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Microbial Pathogenesis > Lecture 3 Immunity (E1) > Flashcards

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
Q

TH2

A

CD4 response important for antibody protections
Class II up-regulation on B-cells. DC’s and Macrophages
Allergic responses, Eosinophil toxins ADCC

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25
Q

TH17

A

CD4 response activates neutrophils, epithelial cells

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26
Q

MHC-I (Major histocompatibility Complex)

A

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

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27
Q

MHC-II

A

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

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28
Q

Peptide Loading

A

A short lived mutlisubunit membrane protein complex that is located in the ER. It orchestrates peptide translocation and selection by MHC-I molecules

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29
Q

Lymph node

A

Antigen presenting cells (dendritic)
T-cell zones- Cortex Paracortex
B-Cell zones- Primary follicle
Germinal center of secondary follicle

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30
Q

Primary Lymph node organ

A

Bone Marrow
Thymus
Development

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31
Q

Secondary Lymph node organ

A

MALT (BALT, GALT)
Lymph nodes
Spleen
Activation

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32
Q

Peyer’s patch

A

In the gastrointestinal tract
Protect the digestive system against harmful pathogens and monitor the commensal bacteria population

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33
Q

M-cell

A

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
Q

Antigen presentation

A
  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
Q

Classical pathway

A

Antibody (IgM or IgG) binds to pathogen surface+ complement (C1qr2s2) Induction

36
Q

Lectin pathway

A

mannose binding protein attaches to pathogen
surface

37
Q

Alternative pathway

A

spontaneous C3b production attaches to
pathogen surface

38
Q

Complement

A

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
Q

C3b, C3a

A

C3b- main effector molecule of the complement system
C3a- a peptide mediator of inflammation

40
Q

C1Q

A

A complement component that is a soluble protein complex acting as a key bridge between innate and adaptive immune responses

41
Q

C5b, C5a

A

Part of complement system
C5a- helps in chemotaxis
C5b- builds the primary part of the complement membrane attack complex

42
Q

Barriers (Chemical, physical, Genetic)

A
43
Q

Normal Flora

A

Bacterial that the body uses and has homeostasis, help eachother

44
Q

Toll like receptors 1-9

A

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
Q

Diapedesis

A

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
Q

Sepsis

A

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
Q

Adjuvant

A

Substance that promotes immune response to immungen

48
Q

Hapten

A

Incomplete immunogen that cannot initiate response but can be recognized by antibody when conjugated to a carrier

49
Q

Carrier

A

Protein modified by hapten to elicit response

50
Q

Epitope

A

Minimal molecular structure recognized by immune response

51
Q

Immunogen

A

Substance capable of eliciting an immune response

52
Q

T-dependent antigens

A

Antigens that MUST be presented to T-helper cells to assist B cells for antibody production (class switching to IgG or IgA)

53
Q

T-independent antigens

A

Antigens with large, repetitive structures (e.g. bacteria, flagellin, lipopolysaccharide, polysaccharide). Do not require antigen presentation for antibody production (IgM)

54
Q

Memory

A

Adaptive response that produces high number of specific antigen responsive cells

55
Q

Self-tolerance

A

Suppression of immune response vs self-antigens

56
Q

Central immune tolerance

A

Generated in bone marrow or thymus during development (clonal deletion)

57
Q

Peripheral immune tolerance

A

Generated in peripheral organs or tissues(clonal anergy)

58
Q

Variable regions

A

Basic antibody structure
N terminus, has Ag binding site

59
Q

Constant regions

A

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
Q

VDJ-regions

A
61
Q

Class switching

A

Switching class of antigen presenting molecules for an immune response (add more after reading chapter)

62
Q

Antibody functions (slide 57)

A
63
Q

Primary antigen challenge

A

Expansion, memory (first time exposure)

64
Q

Secondary antigen challenge

A

Expansion, somatic hypermutation, more memory, a way faster immune response with more of a response

65
Q

CD3

A

CD3 Complex- Signaling
TCR

66
Q

CD4

A

Helper cells

67
Q

CD8

A

Cytotoxic cells

68
Q

IL-2

A

Promotes T, B, and NK cell growth
Regulatory, Treg requires this (lymph node, spleen, tissue)

69
Q

IL-1

A

Can cause septic shock if too activated

70
Q

TNF-alpha

A

Can causes septic shock if too activated

71
Q

IL-4

A

Induced TH2 bc of parasites
T-cell growth factor, stimulates immunoglobulin class switch (IgG, IgE), activation of mast cells, M2 (alternative) macrophage

72
Q

IL-5

A

(TH2) B-cell and eosinophil growth factor, stimulates Ig class switch(IgG, IgA)

73
Q

TGF-beta

A

Promotes inflammation and cytoxicity (TH1)

74
Q

INF-y

A

Antivates M1 (inflammatory) macrophages; promotes B-cell production of IgG; Inhibits TH2

75
Q

Antimicrobial peptides

A
76
Q

Defensins

A

Part of innate defense system
Disrupt membranes

77
Q

Neutralization

A

Antibodies do this to toxins and toxic enzymes
TH2 response through Ig (IgG and IgA) can block attachment of fungi and toxin action

78
Q

Hypersensitivities

A

Has 4 types of reactions, the bodies reaction to harmful and not harmful things in the world

79
Q

Type-1

A

IgE-Mediated; quick onset after exposure
Allergic

80
Q

Type-2

A

(IgG, IgM)
Cytotoxic/antibody mediated
Ex: Hemolytic reactions, Goodpasture syndrome
Hyperacute graft rejection
Cytotoxic

81
Q

Type-3

A

Immune complex/IgG/IgM Mediated
Ex: Hypersensitivity pneumonitis
Systemic Lupus erthematosus
Serum sickness
Immune complex deposition

82
Q

Type-4

A

Delayed or cell mediated
ex: Chronic graft rejections
PPD test
Latex
Nickel
Poison ivy
Delayed

Microbial Pathogenesis (11 decks)

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