1
Q
1st Line of Defense
A
- Intact skin
- Mucous membranes and their secretions (acidity)
- Normal microbiota
2
Q
2nd Line of Defense Innate Immunity
A
1) Defensive Cells i.e. phagocytes, mast cells, basophils and natural killer cells
2 Inflammation and fever
3) Antimicrobial substances and Interferons
3
Q
3rd Line of Defense aka Adaptive Immunity
A
- Specialized lymphocytes i.e. t-cells and b-cells
- Antibodies
- APCs
4
Q
Natural Killer Cells
A
- Kill infected target cells by releasing granules that contain perforin and granzymes
- Eliminate virus-infected cells and tumor cells
- Non-phagocytic: attaches to target cell and showers it with cytokines that destroy it (similar to action of Tc cells)
5
Q
How does inflammation fight invading pathogens?
A
Confines and destroys microbes and initiates tissue repair
6
Q
Antimicrobial Peptides (AMPs)3 MOAs
A
- Inhibit cell wall synthesis
- Forms pores in plasma membrane that cause lysis
- Destroys DNA and RNA
7
Q
AMP Glycoproteins produced by Lung Tissue
A
1) Collectins - Surfactant proteins A through D (opsonize pathogens)
2) Mannose-binding lectin (binds sugars found on microbe surfaces and Activates Complement System
8
Q
Normal Flora
A
- Competes with pathogens
- Block attachment and inhibits colonization
- Produce vit. k and biotin
- Can become opportunistic (i.e. strep, pseudomonas and candida)
9
Q
Granuloma
A
In presence of chronic inflammation, the immune system walls off infectious organisms, which may calcify overtime (i.e. fungal or TB infection in lungs)
10
Q
3 Plasma Protein Systems in Inflammation
A
1) Compliment System - Signals immune system, opsinizes microbes, destroys pathogens
2) Clotting System - Activates platelets/fibrin and limits spread of damage/infx
3) Kinin System - Produces bradykinin which enhances inflammation and vasodiation
11
Q
4 molecules involved in healing and tissue repair after acute inflammation?
A
1) IFN-y activates macrophages
2) TGF-β stimulates fibroblast growth
3 and 4) VEGF and FGF-2 - Angiogenic Factors that stimulate endothelial and fibroblast growth
12
Q
Erythrocyte Sedimentation Rate (ESR)
A
- A type of blood test that measures how quickly RBCs settle at the bottom of a test tube.
- RBCs normally settle slowly. A faster-than-normal rate may indicate inflammation in the body.
- Fibrinogen and Roleaux formatin increases ESR
13
Q
Cytokines
A
1) Interleukins (ILs)
2) TNF-α
3) TGF-β
4) Interferons
14
Q
Interleukins (ILs)
A
- 2 Major proinflammatory ILs: IL-1 & IL-6
- Produced by macrophages & lymphocytes
- Alter adhesion molecule expression
- Attract leukocytes & induce proliferation
15
Q
TNF-α
A
- Proinflammatory
- Produced by macrophages/mast cells
- Induces fever
- Long term causes cachexia & thrombosis
16
Q
TGF-β
A
- Produced by many types of cells in response to inflammtion
- Induces cell division & differentiation
17
Q
Interferons
A
- Type I - Released from virally infected cells - Interferes w/viral replication
- Type II - Released by lymphocytes – ↑ macrophage killing (viruses and bacteria)
18
Q
Cellular Products of Inflammation
A
1) Histamines
2) Leukatrienes
3) Protaglandins
4) Platelet Agregating Factor
19
Q
Histamines
A
- H1 receptor = vasodilation, bronchoconstriction, ↑ vascular permeability.
- H2 receptor = inhibits neutrophils; ↑ gastric acid
- H3 receptor = in CNS - regulates release of other neurotransmitters; ↑ cognitive function
- H4 receptor = in Hemopoietic tissue – regulates Eosinophil migration; involved w/activation of dendritic cells and T-cell differentiation
20
Q
Leukatrienes
A
- From mast cell membrane arachidonic acid via lipoxygenase pathway
- Effects similar to Histamine (H1)
21
Q
Protaglandins
A
- From mast cell membrane arachidonic acid via cyclooxygenase pathway
- 5 classes – A, B, D, E, F
- Enhance inflammation; PGE ↑ vasc. Perm. & smooth m. contraction
22
Q
Platelet Agregating Factor
A
- Produced by mast cells & WBCs
- Activates platelets & has same effect as Leukotrienes
23
Q
Effects of Histamine on the following cells:
1) Smooth Muscle Cell
2) Endothelial Cell
3) Neutrophil
4) Mast Cell
5) Parietal Cell of Stomach Mucosa
A
1) Smooth Muscle Cell and Endothelial Cell - Contraction
Bronchoconstriction, edema, vasodilation
2) Neutrophil and Mast Cell - Neutrophil migration and Enhanced inflammation
3) Parietal Cell of Stomach Mucosa - Secretion of gastric acid
24
Q
Eosinophils
A
- Defend against parasites
- Involved in allergic rxns
- Regulate & degrade vasoactive substances released by mast cells
25
Neutrophils (PMNs)
- Phagocytize microorganisms and cellular debris soon after injury (first responders)
- Secrete chemicals that call in longer-acting phagocytes
26
Macrophages
Phagocytize microorganisms and cellular debris
Secrete chemicals that promote tissue healing
Activate adaptive immunity
27
Endogenous VS. Exogenous Pyrogens
1) Endogenous - Endotoxins of pathogens like lipopolysaccharide (LPS) component of gram negative bacteria cell wall.
