Immunity Flashcards
(121 cards)
1
Q
1st line of defense (MIN)
A
Intact skin
Mucous membranes
normal microbiota
2
Q
2nd Line of defense (MINCAPFI)
A
Mass cells and Basophils (inflammatory response)
Inflammation
Natural killer cells
Complement system
Anti-microbial substance
Phagocytes DEMMN(neutrophils, monocytes; eosinophils,
dendritic cells, and macrophages)
Fever
Interferon
3
Q
3rd line of defense
A
Specialized lymphocytes T and B cells Antibodies T lymphocytes Antigen presenting cells B lymphocyts
4
Q
Prevents microbes from entering airway
A
Epiglottis
5
Q
Tears contain ______ which destroy cells walls, gram positive bacteria
A
Lysosomes.
6
Q
Traps microbes in respiratory adn GI tract
A
Mucous
7
Q
Phagocytes
A
Cells such as neutrophils, eosinophisl, dendritic cells, and macrophages.
8
Q
Fever
A
Intensifies the effects of interferons, inhibits growths of some microbes, speeds up body reactions that aid repair.
9
Q
***Interferons
A
Protect uninfected host cells from Viral infection
Interferes with viral replication
10
Q
Granuloma -
A
Immune system walls off infectious organisms (fungal or tuberculosis Infections in the lungs). May calcify over time.
11
Q
is ongoing inflammation. It can be
caused by foreign bodies, persistent pathogens, and autoimmune diseases.
A
Chronic inflammation.
12
Q
Short term inflammatory response to an insult to the body
A
Acute inflammation
13
Q
*****Repair and healing process
A
*****IFN-gama (activates macrophages)
TGF-B - (Stimulates fibroblast growth)
Angiogenic factors [VEGF, FGE-2} stimulates endothelial and fibroblast growth
14
Q
Cellular injury –> Mast cell degranulation
A
Histamine is released
15
Q
Cellular injury –> activation of plasma systems. Mast cell degranulation
A
Histamine is released
16
Q
*****Mediators of Inflammation
A
Vasodilation: Prostaglandins, Histamine, Nitric Oxide
Vascular permeablity: Histamine, bradykinin, leukotrienes and , PAF
Pain: Prostaglandins, bradykinin
Systemic effects
Fever : Il-1 , Il-6, TNF alpha, prostaglandins
Acute phase reactants
Leukocytosis
17
Q
Endogenous pyrogens
A
Prostaglandin-E2 (PGE2) IL-1 IL-6 TNF-α interferon-γ
18
Q
Endotoxins of pathogens:
A
lipopolysaccharide (LPS) component of gram negative bacteria cell wall
19
Q
Eosinophrils
A
- Fight PARASYTIC worms infction
2. Regulate and degrade substances.
20
Q
Neutrophyils (PMN) most ABUNDANT
A
Phagocytize microorganisms and cellular debris soon after injury FIRST RESPONDERS
Secrete chemical
21
Q
Natural Killer cells
A
Eliminate virus infected cells and tumor cells
DESTROY TUMOR/CANCER CELLS
22
Q
Neutrophyils (PMN) most ABUNDANT
Both (shower and
A
Phagocytize microorganisms and cellular debris soon after injury FIRST RESPONDERS
Secrete chemical
23
Q
Natural Killer cells
A
Eliminate virus infected cells and tumor cells
DESTROY TUMOR/CANCER CELLS
non-PHAGOCYTES, shower with citokines that destroy
24
Q
Macrophages
A
Phagocytize microorganinsm and cellular debris
Secrete chemicals that promote tissue healing
Activate adaptive Immunity.
25
Production
| What is arachidonic acid?
Cell membrane PHOSPHOTIDYLCHOLINE gives-->
Phospholipase A2 --> membrane protein Splits into Arachidonic acid and PAF
Arachidonic acid is a 20 carbon polyunsaturate fatty acid precursor to pro-inflammatory molecules
Arachidonic acid gives 2 cyclooxygenase (forms and gives us Prostaglandins 2) and 5-Lipoxygenas (which produces inflammatory leukotrienes)
26
Production of lipid vasoactive substance by mast cells.
Phospholipase A2 -membrane protein
| Arachinoic acid precorse to cyclooxygenase (gives us Prostaglanding 2
27
Most NSAIDS are
cyclooxygenase
28
Too much ASA
Bleeding
29
Complement system (3) main action.
