Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BLD + Pharm > BLD434 Section 1 > Flashcards

BLD434 Section 1 Flashcards

Immunology (86 cards)

Start Studying
1
Q

Antigen

A

pathogen component that binds to BCR or TCR

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

Innate Immunity

A

First line of defense (Non-specific) - Inflammation
- rapid pathogen recognition response (hours)
- fixed - based on the inherited receptors
- limited # of specificities
- constant during response
- neutrophils, eosinophils, basophils, mast cells, monocytes (B)/phagocytes (T), DC, NK cells, ILC

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

Adaptive Immunity

A

Third line of defense. Antigen-specific
- Slow pathogen recognition response
- Variable (not based on inherited genes)
- Numerous highly selective specificities
- Improves during response and each time infected
- B cells (plasma cells, CD19 and CD20), B-1 forms before birth, B-2 forms after birth
- T cells (CD3) - Helper T cells & T regulatory cells (CD4), Cytotoxic T cells (CD8)

Main advantages: more powerful & long-lasting protection (memory)

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

CD antigen (marker)

A

“clusters of differentiation” - cell surface molecules that identify immune cells

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

Sebum

A

Substance secreted by sebaceous glands that contains fatty acids and lactic acids which inhibit bacterial growth at the skin surface.

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

Lysozyme

A

Enzyme contained in tears and saliva that kills bacteria by degrading their cell walls.

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

Polymorphonuclear

A

having a nucleus with several lobes and a cytoplasm that contains granules (ex: neutrophils, eosinophils, basophils)

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

Primary lymphoid tissue

A

Bone marrow - where B & T cells form and multiply. where B cells mature.
Thymus - where T cells mature.

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

Secondary lymphoid tissue

A

Filters extracellular fluids for antigens and microorganisms. Site for lymphocyte activation by antigens, which develop into effector cells.
- Lymph nodes, spleen, tonsils, Peyer’s patches , appendix.

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

Lymph

A

fluid and cells (including WBCs) that are transported to the lymphatics and into the bloodstream
- Attack bacteria in the blood and body tissues

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

Naive lymphocyte

A

Immature B or T lymphocytes that have not been activated by an antigen

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

PALS (Periarteriolar lymphoid sheath)

A

A portion of white pulp in the spleen that is occupied by T cells.

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

GALT (Gut-associated lymphoid tissue)

A

Tonsils, adenoids, appendix, Peyer’s patches of the gastrointestinal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

BALT (Bronchial-associated lymphoid tissue)

A

aggregates of the respiratory epithelium
- mucosal lymphoid tissue in the walls of airways (respiratory tract, bronchi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MALT (Mucosa-associated lymphoid tissue)

A

Secondary lymphoid tissue that initiates immune responses to specific antigens along mucosal surfaces (ex: vaginal tract)

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

Mature immune cells from the common Myeloid precursor

A

Monocytes/Macrophages, Neutrophils, Eosinophils, Basophils, Mast cells, DC cells

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

Mature immune cells from the common Lymphoid precursor

A

B cells, T cells, NK cells, ILC (innate lymphoid cells)

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

Monocytes vs Macrophages

A

Same cell but is called a monocyte (inactive) when in the blood and a macrophage (active) when in tissue. Macrophages are phagocytic while monocytes are not

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

Polymorphonuclear leukocytes (granulocytes) of the blood - color of granules & # of lobes

A

Neutrophils (2-5 lobes) - pink/blue/lilac
Eosinophils (2 lobes) - orange-pink
Basophils (2 lobes) - purple-black

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does a naive lymphocytes enter a lymph node?

A

Naïve lymphocyte enters a lymph node via afferent lymphatic vessels and drains through the efferent lymphatic vessel in the medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

M cell (Microfold cell)

A

Specialized intestinal epithelial cells covering GALT mucosa – Transport antigens to lymphoid follicles to initiate an immune response. Long-lived.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does an antigen enter a lymph node?

A

Antigen enters lymph node via fluid draining from tissues (due to inflammation) in afferent lymph vessels

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

Where are B & T lymphocytes primarily located in the lymph node?

A

B cell - Lymphoid follicles in the cortex (circular areas in the outer part)
T cell - Medulla (middle part)/ T-cell area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where are B & T lymphocytes primarily located in the white pulp of the spleen?

A

Active B cell - Germinal center
Inactive B cell - lymphoid follicles
T cell - PALS (periarteriolar lymphoid sheath)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
C (Complement proteins)
soluble zymogens (inactive enzymes) in the blood that are part of the innate immune system First line of defense against infection
26
Defensins
small amphipathic proteins inserted into pathogenic membranes to cause lysis. Defend against bacterial, viral, and fungal infections
27
Opsonization
Coating or binds to the surface of a pathogen to help phagocytosis.
28
Complement fixation
Opsonization where C3b is the opsonin. - C3b is covalently bonded to the pathogen's surface to mark it as a target for destruction by a phagocyte
29
Anaphylatoxin
Complement fragments that float away (C3a, C4a, C2b) - Substance that activates blood vessel endothelial cells to initiate inflammation by: causing degranulation, increasing vascular permeability and vasodilation.
30
Chemoattractant
A chemical substance that creates a gradient to attract cells (from low to high concentration) towards an infection
31
4 Main Functions of complement proteins in immune system
- opsonization - anaphylatoxin - chemoattraction - direct lysis (pore formation - C9)
32
List the 3 Complement Pathways and what initiates them
- Classical (Antibody-initiated, C1 binds) - CRP initiates without antigen binding - Lectin (MBL binds) - Alternative (spontaneous hydrolysis of C3, Factor B binds)
33
C3 covertase (Classical and Lectin)
C4b2a
34
C3 convertase (Alternative)
C3bBb
35
C5 convertase (Classical and Lectin)
C4b2a3b
36
C5 convertase (Alternative)
C3bBb3b
37
Major advantage that complement has compared to antibody in tagging pathogens for disposal?
Complement binds covalently (strong and permanent) to pathogen surface, while antibody binds non-covalently (not as strong and can be reversible)
38
Explain the similarities and differences between iC3 vs iC3b and iC3Bb vs C3bBb. Identify which are enzymatically active and which have been inactivated.
iC3 - inactive - soluble - can bind Factor B to be cleaved into iC3b iC3b: - inactive (C3b, by Factor I) - opsonin - bind to Factor D to be cleaved into iC3bBb iC3Bb: - active - soluble - C3 convertase of alternative pathway C3bBb: - active - fixed (covalently bonded to pathogen surface) - C3 convertase of alternative pathway
39
Which complement component fragment provides the greatest amount of amplification of the complement cascade, and why (i.e, C2b, C3b, C4b, C5b?)?
C3b - provides a way to activate the alternative pathway and add exponential activation of complement proteins.
40
Complement proteins of the MAC
C5b, C6, C7, C8, C9
41
Which complement component polymerizes a pore in the pathogen membrane?
C9
42
What protein can amplify complement activation? Which complement pathway? What mechanism?
Properdin (Factor P) binds to C3bBb (alternative C3 convertase) bound to a pathogen surface and protects it from protease degradation (Bacteria and parasites secrete proteases around their surface). Amplifies the alternative pathway.
43
List the two points at which complement activation can be inhibited, and identify the product of C3b cleavage produced by Factor I.
- Inactivate C3 convertase - Prevent MAC formation Product = iC3b
44
Describe how a2-macroglobulins, pentraxins and defensins function in innate immune system protection of the body.
- a2-macroglobulins inhibit proteases - Pentraxins enhance phagocytosis - Defensins are antimicrobial peptides that disrupt microbial membranes & cause lysis
45
Neutrophils
- short-lived - highly mobile - crucial in early stages of infection - die after they phagocytize by apoptosis - enter inflammatory site when called upon
46
Macrophages
- Long-lived - Tissue residents - First to respond - Detect danger infection signal using inflammatory cytokines - Clean up mess after pathogen is killed - Help in tissue repair - Function as sentinels (guards)
