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Step 1 Shit I'm Forgetting/embryogology > Immunology > Flashcards

Immunology Flashcards

1
Q

Endotoxin binds to what?

A

Lipopolysaccharide -> binds to LPS- bind protein (found in plasma) -> binds to CD14 on macrophages -> triggers TLR4

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2
Q

Peptidoglycan cell wall binds to what?

A

NOD receptors (intracellular) aka nucleotide- binding oligomerization domains-> cytokine expression

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3
Q

Mannose is what? and binds to what?

A

Polysaccharide on bacteria and yeast -> mannose-binding lectin (MBL) from liver -> activates lectin pathway of complement activation

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4
Q

What are pattern recognition components that activate an innate immune response?

A

-lipoteichoic acid on gram positive bacteria, double stranded RNA, unmethylated DNA, mannose, peptidoglycan cell wall, endotoxin

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5
Q

What are the key surface receptors on macrophages?

A

CD14, Fc receptor, C3b receptor

T cell molecules: MHC II, B7, CD40

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6
Q

What does CD14, Fc receptor and C3b receptor bind to?

A

CD14-LPS (gram negative)
Fc receptor- binds to Fc (antibodies)
C3b receptor- C3b (complement)

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7
Q

What does B cell molecules receptor bind to: MHCII, B7, CD40?

A

MHCII- CD4
B7-CD28
CD40-CD40L

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8
Q

What cytokines are produced by macrophages?

A

IL-1 and TNF-alpha

-IL-6, IL-8, IL-12

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9
Q

What does IL-1 do?

A
  • Increases synthesis of endothelial adhesion molecules-> allows neutrophils to enter inflamed tissue
  • Endogenous pyrogen-> causes fever
  • Acts on hypothalamus
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10
Q

What does TNF-alpha do?

A

-Increases synthesis of endothelial adhesion molecules-> allows neutrophils to enter inflamed tissue
- Vascular leak-> septic shock if severe
-“cachectin: inhibits lipoprotein lipase in fat tissue
Reduces utilization of fatty acids -> cachexia

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11
Q

What does IL-6 do?

A

Fever

Stimulates acute phase proteins production in liver

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12
Q

What does IL-8 do?

A

Attracts neutrophils

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13
Q

What does IL-12 do?

A

Promotes Th1 development (cell mediated response)

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14
Q

What are the opsonins?

A

Attracters of neutrophils- IL-8, C5a, and IgG

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15
Q

What surface markers do natural killer cells present with?

A

CD16- binds Fc of IgG

CD56- NCAM-useful marker for presence of NK cells

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16
Q

What cytokines do Th1 cells secrete?

A

-IL-2, IFN-gamma

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17
Q

What does IL-2 do?

A
  • mostly from Th1 cells
  • T-cell growth factor
  • stimulates growth of CD4, CD8 T cells
  • Also activates B cells and NK cells
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18
Q

What does IFN-gamma do?

A
  • since it’s secreted by Th1 cells -> activate even more Th1 cells and suppresses Th2 cells
  • Activates macrophages (phagocytosis/killing)
  • More MHC class I and II receptor expression from the APC (II) and all other cells (I)
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19
Q

What are the Th2 cytokines?

A

IL-4, IL-5, and IL-10

20
Q

What does IL-4 do?

A
  • Activates Th2 cells/suppresses Th1 production

- Promotes IgE production (parasites)

21
Q

What does IL-5 do?

A
  • Activates eosinophils (helminth infections)

- Promotes IgA production (GI bacteria)

22
Q

what does IL-10 do?

A
  • Inhibits Th1 production
  • “Anti-inflammatory” cytokine only
  • No pro-inflammatory effect
23
Q

Why is Th1 important?

A

Important for many intracellular infections

-works against infections that antibodies are not effective against

24
Q

How are giant cells formed from?

A

Formed from macrophages

25
Q

Mechanism of granuloma production

A

Th1 cells secrete IFN-gamma -> activates macrophages -> macrophages secrete TNF-alpha -> promotes granuloma

26
Q

What is IL-12 receptor deficiency?

A
  • IL-12 cannot trigger differentiation T-cells into Th1 cells
  • No Th1 cells to produce IFN-gamma
  • Increased susceptibility to intracellular infections -> mycobacterial infections, disseminated salmonella, disseminated bacillus calmette- guerin (BCG) after vaccine
27
Q

MHC Class I

A

Binds TCR and CD8

-One “heavy chain” plus beta-microglobulin

28
Q

What ligand does CD8 T-cells produce to induce apoptosis?