1. Chemical signaling. Through NAFTATOXINS (tell white blood cells to kills bacteria , like smelling smoke)
2. Starts putting protein molecule on the bacteria, so macrophages destroy. OPSONIZATION- Mark something so macrophages can attack and destroy.
3. Punches holes in bacteria wall. (Membrane attack complex)
30
******________ bind to the cell membrane of the pathogen that activates it, labeling it for ___________
IgG & C3b; phagocytosis (opsonization)
31
Interferon α -
Produced by Monocytes, has Antiviral action, increases expression of MHC I can be used to treat Hep. B, C
32
Interferon β -
produced by Fibroblasts, has Antiviral action, increases expression of MHC I can be used to treat MS
33
Interferon γ -
produced by NK, Tc(CD8), Th(CD4)
| Activates Macrophages, increases expression of MHC II, can be used in treatment of cancer
34
T-cell development in the Thymus (Cortex)
Step 1: Recognize foreign antigen
| Step 2: Regonize self antigen
35
Where T cells are tested
Thymus
36
Where B cells are tested
Bone marrow
37
Thymic epithelial cells mechanism of action:
present MHC proteins to the untrained thymocytes
Thymocytes that succesffully bind to the protein MHC continue while those that cannot undergo APOPTOSIS (this is positive selection selecting those that binds)
38
CD 8 becomes
Cytotoxic T cells.
39
Which Ig Active against parasites; important mediators of allergic responses
IgE
40
IgE
- Active against parasites; important mediators of allergic responses
41
Produced during the primary response to an antigen; are the largest Igs (pentamer)
IgM
42
- Active against parasites; important mediators of allergic (attach mast cells and basophils) responses
IgE
43
Produced during the primary response to an antigen; are the largest Igs (pentamer)
IgM
44
IgM
Produced during the primary response to an antigen; are the largest Igs (pentamer)
45
Most abundant class of Igs; transported across the placenta
IgG
46
Has subclasses; one subclass is most abundant in body secretions
IgA
47
Has subclasses; one subclass is most abundant in body secretions
IgA
48
IgA
Has subclasses; one subclass is most abundant in body secretions
49
Serve as surface receptors on developing B lymphocytes
IgD
50
Serve as surface receptors on developing B lymphocytes
IgD
51
IgD
Serve as surface receptors on developing B lymphocytes
52
Dendritic cells (CL -PM)
Capture Antigen from invading pathogen in epithelial tissue
Leave epithelium and migrate to lymphatic vessel
Presents Antigen to immature T cells
Mature T cells multiply and proliferate
53
Type I hypersensitivity
IgE Medicated hypersensitivity
causes localized and systemic anaphylaxis, seasonal allergies including Hay fever, food allergies such as those to shellfish and peanus , hives and eczema
54
Type II hypersensitivity
IgG - Mediated Cytotoxic Hypersensitivity.
Red blood cells destroyed by complement and antibody during a transfusion of mismatched blood type or during erythropoiesis fetalis
55
Type III Hypersensitivity
Immune complex Mediated Hypersensitivity
| Most COMMON FORMS of immune complex disease are seen in GLOMERULONEPHRITIS< RA, and SLE
56
Type IV Hypersensitivity
Cell- Mediated Hypersensitivity
| Most common forms are contact dermatitis, Tuberculin reaction, Autoimmune disease such as DM I, MS and RA
57
****General Four MECHANISMS of Antibodies
Virus neutralization by blocking docking to host cells
Toxin neutrolization
Activate complement-mediated killing
Phagocytosis via opsinisation
58
*****Class II MHC Distribution
Presents_____
Reacts with _______
B cells, APCs, and some epithelial cells
Exogenous antigens derived from extracellular organisms
CD4 on Th cells
59
******Class I MHC Distribution -->
Presents_____
Reacts with _______
All nucleated cells and platelets
Endogenous antigens (8-10 amino acids)derived from INTRACELLULAR PROTEINS
CD-8 on Tc Cells
60
ADCC
Antibody dependent CYtotoxic cell
Does not use CD8 or MHC
Binding to antiboeis
Has receptors for those antibodies.
61
Epitomes
Specific regions for binding for antigen.
62
Stages of B cell development in bone marrow.
