Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Immunology > Immune response > Flashcards

Immune response Flashcards

(104 cards)

Start Studying
1
Q

Acute phase reactants - definition

A

Factors whose concentrations change significantly in response to inflammation

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

Acute phase reactants produced by (when, and induced by)

A

produced by liver in both acute and chronic inflammatory states
Notably induced by Il-6

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

Acute phase reactants - types and the way that they change

A

upregulated: 1. C-reactive protein 2. Ferretin 3. Fibrinogen 4. Hepcidin 5. Serum amyloid A down
downregulated: 1. albumin 2. transferrin

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

C-reactive protein - function and clinical relevance

A
  1. opsonin (enhances phagocytosis)
  2. Fixes complement
    - -> Measured clinically as a sign of ongoing inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ferritin - function (as an acute phase reactant)

A

Binds and sequesters iron to inhibit microbial iron scavenging

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

Fibrinogen - function (as an acute phase reactant)

A
  1. coagulation factor

2. promotes endothelial repatir

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

Hepcidin - function

A

decreases iron absorption (by degrading ferroportin) and decreases iron release (from macrophages) –> anemia of chronic disease

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

Acute phase reactants - serum amyloid A?

A

prolonged elevation –> amyloidosis

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

Acute phase reactants - albumin

A

reduction conserves aminoacids for positive reactants

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

Acute phase reactants - transferrin

A

internalized by macrophages to sequester iron

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

Complement is produced by …/ play role in …. (generally)

A

liver / role in innate immunity and inflammation

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

Membrane attach complex (MAC) defends against

A

Gram (-) bacteria

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

Complement activation - pathways (generally mediated by)

A
  1. classic pathway - IgG or IgM mediated
  2. Alternative pathway - microbe surface molecules and spontaneous
  3. Lectin pathway - mannose or other sugars on microbe surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

complement function (and which types)

A
  1. oponization: C3b
  2. anaphylaxis: C3a, C4a, C5a
  3. neutrophil chemotaxis: C5a
  4. cytolyisis by MAC: C5b-9
  5. helps cliar immune complex: C3b
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

primary opsonins in bacterial defence

A
  1. C3b

2. IgG

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

beside phagocytosis enhancement , C3b also help

A

clear immune complexes (C3b-tagged immune complex is destroyed)

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

Complement inhibitos

A
  1. Decay-accelerating factor (DAF, aka CD55)

2. C1 esterase inhibitor help prevent complement activation on self cells (eg. RBCs)

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

Decay-accelerating factor (DAF) is aka

A

CD55

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

complement activation - alternative pathway

A
  • C3 + spontantenous/microbial surface –> C3b
  • C3b + Bp factor (B+D–>Bd) –> C3Bd convertase
  • C3bBd (C3 convertase) + C3 –> C3a + C3b
  • C3b + C3bBd –> C3bBd3b (C5 convertase)
  • C3bBd3b + C5 –> C5a + C5b
  • C5b + C6-9 –> mac –> lysis, cytotoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

complement activation - classic pathway

A
  • C1 + antigen-antibody complex (IgM, IgG) –> activate C1
  • activated C1 + C4 + C2 –> C4a + C4b + C2a + C2b
  • C4b + C2b –> C4b2b (C3 convertase)
  • C3b + C4b2b –> C4b2b3b (C5 convertase)
  • C4b2b3b + C5 –> C5a + C5b
  • C5b + C6-9 –> mac –> lysis, cytotoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

complement activation - lectin pathway

A

C1 + Microbial surface (eg. maltose) –> C1 like complex (activated C1)

  • activated C1 + C4 + C2 –> C4a + C4b + C2a + C2b
  • C4b + C2b –> C4b2b (C3 convertase)
  • C3b + C4b2b –> C4b2b3b (C5 convertase)
  • C4b2b3b + C5 –> C5a + C5b
  • C5b + C6-9 –> mac –> lysis, cytotoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

C2 historically

A

the larger fragment of of C2 was called C2a but is now referred to as C2b

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

Complement disorders - types

A
  1. C1 esterase inhibitor deficiency
  2. C3 deficiency
  3. C5-9 deficiency
  4. DAF (GPI-anchored enzyme) deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

C1 esterase inhibitor deficiency?

