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

vaccination

A

severe disease is prevented by prior exposure to the infectious agent in a non-disease form

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

first vaccination

A

small pox in Asia a long time ago

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

Edward Jenner

A

cowpox as vaccination against smallpox in 1796

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

1979

A

smallpox officially eradicated

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

commensal organisms

A

500+ microbial species that live in a healthy human

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

flora

A

the community of microbial species that lives in a particular niche in the human body

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

Role of commensal organisms

A

digest food, vitamin synthesis, disease protection

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

colicin

A

antibacterial protein secreted by E. coli that help protect us from disease besides competition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathogenic Organisms

A

any organism with the potential to cause disease is a pathogen. can be common like influenza or opportunistic. evolve to invade host, replicate, transmit

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

Types of Pathogens

A

bacteria, viruses, fungi, parasites

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

First Line of Defense

A

skin and mucus secreted by epithelial which is continuous with the skin and the mucus connects it all

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

Mucus

A

contains proteins, peptidoglycans, and enzymes to protect from damage and infection

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

Epithelial Fatty Acids and Lactic Acids

A

inhibit cell growth

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

Epithelial Defensins

A

perturb membranes or bacteria, fungi, and bacteria

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

Epithelial Lysozyme

A

degrades cell walls of bacteria

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

Epithelial Acid

A

the lower pH of environment

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

pathogen recognition

A

involves soluble proteins and cell-surface receptors that bind to the pathogen or to human cells and serum proteins that are altered in the presence of pathogen

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

pathogen destruction

A

involves effector mechanisms that kill and eliminate the pathogen

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

effector mechanisms

A

provided by effector cells that engulf foreign entities and complement, which helps mark pathogens and can attack pathogens as well

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

Inducing Inflammation

A

1) cytokines induce local capillary dilation (warm red skin)
2) vasodilation introduces gaps in endothelium for increased plasma leakage (edema swelling pain)
3) cytokines change adhesive properties of vascular endothelium to recruit WBC

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

Adaptive Immunity

A

Highly specific lymphocytes that have unique receptors that are formed by genes being cut, spliced, and modified during lymphocyte development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clonal Selection

A

during pathogen recognition, only the lymphocytes that recognize the pathogen are selected for to participate in the immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clonal Expansion

A

the selected lymphocytes then proliferate to produce large numbers of effector cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

immunological memory

A

during clonal selection, some lymphocytes differentiate into memory cells to allow for eliciting of stronger faster immune responses upon subsequent exposure

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

pluripotent hematopoietic stem cells

A

cell that all blood cells differentiate from

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

hematopoiesis

A

process by which leukocytes are continuously generated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Lineage of Hematopoietic Stem Cells

A

self-renewal, erythroid, myeloid, lymphoid

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

Erythrocytes

A

red blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Megakaryocytes

A

platelet producing cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Myeloid Progenitors

A

granulocytes, monocytes, mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

granulocytes

A

polymonrphonuclear leukocytes which includes neutrophils, eosinophils, and basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

monocytes

A

which are progenitors of dendritic cells and macrophages

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

mast cells

A

involved in inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

neutrophil

A

most abundant of all leukocytes and is phagocyte that can work under anaerobic conditions. short lived and die at infection making pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

phagocyte

A

specialized in capture, engulfment, and killing of microorganisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

eosinophil

A

granulocyte that defends against intestinal parasites

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

basophil

A

is implicated in regulating the immune response to parasites (because of low abundance, little is known about basophils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

macrophage

A

a scavenger and expert phagocyte, generally the first phagocyte to sense an invading microorganism that also makes cytokines

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

dendritic cells

A

act as cellular messengers to call up an adaptive response when necessary

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

Lymphoid Progenitors

A

gives rise to large granular lymphocytes and small lymphocytes

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

large granular lymphocytes

A

natural killer cells

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

small lymphocytes

A

B cells and T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Natural Killer Cells

A

important in viral infections as they kill virus-infected cells and secrete cytokines that block viral replication in infected cells

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

B Cells

A

utilize immunoglobulins as cell-surface receptors for pathogens. can further develop into plasma cells which secrete antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

antibodies

A

soluble immunoglobulins

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

T Cells

A

utilize T-Cell Receptors (TCR) as cell-surface receptors for pathogens. can further develop into cytotoxic t-cells or helper t-cells