```
Stages
Stem cell
Pro B cell (early, late)
Pre-B cells
Immature B cell
Naive B cell
Mature B cell
```
63
1st step of complement system
IgE to bindg
64
Dendritic Cells short version
Capture antigen from invading pathogen in epithelia tissue
Types of APCs
IN skin
65
Antigen processing and presentation
Reaction when presented to pathogen
| Autoimmune dysfunction.
66
```
How does Superantigen cause TSS?
Bind to MHC class II antigen
```
Kills all viruses (does not specifically target any particular cell)
STAPH AUREUS EXAMPLE: Toxic Shock syndrome.
The superantigen binds to all T-cells not specific one.--> RELEASE OF EXCESSIVE IL-2
67
Toxic Shock syndrome can cause
Rash
| Desquamation of hands
68
2 types of adaptive immunity
Naturally acquired
| Artificially Acquired.
69
Mucosal immune Response
MALT such as Peyer’s patches (tonsils) of the small intestine generate ______immunity. Microfold cells (M cells) transport ________
IgA immunity.
antigen inside the body. Dendritic cells then take the antigen to the regional lymph nodes, where an immune response is mounted.
70
Acute Inflammatory Response system
Cellular injury or pathogenic invasion leads
to:
mast cell degranulation
activation of plasma systems
Release of cellular produces
71
Complement clotting kinin leads to
```
Vasodilation
Vascular permeability
Cellular infiltration
Thrombosis
stimulation of nerve endings
```
72
Mediators of inflammation: What limit inflammation
IL-10 (inhibits cytokine production)
TGF-B (inhibits macrophage proliferation)
ECF-A (Attracts eosinophils)
Histaminage, arylsulfatase (destroy histamine and leukotrines)
73
Mediators of inflammation: Vascular Permeability
Histamine
Bradykinin
Leukotrienes
PAF
74
Intact skin forms a physical barrier to entrance of microbes
Epidermis of the skin
75
Inhibit entrance of many microbes, but not as effective as intact skin
Mucous membranes.
76
Traps microbes in respiratory and GI tract
Mucous
77
Provide tears that wash away microbes: tears contain lysozyme which destroy cells especially GRAm POSITIVE BACTERIA
Lacrimal apparatus.
78
Dilutes and washes microbes from mouth
Saliva
79
Filters and traps microbes and dust in nose
Hairs
80
Together with mucous form a ciliary escalator which traps and remove microbes from upper respiratory tract
Cillia
81
Prevents microbe from entering ear
Earwax
82
Washes microbes from urethra to prevent colonization
Urine
83
Move microbes out of body
Vaginal secretions
84
Expel microbes out of body
Peristalsis
Defecation
Vomiting
Diarrhea
85
Component of First line defense: Chemical factors
| SUP VEGS
```
Sebum
Urine
Perspiration
Vaginal secretion
Earwax
Gastric juice
Saliva
```
86
Both chemical and physical Factors of 1st line defense
Saliva
Urine
Vaginal secretions
Earwax
87
Components of 2nd line of defense
Defensive cells
Inflammation
Fever
Antimicrobial Substances
88
Components of 2nd line of defense : Defensive cells are
Phagocytes and
| Natural killer cells
89
Components of 2nd line of defense : Confine and destroys microbes initiate tissue repair
Inflammation
90
Components of 2nd line of defense : Intensify the effects of interferons, inhibits growth of some microbes and SPEED UP THE BODY REACTION that aid repair
Fever
91
Components of 2nd line of defense : Kill infected target cells
Kills infected target cells by releasing granules that contain PERFORIN and GRANZYMES --> PHAGOCYTES THEN KILL THE INFECTED MICROBES.
92
Components of 2nd line of defense : Phagocytosis such a neutrophyills, eosinophils, dendritic cells and macrophages
Phagocytes
93
Phagocytes are
neutrophils
Eosinophils
Dendritic cells
macrophages
94
Antimicrobial substance : Complement system
Causes cytosis of microbes, promotes phagocytosis, and contributes to inflammation
95
Interferons function?
Protect FROM VIRAL INFECTION.
96
Inhibit growth of certain bacteria by reducing iron
Iron binding proteins.
97
Describe arachadonic acid. Explain its role in the inflammatory response?