A

causes hereditary angioedema due to upregulated activation of kallikerein –> increased bradykinin –> VASODILATION, PERMEABILITY, INCREASES PAIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
contraindicated in C1 esterase inhibitor deficiency? (why)
ACE inhibitors | because ACE inhibits bradykinin
26
C3 deficiency?
1. increases risk of severe, recurrent pyogenic sinus and respiratory tract infection 2. increased susceptibility to type III hypersensitivity reaction (C3b helps to clear ICs)
27
C5-9 deficiency?
Terminal complement deficiency increases susceptibility to recurrent Neisseria bacteremia
28
DAF (GPI-anchored enzyme) deficiency
Causes complement-mediated lysis of RBCs and paroxysmal noctural hemoglobinuria
29
Important cytokines secreted by macrophages
IL-1, 6, 8, 12, TNFa
30
Important cytokines secreted by ALL T cells
IL-2, IL-3
31
Important cytokines secreted from Th1 cells
Interferon γ
32
Important cytokines secreted from Th2 cells
IL-4, 5, 10, 13
33
IL-1 is AKA
osteoclast-activating factor
34
IL-1 causes
1. fever 2. acute inlammation 3. Cachexia
35
IL-1 causes acute inflammation - mechanism
1. acivates endothelium to express adhesion molecules | 2. induce chemokine secretion to recroit WBCs
36
IL-6 -->
1. fever 2. stimulates production of acute-phase proteins 3. Cachexia 4. Th --> Th17 (with il-6)
37
IL-8 -->
major chemotactic factor for neutrophils
38
IL-12 -->
1. induce differentiation of T cells into Th1 cells | 2. Activates NK cells
39
TNF-a -->
1. mediates septic shock 2. Cachexia in malignancy 3. acute inflammation (WBC recruitment, activates endothelium, vascular leak) 4. Apoptosis (instrict pathway) 5. induce and maintains granuloma formation
40
IL-2 -->
stimulates growth of helper, cytotoxic and regulatory T cells and NK cells
41
IL-3 -->
supports growth and differentiateion of bone marrow stem cells (function like GM-CSF)
42
INF-γ is secreted by
NK cells and T cells in response to il-12 from macrophages
43
INF-γ -->
1. stimulates macrophages to kill phagocytosed pathogens 2. Inhibits differentiation of Th2 3. activates NK cells to kill virus infected-cells 4. increases MHC expression and antigen presentation by all cells
44
IL-4 -->
1. induce differentation of T cells into Th2 2. Promotes growth of B cells 3. Inhibit Th1 differentiation 4. Enhance class switching to IgE and IgG
45
IL-5 -->
1. Promotes growth and differentation of B cells 2. Enhance class switching to IgA 3. Stimulates growth and differentiation of eosinophils
46
IL-10 -->
1. attenuates inflammatory response 2. decreases expression of MHC II and Th1 cytokines 3. Inhibits activaed macrophages and dendritic cells 4. Inhibit differentiation of Th to Th1
47
beside Th2 cells, il-10 is also secreted by
T reg cells
48
cytokines that attenuate the immune response
1. TGF-β | 2. IL-10
49
Respiratory burst is AKA, and definition
oxidative burst | is the rapid release of ROS from different types of cells.
50
Respiratory burst (oxidative burst) plays important role in
immune response --> rapid release of ROS
51
ROS - pathway
O2 + NADPH --> 02- + NADP+ (NADPH oxidase) 02- --> H202 (Superoxide dismutase) H20 --> a. H20 + 02 (bacterial catalase) b.H20 + CL- --> HCLO (Myeloperoxidase) --> destroys bacteria c. glutathione pathway 02-->superoxide anion HCLO-->Bleach (Hypochlorite) H202-->Hydrogen peroxide
52
glutatione pathway
NADP+ + Glucose-6-P --> NADPH + 6-phosphpgluconate (G6PD) NADPH + oxidazed Glutathione --> NADP+ + reduced glutathione (Glutathione reductase) REDUCED GLUTATHIONE destroys H202 reduced glutathione + H202 --> oxidazed Glutathione + H2O (Glutathione peroxide) Glutathione enzymes (peroxidase and reductase requires selinium)
53
NADPH oxidase deficiency
chronic granulomatous disease
54
Patients with chronic granulomatous disease -->
can untlize H2O2 by invading organisms and convert it to ROS. High risk at CAT+ species capable of neutralizing their own H2O2, leaving phagocytes without ROS for fiighting infections
55
Pyocyanin of P. aeruginosa - function
generate ROS to kill competing microbes
56
Lactoferrrin is a
protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation
57
NAPDH - role in ROS
it plays a role in both creation and neutraliation of ROS
58
Myeloperoxidase - function and appearance
H20 + CL- --> HCLO3 (Myeloperoxidase) --> destroys bacteria | blue green heme-containing pigment that gives sputum its color
59
Interferons structure
glycoproteins
60
Interferons -a - β function
a part of innate host defense against both RNA + DNA viruses
61
Interferons are glycoproteins synthesizes by (and function)
virus infected cells that act locally on unifected cells priming them for viral defense by helping to selectively degrade viral nuclei acid and protein
62
interferons as drugs - clinical use
Interferons - α: 1. chronic hepatitis B, C 2. Kaposi sarcoma 3. hairy cell leukemia 4. condyloma acuminatum 5. renal cell carcinoma 6. malignant melanoma Interferons - β: multiple sclerosis Interferons - γ: chronic granulomatous disease