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

Immunoglobulins

A

on B-cells and contain a heavy chain and light chain

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

T-Cell Receptors

A

have an alpha-chain and a beta-chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

antigen

A

any molecule recognized by immunoglobulin, antibody, or T-Cell receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

variable region

A

specific for each antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

constant region

A

binding sites for phagocytes, inflammatory cells, complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Antibody Action

A

soluble proteins secreted by plasma cells that can either be neutralizing or opsonizing

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

Neutralizing Antibodies

A

antibodies that bind to molecules and prevent them from functioning (typical targets are toxins and pathogen surfaces molecules needed for binding to target cells)

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

Opsonizing Antibodies

A

antibodies that bind to molecules to tag them for destruction by phagocytosis or attack using the complement system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Major Lymphoid Tissues

A

bone marrow, thymus, spleen, adenoids, tonsils, appendix, lymph nodes, Peyer’s patches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Primary/Central Lymphoid Tissue

A

where lymphocytes develop and mature (bone marrow and thymus - B cells develop and fully mature in bone marrow, T cells begin development in bone marrow but fully mature in Thymus)

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

Secondary/Peripheral Lymphoid Tissue

A

where mature lymphocytes become stimulated to respond to pathogens (all other lymphoid tissues)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Lymph Nodes

A

lie at the junction of the lymphatics, which collect plasma (fluid that leaks from blood vessels)

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

Lymph return

A

lymph is returned to the blood chiefly through the thoracic duct into the left subclavian vein in the neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Mature B and T Cell Movement

A

through the body by both blood and lymph. once in capilaries close to node or 2nd tissue, lymphocytes can exit into node

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

B and T Cells in Lymph Nodes

A

1) lymphocyte encounters pathogen and remains in lymph node

2) lymphocyte can exit via the efferent lymph and eventually return to blood

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

Lymph Circulation with Infection

A

pathogens, pathogen components, and pathogen-infected dedritic cells are carried by the lymphatics to the lymph node (draining) leading to swollen glads

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

Lymph Node Filter

A

The lymph node filters pathogens and other foreign material so that it doesn’t reach the blood and can stay for activating lymphocytes

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

Draining Lymph Node

A

pathogens and pathogen-carrying dendritic cells enter the draining lymph node through the afferent lymphatics

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

Effector Cell genesis

A

in draining lymph node, pathogens are phagocytosed by MO or pathogens and their products are sensed by B and T cell receptors which causes the b cells and t cells to divide and differentiate into effector cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Pathogens in blood

A

either blood-born or if not removed from draining nodes. the spleen can then filter and splenic MO and dendritic cells can take them up and stimulate b and t that arrive in spleen from blood

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

Spleen

A

removes damaged and senescent red blood cells and serves as a peripheral lymphoid tissue for blood-borne pathogens

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

Spleen Red Pulp

A

where red blood cells are monitored and removed

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

Spleen White Pulp

A

where white blood cells provide adaptive immunity

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

Asplenia

A

rare genetic disorder where there is no spleen - susceptible to infections with encapsulated bacteria but can be treated through vaccination with capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Respiratory and GI environments

A

harbor the largest and most diverse populations of microorganisms, making them vulnerable to infection and heavily invested with 2nd lymphoid tissue (mucosa-associated lymphoid tissue)

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

Gut-Associated Lymphoid Tissue

A

GALT - tonsils, adnoids, appendix, Peyer’s patches

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

Bronchial-Associated Lymphoid Tissue

A

BALT - line respiratory epithelium

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

M-Cells

A

specialized cells that directly deliver pathogens that arrive at the mucosa-associated lymphoid tissue across the mucosa

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

Movement of Lymphocytes in GALT and BALT

A

lymphocytes enter mucosa-associated lymphoid tissue from the blood and exit from the lymphatics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Pathogen Location

A

can be intracellular or extracellular and divided into more sub-groups which makes how the immune system responds different (extracellular needs soluble)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Complement

A

one of the first lines of defense in innate is a system of soluble proteins that are constitutionally made by the liver and transported in blood, lymph, and extracellular fluids. many components are proteases that circulate as zymogens. 30+ proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

zymogens

A

inactive precursors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

complement activation

A

series of protease cleavages triggered by infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Complement component 3 (c3)