20- Carbon polyunsaturated fatty acid precursor to pro-inflammatory molecules (Cyclooxygenase and 5-Lipooxygenase)
98
Precursor of Arachidonic acid
Phospholipase A2
99
T Cell development in the THYMUS (MEDULLA)
The surviving thymocytes move to the thymic medulla where they encounter antigen-presenting cells (APCs) . These APCs present self-antigents from other body ceslls. Thymocytes that bind with the self-antigens undergo apoptosis, as this indicates that they will attack body cells. This is called NEGATIVE SELECTION (selection for cells that don't bind)
100
T-cell development in the thymus MEDULLA is the one with the _________ for cells that _____ bind
Negative selection, don't
101
Effects of Histamine on Target cells : H1
```
Target cells (SENM)
Smooth muscle cell; endothelial cell; Neutrophil ; Mast cell
```
Effect of histamine:( Smooth muscle cell) Contraction --> Bronchoconstriction
Effect of histamine on Endothelial Cells:
Contraction (Retraction at endothelial junction)--> Edema and vasodilation
Effects of histamine on Neutrophils:
Increased chemotaxis --> Neutrophil migration
Effects of histamine on Mast cell
Prostaglandin synthesis --> Enhanced Inflammation.
102
Effects of Histamine on Target cells : H2
Target Cell:
Parietal cell of stomach mucosa
Effect of histamine --> secretion of gastric acid
```
LENM
Lymphocyte : Decreased activity
Eosinophils: decreased activity
Neutrophil: Decreased chemotaxis
Mast cell: Decreased granulation.
```
103
Explain mast cell degranulation
Degranulation is a cellular process that releases antimicrobial cytotoxic or other molecules from secretory vesicles called granules found inside some cells. It is used by several different cells involved in the immune system, including granulocytes (neutrophils, basophils, and eosinophils) and mast cells.
104
Inflammatory Phases 2 fates
Cellular injury --> Acute inflammatory --> healing
| Cellular injury --> Acute inflammatory --> Chronic inflammatory --> Glanuloma formation --> Healing
105
Actions of PGD2 (VIBE)
Vasodilation
Increased capillary permeability
Bronchoconstriction (smooth muscle contraction)
Enhanced inflammation
106
Actions of PAF (VEBEF VI)
```
Vasoconstriction
Enhanced Inflammation
Bronchoconstriction
Eosinophils chemotaxis
Platelet activation (VI) at low PAF
```
107
Actions at H1 receptor
GTP converted to cGMP--> increasing level (cell activation)
108
Actions at H2 receptor
ATP converted to cAMP --> increasing level -->Cell INACTIVATION
109
Degranulation immediate response
| 1. Histamine --> vascular effects
Vasodilation--> Increased permeability --> Exudation
110
Degranulation immediate response
| 2.Neutrophil chemotactic factor
Neutrophils attracted to site --> Phagocytosis
111
Degranulation immediate response
| 3. Eosinophils chemotactic factor
Eosinophils attached to site -->Phagocytosis
112
Synthesis long term response
| Leukotrienes and Prostalginding E- series
Vascular effects--> Dilation and increased permeability--> EXUDATION
113
T cells and B cells can be activated only by
exposure to a specific antigen at a specific site in a plasma membrane.
114
When an antigen is bound to a Class II MHC protein, it can activate a ________ cell.
B helper Cells
115
Class II MHC molecules are found on which of the following?
Lymphocytes and APCs
116
When an antigen is bound to a Class I MHC molecule, it can stimulate a ________ cell.
CYTOTOXIC T cells
117
Cell mediated immune response in order: Several cycles of mitosis occur.
2. Antigen is engulfed and presented by a macrophage.
3. Cytotoxic T cells migrate to focus of infection.
4. T cells with specific receptors recognize the antigen.
5. T cells differentiate into cytotoxic T cells or T memory cells.
6. Cytotoxic T cells release perforin and/or lymphotoxin.
B) 2, 4, 1, 5, 3, 6
Antigen is engulfed and presented by a macrophage
T cells with specific receptors recognize the antigen
Several cycles of mitosis occur.
T cells differentiate into cytotoxic T cells or T memory cells.
Cytotoxic T cells migrate to focus of infection.
Cytotoxic T cells release perforin and/or lymphotoxin
118
Immunity that results from antibodies that pass through the placenta from mother to fetus is called ________ immunity.
Naturally acquired passive
119
The first line of CELLULAR DEFENSE Against PATHOGENS
Phagocytes
120
Most of the lymph returns to the venous circulation by way of the
THORACIC DUCT
121
Lymphatic tissue is found in the greatest quantity in
A) the adult spleen.