63
interferons as drugs - side effects
1. neutropenia 2. myopathy 3. depression 4. flu-like
64
Cell surface proteins - T cells (and briefly their function)
TCR (binfs antigen-MHC complex) CD3 (associated with TCR for signal transduction CD28 (binds B7 on APC) CXCR4/CCR5 (co-receptor for HIV)
65
Cell surface proteins - specific for T helper
CD4 | CD40L
66
Cell surface proteins - specific for Cytotoxic T cell
CD8
67
Cell surface proteins - reg T cells
CD4 | CD25
68
Cell surface proteins - B cells
Ig , CD 19, CD20, CD21, CD40, MHC II, B7
69
receptor of EBV in B cells
CD21
70
Cell surface proteins - NK cells (and characteristics)
CD16 --> binds FC of IgG --> antibody dependent cell-mediated cytotoxicity CD56 --> unique marker for NK cells
71
Cell surface proteins - hematopoetic stem cells
CD34
72
Cell surface proteins - Macrophages
CD14, CD40, CCR5, MHCII, | B7 (CD80/86), Fc and C3b receptos
73
Macrophage - function of CD14
receptor for PAMPS | co-receptor of Toll-like receptor
74
Anergy?
state during which a cell cannot became activated by exposure to its antigen
75
T and B cells anergy
when exposed to their antigen without constimulatory signal (signal 2). Another mechanism of self-tolerence
76
Superantigens are produced by
1. S. aureus (TSST-1) | 2. S. pyogenes (exotoxin A)
77
superantigens action
cross link the β region of the T-cell receptor to the MHC II on APC --> can activate any CD4+ T cell --> massive release of cytokines
78
endotoxins/LPS acion
directly stimulate macrophage by binding to endotoxin receptor TLR4/CD14 Th cells are not involved
79
examples of antigenic variation
Parasites - trypanosomes (reccuring fever) Viruses - influenza, HIV, HCV Bacteria: a. Salmonella (2 flagerllar variants), Borrelia recurrentis (relapsing fever), N. gonorrhoeae (pilus protein)
80
antigenic variation - mechanism
some mechanism for variation include DNA rearrangementt and RNA segment reassortment
81
Passive vs active immunity according to mechanism of acquisition and onset
Passive --> receiving preformed antibodies --> rapid | Active --> Exposure to foreign antigens --> slow
82
Passive vs active immunity according to duration
Passive --> short span of antibodies (hald-life = 3 weeks) | Active --> long lasting protection (memory)
83
Passive immunity - example (4)
1. IgA in breast milk 2. maternal IgG crossing placenta 3. antitoxin 4. humanized monoclonal antibody
84
Active immunity - examples (3)
1. Natural infection 2. Vaccines 3. Toxoid
85
combined passive and active immunization can be given for
hepatitis B or rabies exposure
86
humanized monoclonal antibody - definition
combined human antibody with a small part of a mouse monoclonal antibody. The mouse part binds the antigen and the human part makes it less likely to be destroyed by the body's immune system.
87
unvaccinated patients are given preformed antibodies (passive) after exposure to
1. Tetanus toxin 2. Botulinum toxin 3. HBV (both passive and active) 4. Varicella 5. Rabies
88
Vaccination induces
an active immune response (humoral/or cellular) to specific antigens
89
Viral vaccines - categories and viruses
A. Live attenuated vaccines (1. smallpox 2. yellow fever 3. rotavirus 4. VZV 5. Sabin polio 6. Influenza (intransal) 7. Measles 8. Mumps 9. Rubella) B. Killed (1. Rabies 2. Influenza (injected) 3. Salk Polio 4. HAV) C. Subunit (1. HBV (antigen=HBsAg) 2. HPV (types 6, 11, 16, 18))
90
Life attenuated vaccine - description
Microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host --> induces cellular and humoral responses
91
inactivated or killed vaccine - description
Pathogen is inactivated by heat or chemicals --> maintaining epitope structure on surface antigens is important for immune response --> mainly induces a humoral response
92
Life attenuated vaccine vs inactivated or killed vaccine according to immune response
Life attenuated --> cellular and humoral responses | Inactivated or killed --> humoral response
93
Life attenuated vaccine - pros and con
Pros: induce strong, often lifelong immunity Con: may revert to virulent form
94
Life attenuated vaccine is often contraindicated in
pregnancy and immunodeficiency
95
Life attenuated vaccine - HIV
MMR and VZV if cd more than 2 hundred
96
inactivated or killed vaccine - pros and con
Pro: safer than live vaccine Con: weaker immune response (booster shot usually required)
97
Fibrinogen correlates with
ESR
98
B7 is aka (and is found at)
CD 80/86 | B cells and macrophages
99
CD 40 is found in
B cells and macrophages
100
LPS binds to (receptor)
TLR4/CD14
101
live attenuated vaccine but not for virus
BCG | salmonella typhi
102
CD55?
DAF
103
BCG developed from
Mycobacterium bovis
104
influenza vaccine
1. live --> intranasal | 2. killed --> injected

Immunology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions