Lecture 3 Immunity (E1) Flashcards

Ch 7,8,9,10

1
Q

Antibody

A
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2
Q

Antigen

A

Substance recognized by the immune response

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3
Q

IgG, IgM, IgA, IgE, IgD

A

Ig- Immunoglobulin
Products and subsets of B-cells
G- most common
M- maternal
A-
E-allergerns
D-

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4
Q

Cytokine

A

Proteins made by a cell that affect other cells (paracrine/autocrine)

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5
Q

Chemokine

A

Chemoattractant molecules (migration, activation)

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5
Q

T-Cell (lymphocytes)

A

CD4 Helper cells (immune help), Treg- suppress, MHC-II restricted cytokine production
CD8 cytotoxic cells- Memory, MHC-I restricted cytolysis
TCR never soluble (a/b, a/a, y/)
CD3- all, CD2, CD4, CD8, 60-80% of lymphocytes in blood)
(T-cells require antigen presentation)

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6
Q

B-cell (lymphocytes)

A

Antibody producers(BCR, soluble), antigen presenters(MHC-II), MEMORY
IgM, IgD, IgG, IgA, IgE, or cytokines
Plasma cell- terminally differentiated antibody factories
Memory cells: long-lived, anamnestic response

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7
Q

NK Cell

A

Natural Killer Cells
Fill in the gap to cover immune evasion mechanisms of pathogens and tumors
(An innate lymphoid cell, along with ILC)

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8
Q

Neutrophil

A

Phagocytosis (major players from bacteria)
many surface receptors for bacterial antigens/lectins (PAMPS)
Surface opsonin receptors for antibody (FcgR), C3b
Source of pus (suppurative-mostly dead neutrophiles)
Very short lived, ~3 days, no mitochondria
-Neutropenia: susceptible to bacterial infections
-Neutrophilia: probably have an infection

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9
Q

Macrophage

A

3-8% of peripheral blood
M$-Long lived, mitochondria
1. phagocytosis
2. Surface markers- FcyR-I, II, III, CRs, Toll like receptors (TLR)
3. MHC-II antigen presentation to CD4 T-cells
4. Cytokines
a. Tissue repair
b. Antimicrobial/ inflammatory (IL-1, 6, 12, TNF-a)
Know surface structure and function

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10
Q

Dendritic Cell

A

Are major antigen presenter (to native T-cells)- Part of innate immunity but contribute to adaptive immunity
-Several flavors- Langerphans, plasmacytoid, ect
-Immature in tissues- Good Phagocytes
-Mature in lymph node- Good antigen presenter (MHC- I & II)

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11
Q

Eosinophil

A

Preformed cytoplasmic granules with anti-microbial substances
Circulate in blood, anti-parasitic response

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12
Q

Mast Cell

A

Preformed cytoplasmic granules with anti-microbial substances
Surface tissues, (skin, mucosa)

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13
Q

Basophil

A

Preformed cytoplasmic granules with anti-microbial substances
Similar granules to Mast cells, circulate in blood

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14
Q

Interferon

A

Class of Cytokines noted for anti-viral and other effects (INF- alpha, beta, y)

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15
Q

DAMP/PAMP

A

Tissue damage and infection trigger host responses recognized by host receptors on immune and other cells activate innate and inflammatory response
Pathogen-associated molecular pattern receptors (PAMPs)
Damage-associated molecular patterns (DAMP)
-Activation of innate immune system
TLR4-Viruses (GP cell surface), Fungi (Mannan cell surface), protozoa (GPI anchors, cell surface)
TLR4, CD14- Gram-Negative bacteria(LPS cell surface)

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16
Q

TLR and others

A

Toll like receptors (TLR)
TLR4-
Microbial activators:
-Bacteria, parasites, host, proteins
-Viruses, parasites, host proteins
Ligand: LPS, fungal mannans, viral glycoproteins, parasitic phospholipids, host heat shock proteins, LDL
*Know other

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17
Q

Innate Immunity

A

Basophils, Esinophils, Neutrophils, Monocytes, macrophage, Dendritic cells, NK cells
Barriers: Physical, Chemical, Complement et al., Genetic

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18
Q

Adaptive Immunity

A

MEMORY
B-Cells
T-Cells
Facilitates, enhances, regulates the innate responses

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19
Q

Opsonization

A

Binding to a pathogen or other material to facilitate phagocytosis

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20
Q

Thymus

A

Where T-cells undergo Maturation after leaving the bone marrow
Primary lymphoid organ

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21
Q

Bone marrow

A

Where both T-cells and B-cells originate before going elsewhere for maturation
Primary lymphoid organ
Cells identified via:
Morphology
staining
fucntion
markers

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22
Q

Phagocytosis

A

Basically eat or surround other cells

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23
Q

TH1

A

CD8 t-cells responses important for bacterial, especially intracellular, infections
Class II up-regulation on DC’s and Macrophages
Cytotoxicity

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24
TH2
CD4 response important for antibody protections Class II up-regulation on B-cells. DC's and Macrophages Allergic responses, Eosinophil toxins ADCC
25
TH17
CD4 response activates neutrophils, epithelial cells
26
MHC-I (Major histocompatibility Complex)
Dendritic Cells 1. Only cell that can initiate a new Tcell response 2. Process antigenic proteins into peptides 3. Increased expression of molecules for antigen presentation MHC I-peptide: CD8 T cells
27
MHC-II
Dendritic Cells 1. Only cell that can initiate a new Tcell response 2. Process antigenic proteins into peptides 3. Increased expression of molecules for antigen presentation MHC II-peptide: CD4 T cells
28
Peptide Loading
A short lived mutlisubunit membrane protein complex that is located in the ER. It orchestrates peptide translocation and selection by MHC-I molecules
29
Lymph node
Antigen presenting cells (dendritic) T-cell zones- Cortex Paracortex B-Cell zones- Primary follicle Germinal center of secondary follicle
30
Primary Lymph node organ
Bone Marrow Thymus Development
31
Secondary Lymph node organ
MALT (BALT, GALT) Lymph nodes Spleen Activation
32
Peyer's patch
In the gastrointestinal tract Protect the digestive system against harmful pathogens and monitor the commensal bacteria population
33
M-cell
Highly active in phagocytosis and transcytosis and thereby take up luminal bacteria and antigens an deliver them to DC's in the M-cell pocket for initiation of mucosal immune response
34
Antigen presentation
1. Antigen uptake: Antigen-presenting cells (APC's), such as dendritic cells and macrophages, ingest pathogens like viruses and bacteria 2. Antigen processing: APC's break down the pathogens into antigenic peptides 3. Antigen display: APC's display the antigenic peptides on their cell surfaces 4. T-cell activation: T-cells recognize the antigenic peptides and are activated
35
Classical pathway
Antibody (IgM or IgG) binds to pathogen surface+ complement (C1qr2s2) Induction
36
Lectin pathway
mannose binding protein attaches to pathogen surface
37
Alternative pathway
spontaneous C3b production attaches to pathogen surface
38
Complement
Classical, lectin, alternative pathways Opsonization, Membrane attack Inflammatory Cleavage Products (C3a, C5a, etc) Is a system of soluble- pattern-recognition receptors and effector molecules that detect and destroy microorganisms
39
C3b, C3a
C3b- main effector molecule of the complement system C3a- a peptide mediator of inflammation
40
C1Q
A complement component that is a soluble protein complex acting as a key bridge between innate and adaptive immune responses
41
C5b, C5a
Part of complement system C5a- helps in chemotaxis C5b- builds the primary part of the complement membrane attack complex
42
Barriers (Chemical, physical, Genetic)
43
Normal Flora
Bacterial that the body uses and has homeostasis, help eachother
44
Toll like receptors 1-9
TLR 1: Activators- Bacteria, Myobacteria, Neisseria meningitidis Ligand- Lipopeptides, Soluble factors TLR 2: Activators- Bacteria Fungi cells Ligand- LTA,LPS,PG,etc, Zymosan, Necrotic cells TLR 3: Activator- Viruses Ligand- Double-stranded RNA TLR 4- another note card TLR 5: Activator- Bacteria Ligand- Flagellin TLR 6: Activator- Bacteria, Fungi Ligand- LTA, lipopeptides, zymosan TLR 7: Activator- Viruses Ligand- Single-stranded RNA, Imidazoquinolines TLR 8: Activators- Viruses Ligand- Single-stranded RNA, Imidazoquinolines TLR 9: Activator- Bacteria, Viruses Ligand- Unmethylated DNA (CpG)
45
Diapedesis
Neutrophil diapedesis- Inflammatory signals 1. activation of DC, Macrophages, and NK cells by IL-12, IFN-y 2. Chemokines act on vessel endothelia Gradient formed from tissue to vessel lumen (runway lights) 3. Vessels interact with circulation immune cells (inflammation)
46
Sepsis
Vascular leakage- septic shock Fever Neutrophil activation SIRS(Systemic inflammatory response syndrome) Heart failure Intravascular thrombosis decreased blood pressure (TNF-a/IF-1 = a little goes a longggg way)
47
Adjuvant
Substance that promotes immune response to immungen
48
Hapten
Incomplete immunogen that cannot initiate response but can be recognized by antibody when conjugated to a carrier
49
Carrier
Protein modified by hapten to elicit response
50
Epitope
Minimal molecular structure recognized by immune response
51
Immunogen
Substance capable of eliciting an immune response
52
T-dependent antigens
Antigens that MUST be presented to T-helper cells to assist B cells for antibody production (class switching to IgG or IgA)
53
T-independent antigens
Antigens with large, repetitive structures (e.g. bacteria, flagellin, lipopolysaccharide, polysaccharide). Do not require antigen presentation for antibody production (IgM)
54
Memory
Adaptive response that produces high number of specific antigen responsive cells
55
Self-tolerance
Suppression of immune response vs self-antigens
56
Central immune tolerance
Generated in bone marrow or thymus during development (clonal deletion)
57
Peripheral immune tolerance
Generated in peripheral organs or tissues(clonal anergy)
58
Variable regions
Basic antibody structure N terminus, has Ag binding site
59
Constant regions
Antibody Stucture Part of C terminus: Cell and complement binding sites (CH2, CH3) - disulfide bonds to hold CH1 and CL-connected to variable region
60
VDJ-regions
61
Class switching
Switching class of antigen presenting molecules for an immune response (add more after reading chapter)
62
Antibody functions (slide 57)
63
Primary antigen challenge
Expansion, memory (first time exposure)
64
Secondary antigen challenge
Expansion, somatic hypermutation, more memory, a way faster immune response with more of a response
65
CD3
CD3 Complex- Signaling TCR
66
CD4
Helper cells
67
CD8
Cytotoxic cells
68
IL-2
Promotes T, B, and NK cell growth Regulatory, Treg requires this (lymph node, spleen, tissue)
69
IL-1
Can cause septic shock if too activated
70
TNF-alpha
Can causes septic shock if too activated
71
IL-4
Induced TH2 bc of parasites T-cell growth factor, stimulates immunoglobulin class switch (IgG, IgE), activation of mast cells, M2 (alternative) macrophage
72
IL-5
(TH2) B-cell and eosinophil growth factor, stimulates Ig class switch(IgG, IgA)
73
TGF-beta
Promotes inflammation and cytoxicity (TH1)
74
INF-y
Antivates M1 (inflammatory) macrophages; promotes B-cell production of IgG; Inhibits TH2
75
Antimicrobial peptides
76
Defensins
Part of innate defense system Disrupt membranes
77
Neutralization
Antibodies do this to toxins and toxic enzymes TH2 response through Ig (IgG and IgA) can block attachment of fungi and toxin action
78
Hypersensitivities
Has 4 types of reactions, the bodies reaction to harmful and not harmful things in the world
79
Type-1
IgE-Mediated; quick onset after exposure Allergic
80
Type-2
(IgG, IgM) Cytotoxic/antibody mediated Ex: Hemolytic reactions, Goodpasture syndrome Hyperacute graft rejection Cytotoxic
81
Type-3
Immune complex/IgG/IgM Mediated Ex: Hypersensitivity pneumonitis Systemic Lupus erthematosus Serum sickness Immune complex deposition
82
Type-4
Delayed or cell mediated ex: Chronic graft rejections PPD test Latex Nickel Poison ivy Delayed