47
IL-1B
inflammatory cytokine released by macrophages that enhances the effects of TNF-a and IL-6 - Activates vascular endothelium and lymphocytes; local tissue destruction, increases access of effector cells
48
TNF-a
- inflammatory cytokine produced by macrophages - makes blood vessels more permeable so cells, fluid, and soluble effectors can enter infected tissue. - Can cause septic shock if produced in abundance
49
IL-6
- inflammatory cytokine produced by macrophages - induces metabolism of fat and muscle cells --> heats infected tissue - Induces the production of acute-phase proteins CRP and MBL to activate complement opsonization
50
CXCL8
- chemokine released by macrophages - recruits neutrophils from the blood into infected tissue
51
CCL2
- chemokine released by macrophages - recruits monocytes from the blood to infected tissue
52
IL-12
- recruits and activates NK cells to secrete cytokines to strengthen macrophage response to infection
53
TLR
Toll-like receptors - activate immune cells in innate immunity and are involved in cell signaling & the production of inflammatory cytokines
54
TLR subfamily I
- TLR 1, 2, 4, 6, 10 - Located in plasma membranes of immune cells (mostly granular sites, DC, and some B) - Recognize lipid components in the membranes of pathogens (bacteria, parasites, fungi) to activate macrophage or DC response
55
TLR subfamilies II & III
II = TLR 7, 8, 9, III = TLR 3 homodimer - Located in endosomal membranes - Virus release viral DNA/RNA when phagocytized, and then these TLR will have access, activating immune cells to produce cytokines and other mediators
56
TLR subfamily IV
TLR 5 - Expressed on intestinal epithelial cells in their plasma membrane to recognize bacterial flagellin protein - Activates intestinal epithelium to send immune signals to call in help
57
TLRs located in plasma membrane
TLR subfamilies 1 and 4 - recognize extracellular pathogens - target antigen: bacteria
58
TLRs located in endosomes
TLR subfamilies 2 & 3 - recognize intracellular pathogens - target antigen: viruses (attack gene irregularities
59
NFKB
Protein transcription factor that initiates inflammatory cytokine production and secretion to regulate innate immunity. - Activates transcription of genes for inflammatory cytokines, which are synthesized in the cytoplasm and secreted from the ER
60
IRF3 & IRF7
- phosphorylated and travel to nucleus to act as transcription factors - they induce Type I interferon production and secretion (IFN-a & IFN-B) IRF3 = for single-stranded RNA IRF7 = for double-stranded RNA
61
Type I Interferons
IFN-a and IFN-B, which fight viral infections
62
What is the outcome of activation of MAVS receptors?
MAVS = Mitochondrial antiviral-signaling proteins Type I interferon (IFN-a & IFN-B) production by the cell
63
Plasmacytoid dendritic cells
Dendritic cells specialized in secreting high levels of Type I interferons - response to viral nucleic acid during early infection
64
Respiratory burst
the consumption of O2 by phagocytes, pumping H+ ions out of the phagolysosome, raising the pH and activating neutral proteases to digest the microbes consumed.
65
Chronic Granulomatous Disease - identify the immune system defect
Caused by a mutation of the genes encoding subunits of the NADPH oxidase enzyme complex. Leads to: - Defective respiratory burst - Reduced ability of phagocyte to kill pathogens - Infected cell forms a granuloma, a wall, around itself to prevent infection spread
66
Identify the major macrophage cytokine that triggers the “acute phase” response and the proteins that are produced as a part of the acute phase response.
IL-6 - by inducing liver hepatocytes to produce acute phase proteins (CRP, MBL, LPS-binding protein).
67
Importance of an acute phase reaction (response) and which tissues/organs of the body are primarily responsible?
Response to a pathogen by creating a hospitable environment for pathogens and trying to kill the pathogen until the adaptive immune system can step in. - Liver Acute-phase proteins (CRP and MBL) activate complement opsonization - Bone marrow Neutrophil mobilization (5-day supply) causes phagocytosis - Hypothalamus Increases body temperature via shivering --> decreasing viral and bacterial replication - Fat and muscle cells Metabolism increases body temperature via fever --> decreasing viral and bacterial replication
68
Necrosis
cell death by trauma (inflammation, damage, osmotic pressure) - releases inflammatory cytokines
69
Netosis
Neutrophils get overstimulated and extrude their DNA and granule contents (NETs) to trap extracellular bacteria
70
Trogocytosis
Neutrophils extend membrane to take a "bite" out of a cell (parasite) that is too large to phagocytose.
71
Apoptosis
NK cells and Tc cells induce another cell to digest itself from the inside out. - Virus-infected cells, cancer, damaged cells
72
Pyroptosis
Inflammatory cell death - Macrophages get highly activated and inflammasomes form, leading to the release of inflammatory cytokines (IL-1B) - ALL infections
73
Phagocytosis
Neutrophil and macrophage cell receptors bind to target and wrap its plasma around pathogen and engulfs it in a phagosome.
74
LTi (Lymphoid Tissue inducers)
Responsible for creating lymphoid tissues (lymph nodes and white pulp organization in spleen)
75
NK cells
Cytotoxic ILC of lymphoid lineage - circulate blood & kill infected cells (virus, bacteria, protozoa) - Perforin mediator creates a hole in an infected cell, allowing granzymes in to induce apoptosis. IFN-Y further activates macrophages
76
ILCs (Innate Lymphoid Cells)
- Facilitates the development of secondary lymphoid structures - Secrete cytokines that help to activate the effector cells of innate immunity (e.g. macrophages, granulocytes) & phagocytosis - ILC1, ILC2, ILC3 (Tissue residents - for immediate response)
77
ILC1
- Respond to intracellular infections to any invading pathogen - Either stops the infection or limits its spread until NK cells are recruited from the blood (by IL-12)
78
ILC2
- Present at mucosal surfaces - Respond to large extracellular parasites (i.e. worms)
79
ILC3
- Respond to extracellular bacterial or fungal infections - Abundant in mucosal tissues
80
Type 1 Immunity
- Intracellular bacteria and viruses - Mediated by IFN-Y, NK cells, ILC1, neutrophils - Cell-mediated toxicity (NK cells) & inflammatory activation of macrophages
81
Type 2 Immunity
- Parasites in the gut - Mediated by ILC2, IL-4, IL-5, IL-13, mast cells, eosinophils, and basophils - Non-inflammatory activation of macrophages
82
Type 3 Immunity
- Extracellular bacterial or fungal infections - Mediated by ILC3, which produces IL-17 and IL-22 - Promotes phagocytosis and secretion of antimicrobial peptides
83
How do Type I interferons activate NK cells to combat infections?
(IFN-a and IFN-B) by promoting NK cell maturation and recruitment into virally-infected cells
84
How do Type II interferons activate NK cells to combat infections?
(IFN-Y) - Macrophages produce IL-12 and IL-15, causing NK cells to proliferate and differentiate - NK cells secrete IFN-Y, which binds to and activates macrophages to increase phagocytosis and secretion of inflammatory cytokines to kill ingested viruses
85
Macrophage and NK cell interaction
Synergistic 1. Virus activates macrophage, which then secretes cytokines: - CXCL8 recruits the NK cell 2. IL-12 & IL-15 activate the NK cell via the synapse 3. NK cells proliferate into effector cells and secrete IFN-Y 4. IFN-Y binds to macrophage to increase phagocytosis and cytokine secretion
86
What are the three types of interactions that can occur between DC cells and NK cells?
1. DC cells drive NK cells activation, proliferation, and differentiation - Immature DC cell takes up antigen, gets activated, and secretes IL-15 to drive NK cell proliferation - This produces effector NK cells that secrete cytokines and kill virus- infected cells 2. Abundance of NK cells - NK cells outnumber and kill DC cells - There are enough NK cells to terminate the viral infection, so there's no need to activate adaptive 3. Scarcity of NK cells - NK cells signal DC cells to mature and initiate an adaptive immune response - DC cells move to secondary lymphoid tissues to present antigen - Innate immunity fails; need adaptive

BLD + Pharm (7 decks)

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