2) Exogenous - Prostaglandin-E2 (PGE2), IL-1, IL-6, TNF-α, interferon-γ
28
Alternative Pathway of Compliment Cascade
Factorb + FactorD + Properdin = C3Bb-Bb (C3 Convertase)
29
How are the classical and alternative pathways of the compliment system activated?
1) Classical pathway activation - antigen-antibody complex
| 2) Alternative pathway activation - bacterial endotoxin
30
Describe the Alternative compliment pathway
Activated by endotoxins >>> FactorB + FactorD + Properdin = C3 Convertase >>> C3 splits into C3a and C3b. C3b joins C5 = C5 Convertase. C5 breaks into C5a and C5b. C5b forms the Membrane attack complex (MAC)
31
Membrane Attack Complex (MAC)
Form damaging pores in the plasma membrane of the pathogen
32
Chemotactic Factors of the Compliment Cascade
C3a and C5a - Diffuse away from the pathogen and act as chemotactic agents to attract phagocytic cells to the site of inflammation
33
Opsinin
C3b - When IgG & C3b bind to the cell membrane of the pathogen that activates it, labeling it for phagocytosis (opsonization)
34
The Compliment System
The complement system is a series of proteins constitutively found in the blood plasma.
35
Interferons
- A protein produced by a cell that has been infected with a virus
- Interferon molecules then travel to neighboring un-inffected cells and produce antiviral protein
- Antiviral protein blocks virus from replicating nucleic acid in the unaffected cell
36
Types of Interferons
1) Interferon α
2) Interferon β
3) Interferon γ
37
Interferon α
- Produced by Monocytes
- Has Antiviral action
- Increases expression of MHC I
- Can be used to treat Hep. B and C
38
Interferon β
- Produced by Fibroblasts
- Has Antiviral action
- Increases expression of MHC I
- Can be used to treat MS
39
Interferon γ
- Produced by NK, Tc(CD8), Th(CD4)
- Activates Macrophages
- Increases expression of MHC II
- Can be used in treatment of cancer
40
4 Steps of Phagocytocis
1) Recognition and adherence (binding)
2) Engulfment and formation of phagosome
3) Fusion with lysosome to form phagolysosome
4) Destruction killing and digestion
41
T-cell development in the Thymus (Cortex)
1) Untrained thymocytes from bone marrow enter thymic cortex
2) Thymic epithelial cells present MHC proteins to untrained thrombocytes and they bind together.
- This is called positive selection
3) Thymocytes that survive positive selection become double positive because they receive both CD4 and CD8 receptors.
42
What happens to the thymocytes that fail to bind with MHC proteins in the 2nd step of T-cell development in the thymic cortex.
They undergo apoptosis (cell death)
43
What happens to the thymic epithelial cells after they bind MHC proteins and and receive CD4 and CD8 receptors?
- They move to the thymic medulla
- Come in contact with Antigen Presenting Cells (APCs)
- If they can bind APCs, then they will under apoptosis
- Binding with APCs means they will attack body cells
- This is called negative selection
44
What happens after a cell undergoes negative selection.
Self-tolerant thrombocytes then choose to express CD4 or CD8 receptors, but not both
45
Major Histocompatability Complex (MHC)
- A set of genes that code for cell surface proteins
- Essential for the acquired immune system to recognize foreign molecules
- Determines histocompatibility.
46
Class I MHC vs Class II MHC
1) Class I MHC - Single transmembrane chain α and β2 microglobulin
2) Class II MHC - Two transmembrane chains α and β
47
Distribution of Class I MHC vs Class II MHC
1) Class I MHC - All nucleated cells and platelets
| 2) Class II MHC - B-cells, APCs, and some epithelial cells.
