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Immunology (By: Ben + Dustin) > Midterm I (Ben) > Flashcards

Midterm I (Ben) Flashcards

1
Q

What is the difference between the size of peptide fragments bound by MHC-I vs. MHC-II?

And the difference in how the peptide fragments fit into the MHC molecule?

A
  • MHC-I - binds 8-9 AA peptides w/out overhang
  • MHC-II - binds 11-20 AA peptides w/ overhang
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2
Q

What are the four principles of the adaptive immune response?

A
  1. Antigen Specificity
  2. High Antigen Sensitivity
  3. Memory
  4. Clonal Selection
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3
Q

How does a graph of the number of micro-organisms in an infected individual vs. time look…

for a normal person/someone lacking innate immunity/someone lacking adaptive immunity?

A
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4
Q

What are the components of innate immunity?

(7 items)

A
  • macrophages
  • granulocytes
  • mast cells
  • immature dendritic cells
  • innate lymphoid cells
  • complement
  • natural autoantibodies

MGMIICN

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5
Q

Which antibody type dominates the primary immune response?

And secondary?

A
  • primary = IgM
  • secondary = IgG
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6
Q

What are some pro-inflammatory cytokines?

A
  • IL-1 / 12 / 17 / 18 / 33
  • TNF
  • IFN-y
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7
Q

What are some anti-inflammatory cytokines ?

A
  • IL-10 / 13 / 35
  • IFN-alpha
  • TGF-beta
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8
Q

What is the general structure of most cytokine receptors?

What is one exception?

A
  • most are singe-pass receptors in dimer/trimer form
  • chemokine receptors are 7 TM domain Rs
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9
Q

What are the 4 different classes of chemokines?

How do their structures look?

A

C, CC, CXC and CX3C

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10
Q

What are two innate immunity-related molecules found in saliva?

(Where else are they found? What are their actions?)

A
  • Lactoperoxidase - also in mammary glands/milk, catalyzes H2O2 oxidation of acceptor molecules which then have bactericidal activity
  • Lysozyme - also in sweat/tear fluid, is an peptidoglycan N-acetylmuramyl hydrolase enzyme which cleaves bacterial cell wall components
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11
Q

What are the two types of recruited macrophages based on their activation pathway?

(How are they activated and what are their functions?)

A
  • M1 Macrophages - via IFN-y
    • pro-inflammatory, anti-tumor, host defense
    • (also activated by GM-CSF or LPS)
  • M2 Macrophages - via IL-4 or IL-13
    • wound healing, angiogenesis, scavenging (suppress immune defenses)
    • (also via vit. D, PGE, cortisol, IL-10, M-CSF)
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12
Q

What are 3 types of signals sent to macrophages by apoptotic cells?

(via what molecules?)

A
  1. Find Me - via MCP-1 and IL-18
  2. Eat Me - via P-serine
  3. Tolerate Me - via IL-10, TGF-__B and PGE-2
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13
Q

What is the first (of 3) stage of neutrophil extravasation and the molecules involved?

A

Rolling involves binding of neutrophil membrane PSGL-1 (P-selectin glycoprotein ligand) and endothelial P-selectin.

S-Lex (sialyl-Lewis X, a tetrasacch. carb attached to O-glycans on cell surfaces) may also bind E-selectin

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14
Q

What is the second (of 3) stage of neutrophil extravasation and the molecules involved?

A

Adhesion involves binding of neutrophil membrane integrin LFA-1 (lymphocyte function-associated antigen) to endothelial ICAM-1.

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15
Q

What is the third stage (of 3) in neutrophil extravasation and the molecules involved?

A

Diapedesis** involves chemoattraction of neutrophils by **CXCL8 (AKA IL-8) via their CXCL8-R.

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16
Q

Describe the process of “neutrophil swarm”, including chemical messengers involved.

A
  1. Injury/infection induces LTB4 release in tissues, stimulating rapid neutrophil accumulation.
  2. C3XCL1 “fractalkine” then attracts C3XCR1+ macrophages to the site
17
Q

What are 3 neutrophile effector functions?

A
  1. Phagocytosis - with intravesical killing of pathogens (both O2-dependent + indepedent) and lysosomal degradation
  2. Degranulation - “frustrated phagocytosis” involving release of cytotoxic enzymes
  3. NETosis - release of extracellular DNA traps
18
Q

What are the 3 different categories of dendritic cells (one has two subcategories)?

(and their distinguishing surface markers?)

A
  1. Myeloid (both are CD11c+)
    • Conventional DC1 - CD1c+ (40-50%)
    • Conventional DC2 - CD141+ (5-10%)
  2. Plasmocytoid (40-50%) - eccentric nucleus and high rER content
    • ​​CD123+ and CD11c+
  3. Monocyte-derived
    • ​​(CD14+, CD11b+)
19
Q

What are the 2 categories of phagocytic receptors?

(one has two subtypes)

A
  1. Opsonic receptors
    • Fc and complement receptors
  2. Pattern Recognition Receptors (PRRs)
20
Q

What are 4 categories of Fc receptors?

A
  1. Fc-gamma
  2. Fc-epsilon
  3. Poly-Ig
  4. FcRn
21
Q

What are the functions of Fc-gamma receptors?

A
  • binds IgG
  • facilitates phagocytosis (Fc-gamma-R-I)
  • may suppress B cell function (Fc-gamma-R-IIb)
  • induces macrophage respiratory bursts
22
Q

What are the functions of Fc-epsilon receptors?

A
  • binds IgE
  • high affinity form FcE-R-I on basophils + mast cells plays role in allergy
23
Q

What are the functions of PolyIg receptors?

A
  • binds polymeric IgA
  • plays role in mucosal epithelial transcytosis
24
Q

What are the functions of FcRn receptors?

A
  • In the placenta: binds maternal serum IgG to protect it from degradation during transfer of passive immunity from mother to fetus
  • On luminal side of neonatal gut epithelium: binds IgG from breast milk to protect it from acidic gut pH and aid its absorption
25
Q

What are two oxygen-dependent methods of intravesical killing involving free radicals?

A
  • Peroxidase-independent - NADPH oxidase on phagosome membrane creates O2- which makes H2O2 etc. to kill microbes
  • Peroxidase-dependent - peroxidase enzymes make hypochlorite using H2O2, HClO- then kills microbes
26
Q

Describe the NO Pathway of intravesical killing.

A
  • TNF and IFN-y stimulate iNOS activity, producing NO from O2 and L-Arg
  • NO is toxic to microbes
27
Q

What disease is related to a deficiency affecting intravesical killing mechanisms?

A

Chronic Granulomatous Disease

  • deficiency of phagocyte NADPH oxidase (PHOX)
  • leads to granuloma formation, skin infections and gingivitis
28
Q

What is an example of an activating NK cell receptor?

And an inhibitory one? (With its ligand?)

A
  • NKG2D activates
  • NKG2A inhibits (binds MHC-I)
29
Q

What are the 3 types of innate lymphoid cells?

What do they produce/do?

A
  • Type I: NK cells, make IFN-y
  • Type II: make Th2 cytokines (IL-4/5/9/13)
  • Type III: make IL-17/22
30
Q

Give an example of a signalling pathway set off by a Toll-like receptor.

A

With TLR-4…

  • LPS binds LPS-binding protein (LPB) on receptor
  • IC MyD88 adaptor sets of Ser/Thr Kinases
  • IkB is P-ated and degrades
  • NF-kB is disinhibited + translocates to nucleus
  • co-stimulator and cytokine expression is upregulated (ex: pro-IL-1)
31
Q

What are 5 types of membrane-bound PRRs?

A
  1. NK cell Rs
  2. Complement Rs
  3. Lectins
  4. Scavenger Rs
  5. Toll-like Rs
32
Q

How can TLR activation increase antigen presentation efficiency?

A

by upregulating expression of MHC and co-stimulatory molecule B7 expression

33
Q

What are the plasma membrane TLRs and their ligands?

A
  • TLR1:TLR2 - lipopeptides
  • TLR2 - peptidoglycan
  • TLR4 - LPS
  • TLR5 - flagellin
  • TLR2:TLR6 - lipopeptides
34
Q

What are the endosomal TLRs and their ligands?

A
  • TLR3 - dsRNA
  • TLR7 or TLR8 - ssRNA
  • TLR9 - CpG DNA
35
Q

What are the components of inflammasomes and what do they activate?

A
  • Components: ASC, NLR, Caspase-1
  • Activates IL-1B and IL-18, inducing inflammation

Immunology (By: Ben + Dustin) (12 decks)

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