A

cleaves into C3a and C3b by C3 Convertase (protease). is a zymogen - happens because of exposure of high-energy thioester which can attach to proteins and carbohydrates on pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

C3a

A

chemoattractant for effector cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

C3b

A

attaches to pathogen - complement fixation for tagging pathogen for destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Complement Activation Pathways

A

Alternative Pathway, Lectin Pathway, Classical Pathway

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

Alternative Pathway

A

activated at the start of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Lectin Pathway

A

induced by infection and requires time to gain strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Classical Pathway

A

part of both innate and adaptive immunity and requires binding of either antibody or C-reactive protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Steps of Alternative Pathway

A

1) C3 secreted into plasma, confrontational change makes thioester bond available for hydrolysis
2) hydrolysis of this bond on a subset of C3 forms iC3
3) iC3 can bind factor B making it susceptible to cleavage by factor d releasing small factor Ba while some stays bound forming iC3Bb
4) iC3Bb cleaves C3 into C3a and C3b
5) C3b can bind factor b, get cleaved by factor d, form C3bBb complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

iC3Bb

A

C3 convertase that cleaves C3 into C3a and C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

C3bBb

A

the alternative C3 Convertase - can cleave much more C3 and produces positive feedback rapidly coating pathogen surface

90
Q

Regulate C3b Deposition

A

Factor P prevents C3bBb degradation, factor H and I lower C3 convertase activity - factor H/sialic acid/pathogen evasion. P, H, and I are all soluble

91
Q

complement control proteins

A

regulate complement reactions by mainly stabilizing or degrading C3b at cell surface

92
Q

Properdin (factor P)

A

increases complement activation by preventing the degradation of C3bBb

93
Q

Factor H

A

counters factor P by binding to C3b and facilitates its further cleavage to iC3b by factor I so iC3b cannot form an active C3 convertase

94
Q

Prevent Complement on Human Cells

A

DAF and MCP

95
Q

Lack of factor I

A

immunodeficient patients can lack factor I leading to depletion of C3 - more susceptible to ear infections and abscesses caused by encapsulated bacteria

96
Q

Decay-Accelerating Factor

A

binds C3b of the alternative C3 convertase causing its activation to prevent activation

97
Q

Membrane Co-Factor Protein

A

binds C3b of alternative C3 Convertase like DAF but also inactivates factor I

98
Q

Macrophages and Complement

A

macrophages can be non-specific but have CR1 that can bind C3b, CR3 and CR4 bind iC3b on pathogen surface

99
Q

Opsonization

A

coating of a pathogen with a protein to facilitate phagocytosis

100
Q

Terminal Complement Proteins

A

C5b is the start and C9 is the end

101
Q

C5b genesis

A

C3b can bind to alternative C3 convertase to produce a protease that acts on C5 forming alternative C5 convertase (Bb plus two C3b fragments = C3b2Bb)

102
Q

Membrane Attack Complex

A

C5b bind in succession C6 and C7 and is inserted into the membrane, C8 binds C5b and inserts into lipid bilayer, C8 induces polymerization of C9, forming transmembrane pores

103
Q

C9

A

the subunit of the membrane attack complex that forms transmembrane pores

104
Q

Prevention of Lysis from MAC

A

1) Soluble proteins (S, clusterin, factor j) prevent C5b/C6/C7 binding to cell surface
2) at cell surface homolgous restriction factor (HRF) and CD59 prevent C9 recruitment

105
Q

Paroxysmal nocturnal hemoglobinuria

A

complement mediated lysis of red blood cells caused by lack of CD59 due to loss of GPI anchor

106
Q

C3a and C5a

A

aka anaphylatoxins -

physiologically active - increase local inflammation - can induce anaphylactic shock

107
Q

Anaphylatoxins

A

induce smooth muscle contraction and degranulation of mast cells and basophils, histamine released, increased vascular permeability

108
Q

coagulation system

A

plasma proteins that induce blood clots to prevent pathogen movement and reducing blood loss

109
Q

platelets

A

major component of blood clots - also relase antimicrobial defense mediators like prostaglandins,hydrolytic enzmes, GF

110
Q

kinin system

A

increases vasodilation

111
Q

a-2-macroglobulin

A

protease inhibitor which lures in proteases (from pathogens) to covalently link the protease and envelop the protease

112
Q

“Other Plasma Proteins”

A

coagulation system, platelets, kinin system, protease inhibitors (a-2-macroglobulin)

113
Q

Defensins

A

major family of antimicrobial peptides (35-40 aa rich in Arginine w/ 3 intra-chain disulfides), two classes (alpha and beta), amphipathic (hydrophobic portion penetrates microbial membrane)

114
Q

Pentraxins

A

act as bridging molecules that bind to surface molecule of a pathogen and escort to immune cells (has similar role in innate immune as antibodies in adaptive)

115
Q

Innate Microbial Receptors

A

many are carbohydrates (recognized by lectin receptor (mannose receptor)) and lipids

116
Q

CR3 and CR4

A

complement receptors/cell surface structures

117
Q

scavenger receptors

A

bind to wide array of negatively charged molecules (sulfated polysaccharides, nucleic acids, lipoteichoic acid from Gram-positive cell walls)

118
Q

Bacterial Lipopolysaccharide

A

LPS - gram-negative surface molecule is a binding partner for many receptors

119
Q

Binding Initiates

A

either phagocytosis or secretion of cytokines

120
Q

Phagocytosis

A

receptor-mediated endocytosis begins with pathogen binding to phagocyte, engulfed into vesicle called phagosome, phagosome fuses with lysosome makeing phagolysosome

121
Q

Toll-Like Receptors

A

family of signaling receptors that are specific for a different set of microbial products. Humans have 10 TLR genes to recognize many microorganisms

122
Q

TLR4

A

expressed by macrophages to detect bacterial LPS and related compounds outside of G- Bacteria. Binding causes gene activation of inflammatory cytokines. Also important to prime adaptive.

123
Q

Toll-interleukin receptor and Leucine Rich Region

A

TIR - transmembrane proteins with an extracellular domain for recognizing pathogens (leucine-rich region (LRR)) and a cytoplasmic domain for conveying information

124
Q

Recognition of LPS by TLR4 Components

A

Needs CD14(co-receptor), MD2, TLR4, LPS

125
Q

TLR4 Activation

A

1) LPS recognized by MD2, CD14, TLR4
2) binding of ligand recruits MyD88 to the intracellular side of TLR4
3) MyD88 activates IRAK4 which phosphorylates TRAF6
4) TRAF6 activates kinase cascade activating inhibitor kappaB kinase (IKK)
5) IKK phosphorylates IkB which is degraded releasing txf nuclear factor kappaB (NFkB),
6) NFkB translocates to nucleus and transcription of cytokines (IL-1b, TNF-a, IL-6, CXCL8, IL-12 from MO)

126
Q

IL-6

A

induces fever through increased metabolism

127
Q

TNF-a and IL-1b

A

induces changes in endothelial cell walls to allow effector cells to enter infection area

128
Q

CXCL8

A

a chemoattractant cytokine (chemokine) that recruits neutrophils - acts through G protein linked receptors

129
Q

IL-12

A

activates NK lymphocytes (viral infection)

130
Q

TNF-a The Good

A

local action causes vascular endothelial cells to make platelet-activating factor triggering blood clotting and blockage of local blood vessels thus preventing pathogens from entering blood and causing systemic infection

131
Q

TNF-a The Bad

A

sepsis (infection of blood) can cause widespread TNF-a released by liver, spleen, and other sights causeing massive dialtion of blood vessles/leakage of fluid to tissues = septic shock

132
Q

Septic Shock

A

widespread blood lotting and failure of vital organs (kidneys, liver, heart, lungs)

133
Q

NOD-Like Receptors

A

intracellular sensor that detects presence of bacteria in the cytoplasm - aka nucleotide-binding oligomerization domain proteins

134
Q

muramyl peptides

A

cell wall component that NOD recognizes

135
Q

RIPK2

A

kinase activated by the binding of NOD. then activates NF-kB like in TLR4 signaling causing synthesis of cytokines, chemokines, defensins

136
Q

NOD Problems

A

NOD genes linked to IBD/Crohn’s

137
Q

The Inflammasome Function

A

increase local concentration of procaspase 1 to promote autoproteolysis and activation. More caspase 1 = more inflammation