A

Produce Fas ligand-> binds to Fas (CD95) on surface of cells

  • activation caspases in cytosol-> cellular breakdown -> cell death with no significant inflammation (apoptosis)
  • “extrinsic pathway” of apoptosis
29
Q

What surface markers do Regulatory T cells express?

A

All express CD25 (classical marker)

  • also have CD3/4
  • Produce anti-inflammatory cytokines -> IL-10 and TGF-beta
  • suppresses CD4/CD8 T cells
30
Q

How does a superantigen work?

A

Directly links MHC with T cell receptors -> to illicit response without being processed by APC

  • release a huge amount of cytokines -> IFN-gamma and IL-2 from Th1 cells
  • massive vasodilation and shock
31
Q

What are the 2 superantigens?

A 
Staph aureus- toxic shock syndrome toxin (TSST-1) 
Strep pyogenes (group A strep) -> pyrogenic exotoxin A or C
32
Q

What type of cells do polysaccharide capsules bind to?

A

Polysaccharide capsules of many bacteria can stimulate B-cells but not T cells

33
Q

How are B cells activated?

A
  1. ) T- cell dependent (protein)

2. ) T-cell independent (non-protein)

34
Q

For T-cell dependent activation of B cells what 2 signals are required?

A
  1. ) Cross-linking of receptors bound to antigen

2. ) T cell binding (T-cell dependent activation)

35
Q

What is the mechanism for T cell dependent activation?

A

B cell can present antigen to T- cells via MHC class II-> Binds MHC class II w/antigen to TCR

  • Other T cell to B cell interactions need to occur
    1. ) CD40 (B cells) to CD40 ligand (T cell) -> required for class switching
    2. ) B7 ( B cells) to CD28 (T cell) -> required for stimulation of T-cell cytokine production
36
Q

Mechanism for T cell independent activation

A

Pathogens with many repeating subunits -> bind to multiple B cell receptors -> cluster so many B cell receptors together

37
Q

What are the key points of T cell independent antigen?

A
  1. ) Very important for non-protein antigens -> polysaccharide capsules of bacteria and LPS
  2. ) Weaker response, mostly IgM, no memory
38
Q

What are the 3 conjugated vaccines?

A

All have a non-protein polysaccharide capsule-> peptide antigen

  • H.influenza type B (Hib)
  • Neisseria meningitidis
  • Streptococcus pneumoniae
39
Q

What are the B cell surface proteins?

A 
Proteins for binding with T cells 
1.) CD40 (binding with T-cell CD40L) 
2.) MHC Class II 
3.) B7 (binds with CD28 on T cells) 
Other surface markers- all close to 20 
1.) CD19: All B cells 
2.) CD20: Most B cells, not plasma cells 
3.) CD21 (complement, EBV)
40
Q

What are the triggers of class switching?

A
  1. ) Cytokines (IL-4, IL-5 in Th2 response)

2. ) T-cell binding (CD40-CD40L)

41
Q

Features of IgM

A
  • 1st antibody secreted during infection
  • activates complement-> can activate complement and use c3b as opsonin
  • Prevents attachment of pathogens
  • cannot cross the placenta
42
Q

Features of IgG

A
  • Major antibody of secondary response
  • **only antibody that crosses the placenta-> most abundant antibody in newborns
  • excellent opsonin- IgG1 and IgG3 are best opsonins
  • longest lived of all antibody types (weeks)
  • ** very important for encapsulated bacteria -> b/c it can coat encapsulated bacteria
43
Q

Features of IgA

A
  • mucosal surfaces and mucosal secretions
  • crosses epithelial cells by transcytosis
  • excellent at coating mucosal pathogens-> so they cannot invade -> pathogens sweapt away with mucosal secretions
  • secreted into milk to protect baby’s GI tract
44
Q

What pathogens contain IgA protease?

A

-S.pneumonia, H. influenza, Neisseria (gonorrheae and meningitidis)

45
Q

Features of IgE

A
  • binds to mast cells and eosinophils
  • designed for defense against parasites
  • Mediates allergic reaction: seasonal allergies and anaphylactic shock
46
Q

B cell development timeline

A 
Bone marrow/pre-infection: B cell undergoes VDJ rearrangement 
Lymph nodes/during infections: class switching for more specific response -> somatic hypermutation- stronger antigen binding over time -> Post infection: Memory B cell

Step 1 Shit I'm Forgetting/embryogology (7 decks)

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