48
Presentation of Class I MHC vs Class II MHC
1) Class I MHC - Endogenous antigens (8-10 amino acids) derived from intracellular proteins
2) Class II MHC - Exogenous antigens derived from extracellular pathogens
49
Reaction of Class I MHC vs Class II MHC
1) Class I MHC - CD8 on Tc cells
| 2) Class II MHC - CD4 on Th cells
50
Activation of Helper T cell vs Cytotoxic T cell
1) Th cell - Stimulate b-cells to produce antibodies after binding with MHC II surface proteins on APC
2) Destroy infected body cells after binding to MHC I surface proteins on infected cells.
51
Stages of B-cell development in Bone Marrow
1) Stem Cell
2) Pro B-cell (early, late)
3) Pre B-cell
4) Immature B-cell
5) Naive B-cell
6) Mature B-cell
52
Antibody Characteristics
1) IgE - Active against parasites; important mediators of allergic responses
2) IgM - Produced during the primary response to an antigen; are the largest Igs (pentamer)
3) IgGMost abundant class of Igs; transported across the placenta
4) IgA - Has subclasses; one subclass is most abundant in body secretions
5) IgD - Serve as surface receptors on developing B lymphocytes
53
Direct an Indirect Functions of Antibodies
1) Direct - Virus neutralization by blocking docking to host cell and toxin neutralization.
2) Indirect - Activate compliment mediated killing and phagocytosis via opsonization.
54
Dendritic Cells
1) Capture Antigen from invading pathogen in epithelial tissue
2) Leave epithelium and migrate to lymphatic vessel
3) Presents Antigen to immature T cells
4) Mature T cells multiply and proliferate
55
Antigen
- Presented my APCs (i.e. macrophage) to Th-cells on Class II MHCs.
- Only Th-cells with corresponding receptors are can bind with the APC and stimulate the release of cytokines.
56
Superantigen
- Binds to the outer portion of the APC and outer portion of the Th-cell without specificity.
- Ability to bind without specificity mean that cytokines are released from 20x as many Th-cells.
Excessive cytokine release leads to nausea, diarrhea, and toxic shock syndrome.
57
The Mucosal Immune Response: IgA function
1) MALT such as Peyer’s patches of the small intestine generate IgA immunity.
2) Microfold cells (M cells) transport antigen inside the body.
3) Dendritic cells then take the antigen to the regional lymph nodes, where an
immune response is mounted.
58
2 Types of Adaptive Immunity
- Naturally acquired
| - Artificially acquired
59
Naturally Acquired Immunity
1) Active - Antigens enter the body naturally >>> the body makes antibodies and specialized lymphocytes
2) Passive - Antibodies pass from mother to fetus or to infant via mother's milk
60
Artificially Acquired Immunity
1) Active - Antigens are introduced in vaccines >>> the body makes antibodies and specialized lymphocytes
2) Passive - Preformed antibodies in immune serum are introduced by injection
61
IgE Mediated Immune Hypersensitivity
- Causes localized and systemic anaphylaxis
| - Seasonal allergies including hay fever such as those to peanuts, hives and eczema.
62
IgG Mediated Cytotoxic Hypersensitivity
RBCs destroyed by compliment and antibody during a transfusion of mismatched blood type or during erythroblastosis fetalis
63
Immune Complex Mediated-Hypersensitivity
- Most common form of immune complex disease are seen in glomerulonephritis, RA, and systemic lupus erythematosis
64
Cell-Mediated Hypersensitivity
- Most common forms are contact dermatitis, tuberculin reaction, autoimmune diseases such as DM1, MS, and RA
65
Stem Cells from bone marrow differentiate intzowhich 2 cells?
1) Myeloid progenitor cells
| 2) Lymphoid progenitor cells
66
Myeloid Progenitor Cells Differentiate into which 4 types of granulocytes?
1) Neutrophils, Basophils, Eosinophil, and Monocytes (macrophage and dendritic cells)
67
2 Types AMPs
1) AMPs produced by Epithelial and WBCs: Cathelicidin (α helix shape) and Defensin (β sheet structure)
2) AMPs produced by Lung Tissue: Collectins and Mannose binding lectins
68
How do the following AMPs fight invading pathogens:
1) Cathlicidin
2) Defensin
3) Collectins
4) Monnose binding lectins
1) Cathlicidin - Punch holes in bacterial membranes
2) Defensin - Punch holes in bacterial membranes
3) Collectins - Opsinize pathogens
4) Monnose binding lectins - Activates Complement System
69
3 types of Phagocytes
1) Neutrophils
2) Eosinophils
3) Monocytes (dendritic cells and macrophages)
70
4 Types of Antimicrobial Substances involved in the 2nd line of defense against invading pathogens
1) Compliment System
2) Interferons
3) Iron Binding Proteins
4) Antimicrobial Peptides
CRNA Adv. A&P
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