138
Q

The Inflammasome Steps

A

1) IL-1b secreted by MO bind to IL-1 receptors of the MO to increase proIL-1b production (pathway like TLR4)
2) ProlL-1b activated to IL-1b by protease called caspase 1
3) potassium ions released by MO due to other signals
4) ionic change supports assembly of inflammasome

139
Q

Inflammasome Structure

A

complex of a NOD-like protein NLRP3, and adaptor protein and procaspase 1

140
Q

Neutrophils

A

professional phagocyte aka polymorphonuclear leukocytes, most abundant WBC, 50billion circulting, leave blood when signaled by inflammatory mediators, work under anaerobic conditions, form pus when dead

141
Q

pyogenic bacteria

A

are extracellular bacteria that are pus-forming due to their attack by neutrophils (like S. aureus)

142
Q

Adhesion Molecules

A

needed to move neutrophils from blood to tissue - selectins, vascular addressins, integrins, immunoglobulin-like molecules

143
Q

Neutrophil Inflammatory Mediators

A

CXCL8, C5a, bacterial chemoattractants, induce expression of lignads on endothelial cells of blood vessels to allow for neutrophil binding

144
Q

Extravasation

A

neutrophil migration from blood to tissue

145
Q

Extravasation Steps

A

1: Rolling adhesion
2: Tight Binding
3: Diapedesis
4: Migration

146
Q

Rolling Adhesion

A

selectins on the endothelium bind to Sialyl-Lewis* (carbohydrate on neutropil surface)

147
Q

Tight Binding

A

LFA-1 on neutrophil binds TCAM-1 on endothelium

148
Q

Diapedesis

A

Neutrophil crosses blood vessel wall (adhesion helps)

149
Q

Migration

A

CXCL8 gradient helps

150
Q

Neutrophil Phagocytosis

A

Similar to MO but can recognize wider range or materials but have potent antimicrobial weapons.

151
Q

Neutrophil Phagosomes

A

Fuse with two neutrophil granules Azurophilic (primary) and Specific (secondary) before binding with lysosome

152
Q

Azurophilic granules

A

contain proteins and peptides that disrupt and digest microbes (lysozyme, defensins, proteases)

153
Q

Specific Granules

A

contain lactoferrine (iron and copper sequestration), lysozyme, and NADPH Oxidase

154
Q

NADPH Oxidase

A

produces superoxide radicals which are converted into hydrogen peroxide by superoxide dismutase. Raises pH of phagosome to activate molecules of granules

155
Q

Respiratory Burst

A

consumes oxygen to make two potent cell killers, superoxide radicals and hydrogen peroxide

156
Q

Lack of Respiratory Burst

A

leads to chronic intracellular infections of neutrophils and macrophages that are contained in localized nodules called granulomas

157
Q

Granulomas

A

imprison macrophages that have eaten too many neutrophils

158
Q

Cytokines for Fever

A

IL-1, IL-6, TNF-a act on hypothalamus, muscle and fat cells to generate heat

159
Q

Fever

A

slows bacterial and viral growth and also increases potency of adaptive immunity

160
Q

Acute-Phase Response

A

induced by inflammatory cytokines - liver cells secrete the plasma proteins C-reactive protein and mannose-binding lectin

161
Q

Mannose-Binding Lectin

A

opsonin - binds to carbohydrates on bacteria, fungi, protozoans, and viruses, triggers the lectin pathway of complement activation, doesn’t bind tightly to human

162
Q

C-Reactive Protein

A

opsonin- binds to phosphocholine component of LPS on bacteria and fungi but doesn’t bind to human phosphocholine.

