dendritic cell location

A
  • lymphoid tissue
  • connective tissue
  • epithelium
192
Q

B-cell location

A
  • lymphoid tissue

- blood

193
Q

important functions of antigen presenting cells

A
  • convert protein antigens to peptides and display peptide-MHC complexes (antigen processing)
  • provide stimulus to T-cells (costimulation)
194
Q

antigen processing

A
  • convert protein antigens from extracellular space or cytosol into peptides to display to lymphocytes
  • antigens in acidic vesicular compartments of APCs generate MHC class II associated peptides, antigens in cytosol generate MHC class I associated peptides
195
Q

MHC class II antigen processing and presentation pathway

A

-extracellular antigen

196
Q

MHC class I antigen processing and presentation pathway

A

-cytosolic (endogenous) antigen

197
Q

processing of endocytosed antigens for MHC class II presentation (steps)

A
  1. uptake of extracellular proteins into vesicular compartments of APCs
  2. processing in endosomal and lysosomal vesicles
  3. biosynthesis and transport of MHC class II molecules to endosomes
  4. association with MHC class II molecules in vesicles
  5. expression on APC surface
198
Q

processing of cytosolic antigens for MHC class-1 associated presentation

A
  1. foreign proteins in cytosol
  2. proteolytic degradation of these proteins in proteosome
  3. transport to ER
  4. assembly of peptide: MHC class I complexes in ER
  5. surface expression of peptide MHC class I complexes
199
Q

sources of cytosolic antigens

A
  • proteins found in cytosol, endogenously synthesized
  • viruses or intracellular microbes
  • sometimes endocytosed antigens are presented through MHC class I molecules
200
Q

Class II MHC-associated presentation of extracellular antigen to helper T cells

A
  • induces macrophage activation and destruction of phagocytosed antigen
  • mediated by cytokines
201
Q

Class I MHC-associated presentation of cytosolic antigen to cytotoxic T-lymphocytes

A

-killing of antigen-expressing target cell

202
Q

T-cell receptor

A
  • each T cell has a TCR of one specificity
  • alpha beta TCR is MHC-dependent
  • gamma delta TCR recognizes antigen in MHC-independent manner
203
Q

CD3 complex

A
  • closely associated with TCR
  • does not contribute to TCR specificity (proteins of CD3 are invariant)
  • necessary for cell surface expression of TCR
  • transduces activation signals to nucleus
204
Q

properties of antigens recognized by T-lymphocytes

A
  • most recognize only peptides
  • T-cells specific for amino acid sequences of peptides
  • T cells recognize and respond to foreign peptide antigens only when they are attached to surface of APCs within appropriate MHC context
205
Q

self-MHC restriction

A

-T cells from one individual only recognize foreign peptides presented on their own cell

206
Q

Which T-cells are MHC class II restricted?

A

CD4+

207
Q

Which T cells are MHC class I restricted?

A

CD8+

208
Q

B-cell receptor

A
  • does not interact with MHC molecules
  • recognizes soluble antigens on cell surface
  • recognize peptides, proteins, nucleic acids, polysaccharides, lipids
209
Q

Co-stimulatory molecules

A

-required for full T-cell activation

210
Q

clonal anergy

A
  • when T-lymphocytes stimulated without co-stimulatory signal
  • state of no responsiveness
211
Q

primary lymphoid organs

A
  • sites of lymphocyte development
  • thymus (involutes after puberty)
  • Bursa of Fabricus
  • Peyer’s patches
  • Bone marrow
212
Q

secondary lymphoid organs

A
  • where lymphocytes respond to antigens
  • tonsils
  • spleen
  • lymph nodes
  • Peyer’s patches
  • Bone marrow

immunology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions