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PABI 6100 Immunobiology- Exam > Exam Questions > Flashcards

Exam Questions Flashcards

1
Q

What is tolerance?

A
  • many layers of protection imposed by immune system to prevent reaction of its cells/ antibodies against host components
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2
Q

What are the 3 mechanisms of tolerance?

A
  • Evasion- how location/ sequestration has a role in protecting some sites/ tissue-specific antigens found there from exposure to immune system (passive process)
  • Elimination- mechanisms that remove self-reactive lymphocytes before they can do damage (negative selection)
  • Engagement- cultivating certain self-reactive cells for protection of self structures (regulatory phenotype)
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3
Q

How do regulatory CD4+ T cells (tTregs/ pTregs) inhibit immune responses?

> FoxP3/ CTLA-4/ IL-2R α chain (CD25)

A
  • Contact-Dependent Mechanisms- interaction of CTLA-4 (Tregs) and CD80/86 (APCs) inhibits APC function
    > decreased expression of CD80/86
    > activation of IDO > creating an immunoinhibitory microenvironment
  • Contact-Independent Mechanisms
    > secretion of immune-inhibitory cytokines (IL-10/ TGF-β/ IL-35) into surrounding area > shuts down nearby T cells/ APCs
    > due to high CD25 (IL-2Rα) expression, Tregs absorb IL-2 > prevents expansion of effector T cells
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4
Q

What is linked suppression? > mediated by Tregs

A
  • Tregs can inhibit both effector T cells that share the same antigen specificity/ T cells that recognize other antigens
    > occurs when both Treg/ T-cell recognizing another antigen interact with same APC
  • when a single APC simultaneously interacts with T cells of different specificity > inhibitory signals meant for one can be transmitted to both > leads to spreading of immune suppression to include other antigens
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5
Q

What happens in Hashimoto’s thyroiditis?

A
  • autoantibodies/ TH1 cells specific for thyroid antigens are produced
  • DTH response > thyroid gland infiltration by lymphocytes/ macrophage/ plasma cells
  • inflammatory response caused by antibodies against thyroid proteins
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6
Q

What happens in type 1 diabetes (IDDM)?

A
  • autoimmune attack against insulin-producing beta cells in pancreas
  • starts with CTL infiltration/ macrophage activation (insulitis) > cell-mediated DTH response > autoantibodies/ cytokine release
  • beta-cell destruction mediated by auto-antibodies (ADCC/ antibody-mediated complement lysis)/ cytokines/ lytic enzymes released from activated macrophages
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7
Q

What happens in myasthenia gravis?

A
  • autoimmune disease mediated by blocking antibodies
  • auto-antibodies bind to AChR on muscles > block ACh binding > induce complement-mediated lysis of cells
  • type II hypersensitivity
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8
Q

What happens in lupus?

A
  • auto-antibodies to cells/ cellular components (DNA/ histones/ clotting factors/ RBCs/ leukocytes)
  • immune complexes of auto-antibodies/ antigens deposit along blood vessel walls > type III hypersensitivity
  • complement system activation > MAC/ C3a/ C5a
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9
Q

What happens in multiple sclerosis?

A
  • production of autoreactive CD4+ T cells
  • TH17 cells > IL-17 is hallmark
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10
Q

What happens in rheumatoid arthritis?

A
  • production of antibodies that react with citrullinated protein antigens
  • production of auto-antibodies (RFs) > specific for Fc region of IgG
  • immune complexes formed by RFs binding to normal circulating IgG are deposited into joints
  • activates complement system > type III hypersensitivity
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11
Q

What are 2 systemic autoimmune conditions caused by disruptions in immune regulation?

A
  • APS-1- mutations in AIRE gene > critical for central tolerance in thymus (ensures tissue-specific antigens expressed during T cell development) > both elimination/ engagement
  • IPEX- mutations in FoxP3 gene > master TF associated with regulatory T cells (both tTregs/ pTregs > central/ peripheral tolerance)
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12
Q

What are the 3 categories of current therapies to treat autoimmune disease?

A
  • broad-spectrum immunosuppressive treatments > anti-inflammatory
  • immunosuppression directed at specific cells/ pathways
  • targeted immunotherapy > guide hots cells to new pathway
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13
Q

What are the 5 main mechanisms of action of treatments for autoimmune disease?

A
  • T/ B cell-depleting agents
  • targeting cell trafficking/ adhesion > fingolimod
  • targeting TCR signaling
  • targeting costimulatory/ accessory molecules > CTLA-4
  • targeting cytokines/ cytokine signaling
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14
Q

How are mucosal/ barrier responses typically controlled?

A
  • TH2 response:
    > activation of ILC-2s
    > TH2 specific cytokines > IL-4/ IL-5/ IL-13
    > IgE > recognizes cell surface epitopes of pathogen
    > dimeric IgA at mucosal surfaces
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15
Q

What are the immune mediators for extracellular infections?

A
  • PRRs on phagocytic cells
  • complement system activation
  • antimicrobial compounds
  • IgG/ IgM/ mIgA antibodies
  • TFH/ TH17/ TH2 cells
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16
Q

What are the immune mediators for pathogens in intracellular vesicles?

A
  • TH1 DTH response
  • TH1 cytokine IFN-γ > activates macrophages to digest vesicle-bound agents
17
Q

What are the immune mediators for pathogens within the cytosol? (all viruses)

A
  • detected by cytosolic PRRs (NLRs/ RLRs) > cytokine secretion/ inflammasome activation/ induction of cytotoxic cells to kill infected host cells: NK cells/ CTLs
  • NK cells detect cell surface changes associated with infection/ kill infected host cells via ADCC
  • CTLs activated by cross-presentation of antigen by TH1-licensed DCs > primary adaptive mediators of infected target cell killing
18
Q

What are the mechanisms of antigen delivery from the intestinal lumen to APCs?

A
  • M cells > transcytose antigen/ some microbes from lumen
  • FcRs > carry antigen-antibody complexes across epithelial cells
  • Goblet cells > transcytose small antigens
  • Direct APC contact > APCs can extend their processes into lumen
19
Q

What are the innate immune effector mechanisms that eliminate many viral infections?

A
  • complement activation
  • antimicrobial peptides
  • recognition of viral PAMPs (dsRNA) by PRRs > induces type I IFN expression (IFN-α/ IFN-β)/ inflammasome assembly/ activation of NK cells
20
Q

What is the IFN antiviral pathway?

A
  • IFN-α/ IFN-β bind to/ dimerize IFNAR
  • this recruits/ activates JAK1/ TYK2 > bind/ phosphorylate STAT1/ STAT2 > dimerize/ enter nucleus > stimulate expression of antiviral genes
21
Q

What are the 4 IFN-stimulated antiviral genes?

A
  • PKR- inhibits elf2α > inhibits translation
  • 2’,5’-oligo-A-synthetase > degrades viral/ cellular mRNA
  • Mx proteins- self assemble into ring-like structures > inhibit viral replication
  • IFIT proteins- bind to viral RNA > inhibit translation
22
Q

What are the cell-mediated mechanisms for viral infections?
> required once viral genome integrated into host chromosomal DNA

A
  • CD8+ Tc cells/ CD4+ TH1 cells
  • activated TH1 cells produce IFN-γ (antiviral)/ IL-2 (activates effector T cells)/ TNF-α
  • TH1 cells license DCs for cross-presentation
23
Q

What is required for activation of naive Tc cells by exogenous antigen?

A
  • DC licensing by TH cell
    > DCs internalize/ process antigen via exogenous pathway > present to CD4+ TH cells via MHC II
  • DC cross-presentation > activation of CTLs
    > Th cells are bridge > license DCs to cross-present internalized antigen via MHC I > provide local IL-2 to help activate CTL
24
Q

What 4 strategies do viruses employ to evade host defence mechanisms?

A
  • evade action of IFN-α/ IFN-β
  • inhibit antigen presentation by infected host cells
  • change surface antigens
  • cause immunosuppression
25
Q

What is original antigenic sin?

A
  • Fc regions of antibodies bound to surface of pathogen bind to FcRs on naive B cells > inhibit them from responding to new epitopes
  • no immune response mounted to each new epitope during subsequent pathogen exposures > until pathogen expresses a significant # of unique epitopes/ memory cells can no longer eradicate pathogen
  • primary response > activation of naive B cells
  • secondary response > reactivation of memory B cells
26
Q

What 4 strategies does plasmodium (protozoan parasite) have to evade immune system? > malaria

A
  • changing its surface molecules > continual change in antigens seen by immune system
  • intracellular phases of life cycle > reduce degree of immune activation by pathogen
  • short time circulation in blood > most accessible stage
  • sloughing off its surface antigens > antibodies ineffective

PABI 6100 Immunobiology- Exam (6 decks)

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