163
Q

The Lectin Pathway of Complement Activation

A

mannose-binding protein opsonization is first leading to cleavage of C4 by serine protease associated with mannose-binding protein, cleavage of C2 by same serine protease, associate of C4b with C2a - classical C3 Concertase

164
Q

Nonfunctional Mannose-binding Lectin

A

alleles common (>10%), two nonfunctional alleles susceptibility to meningitis

165
Q

The Classical Pathway of Compliment Activation

A

c-reactive protein opsonization is first step, the association with C1 (protease), cleavage of C4 by C1, cleavage of C2 by C1, associatio of C4b and C2a

166
Q

Sensing Viruses

A

normally intracellular, recognition of cytoplasmic or endosomal nucleic acids, detected by receptors like TLR3, TLR7, or RLR leading signal cascade and txf for type 1 interferones (alpha beta)

167
Q

Type 1 Interferons do

A

block viral repication, signal neighbors about virus, alert immune system cells, promote destruction of virus infected cells by killer lymphocytes

168
Q

Interferon Response

A

changes expression in human genes and increase NK ligands on infected cells and activate NK cells

169
Q

oligoadenylate synthesis

A

blocks viral genome replication

170
Q

protein kinase R

A

inhibits initiation factor elF2 and blocks viral protein synthesis

171
Q

transcription factors

A

activates expression of more interferon

172
Q

NK Cells

A

5-25% of blood lymphocytes, effector functions: cell killing, secretion of cytokines, activated by INF-a, INF-b, IL-12, TNF-a

173
Q

NK Cell Action

A

distunguish between healthy and infected cells based on receptor action and balance of signals from inhibitory and activating receptors

174
Q

Cytotoxic Effector Cells

A

differentiated from NK cells in response to type 1 interferons - release cytotoxic granules to induce apoptosis

175
Q

NK Cells and MO

A

MO recruit NK with IL-12, CXCL8, can then bind in a synapse to form conjugate pair, promotes proliferation and activation of NK cells to secrete cytokine INF-b which induces action of macrophages

176
Q

Dendritic Cells Bridge

A

phagocyte similar to MO, specialize in presenting foreign antigens to adaptive, can be infected by intracellular pathogens and viruses at site of infection

177
Q

NK and Denritic

A

Can form a synapse under viral infections

178
Q

Weird things with NK and Dendritic

A

when more NK than dendritic, NK kill them (maybe limit adaptive response) and when less Nk than dendritic, NK activate the dendritic (induce adaptive maybe)

179
Q

Role of B Cells

A

make antibodies - activation of B cells leads to proliferation and differentiation into effector cells called plasma cells

180
Q

Antibodies Can…

A

prevent pathogen infection, target pathogen for destruction, recognize native macromolecules on the outside of pathogens

181
Q

antibody repertoir

A

variablility in antibodies in an individual can be 10^9 different antibodies

182
Q

B Cells and CD4 Helper T Cells

A

naive B cells come into contact with pathogens in draining lymph node, B cell with right immunoglobulin receptor binds pathogen and engulfs, pathogen peptides presented on MHC class II molecules, CD4 Helper T cells recognize and activate the B Cell

183
Q

Antibody Structure

A

glycoproteins made of four polypeptide chains (2 heavy, 2 light) - disulfide bonds link each light chain to a heavy chain and the heavy chains together

184
Q

Antigen Binding Site

A

formed by the variable regions of heavy and light chains

185
Q

Hinge Region

A

flexible connection of the two antibody fragments Fab and Fc. flexibility allows for Fab fragments to adopt many differnt orientation allowing antibodies to recognize antigens at different distances

186
Q

Fab

A

fragment antigen binding - binds antigen

187
Q

Fc

A

fragment crystallizable (constant) stem region

188
Q

IgM

A

always the isotype used as immunoglobulin receptor on a naive B cell and is the first antibody isotype secreted

189
Q

Improve antibody effectiveness during clonal expansion of b cells

A

1) Somatic Hypermutation

2) Isotype Switching

190
Q

Somatic Hypermutation

A

nucleotide changes in the variable region to allow tighter binding

191
Q

Isotype Switching

A

the isotype is determined by the constant region, B Cells can rearrange the gene to bring a new constant region together with the variable region

192
Q

Antibody Isotypes

A

difference in the heavey chain C region define the five isotopes IgG, IgM, IgD, IgA, IgE (heavy chain is corresponding greek leter) and the light chains have kappa and lambda with no functional differences but abundance changes with organism

193
Q

Immunoglobulin Domain

A

repeating domain found in heavy and light chains

194
Q

Variable Domain

A

Vh and Vl, the amino terminal end of each chain (one domain)

195
Q

Constant Domain

A

light chains have 1, heavy either 3 or 4 depending on isotype

196
Q

Hypervariable Region

A

concentrated area of amino acid differences in the variable regions - three in each variable region surrounded by framework regions - antigen binding is the clustering of hypervariable regions from light and heavy chains

197
Q

Epitope

A

part of the antigen the antibody binds to - mostly carbohydrates and protein components but sometimes DNA and small molecules

198
Q

Multivalent Antigen

A

any antigen that contains more than one epitope or more than one copy of the same epitope

199
Q

linear epitopes

A

are adjacent sugars or amino acids

200
Q

discontinuous epitopes

A

far apart in linear sequence but are close together in three-dimensional structure

201
Q

antigen-antibody interactions

A

noncovalent interactions - hydrophobic, van der Waals forces, electrostatic)

202
Q

Monoclonal Antibodies

A

fusion of B Cells with a tumor cells to form a hybridoma that produces antibodies indefinitely, separation of hybridomas, selection of hybridomas

203
Q

Traditional Antibody Production

A

injection of animal with an antigen and removal of antisera from blood

204
Q

Flow Cytometry

A

lasers see cells surfaces tagged with fluorescent antibodies and get a histogram or dot plot

205
Q

First Monoclonal Antibody

A

mouse antibody that recognized CD3 I cells to prevent rejection after kidney transplant but human body rejects it

206
Q

Chimeric Monoclonal Antibody

A

combine mouse V regions and human C regions (rituximb non-hodgkin B cell lymphoma)

207
Q

Humanize Monoclonal Antibody

A

produced by genetic engineering - only move hyper-variable region of mouse antibodies into human antibodies (omalizumab asthma)

208
Q

Variable Gene Segments

A

Heavy chains and TCRb have V, D, J, light chains have V, J

209
Q

Antibody Diversity?

A

primarily from numerous combos of V, D, and J segments, splicing is imprecise and leads to diversity, also arises from different combos of heavy and light chain and TCRa and TCRb proteins

210
Q

Not B-Cell Immunoglobulins

A

genes are fragmented in gene segments (inherited germline configurations)

211
Q

B Cell Immunoglobulins

A

rearrangement of gene segments allows for production of immunoglobulins, C regions are ready to be made but V regions are encoded by two (Vl) or three (Vh) gene segments that must rearrange to produce and exon

212
Q

V, J, and D stand for

A

variable, joining, diversity

213
Q

Recombination Signal Sequences

A

RSSs - flank the 3’ side of the V segment, both sides of the D segment, and the 5’ side of the J segment - provide recognition sites for the enzymes that cut and rejoin DNA and ensure that gene segments are joined in the correct order

214
Q

V(D)J recombinase

A

set of enzymes responsible for recombining V, D, and J

215
Q

Recombination-Activating Genes

A

RAG-1 and RAG-2 are two proteins of V(D)J recombinase that are specific to lymphocytes

216
Q

Other Recombination components

A

DNA ligase IV, DNA-dependent protein kinase, Artemis (nuclease), and Ku protein

217
Q

RAGs-RSSs

A

RAG complexes interact to align the RSSs and cleave the DNA (forming hairpins) and repair the broken ends of DNA to form the coding joint

218
Q

Junctional Diversity

A

enzymes that open the hairpins and form the coding joint introduce diversity into the third hypervariable region of heavy and light chains

1) nick opens hairpin to create a sequence that would be palindromic in double-stranded DNA (generates P nucleotides)
2) opened hairpins can be shortened by exonucleases or lengthened by terminal deoxynucleotidyl trasferase (TdT) (addition of N nucleotides)
3) base pairing occurs and gaps are filled
- -enzyme definiciencies affect T and B development and cause most sever combined immunodefincienceis.

219
Q

Junctional Diversity Effect

A

increase overall diversity by 3 x 10^7

220
Q

IgM and IgD in Developing Naive B Cells

A

isotype determined by heavy chain but only heavy chain in B cells before they encournter antigen u and deltat – Naive B Cells express both IgM and IgD on surface because of alternative splicing

221
Q

IgM and IgD Alt Splicing

A

transcription produces a transcropt that contains exons for both u and delta heavy chains but not the other isotype genes - splicing removes either u or delta exons

222
Q

Allelic Exclusion

A

only one heavy chain and one light chain are expressed in a developing B cell (single antigen specificity

Immunology (5 decks)

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