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PABI 6100 Immunobiology- Exam > Immunity to Infectious Diseases-1 > Flashcards

Immunity to Infectious Diseases-1 Flashcards

1
Q

What are the 4 major categories of human pathogens?

A
  • viruses
  • bacteria
  • fungi
  • parasites
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2
Q

What is the importance of barriers and vectors in infectious diseases?

A
  • pathogens must breach host physical/ chemical barriers to cause infection > innate immunity
  • vectors (intermediate hosts)- organisms that help infectious agents circumvent host barriers by carrying infection from one organism to another
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3
Q

What are some host barriers to infectious disease?

A
  • epithelial surfaces of body > skin/ GI tract/ respiratory tract/ reproductive tract > monitored by barrier immune systems
  • normal commensal flora at mucosal surfaces completely inhibit binding of pathogens to host cells
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4
Q

How do most vectors work?

A
  • intermediate hosts help infectious agents circumvent host barriers by carrying infection from one organism to another
  • most are blood-sucking anthropods > ticks/ fleas/ flies/ mosquitos
  • breach natural barriers like skin with their bite
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5
Q

What are 3 strategies pathogens have evolved to escape immune destruction?

A
  • growing within host cells
  • expressing molecules similar to host cell membrane molecules
  • continual variation in surface antigens
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6
Q

What happens when a pathogen breaches a host?

A
  • encounters responders of innate immunity
  • innate mechanisms lead to initiation of adaptive mechanisms > cause final eradication of pathogen/ memory response
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7
Q

What are 3 examples of a pathogen breaching a host and encountering innate immunity?

A
  • bacterial LPS (PAMP) stimulates macrophages to produce cytokines IL-1/ IL-6 > activate phagocytosis
  • peptidoglycan on bacterial cell walls activates complement pathway > opsonization/ phagocytosis/ lysis
  • viruses induce production of interferons > antiviral response
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8
Q

What is an example of a way to introduce a barrier to infection in a vector?

A
  • introducing barriers to infection in intermediate hosts can disrupt the life cycle of certain infectious diseases
  • ex) virus transmitted by mosquito bite
    > engineer mosquitos resistant to virus/ release them wild
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9
Q

What is the link between location and immune effector mechanism?

A
  • entry site/ ultimate location of an infectious agent in body determines what immune tools available/ best suited for pathogen detection/ elimination
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10
Q

What are the different entry points for infection?

A
  • contact (eye)
  • wound/ anthropod bite (skin)
  • mucosal surfaces
    > ingestion (GI tract)
    > inhalation (respiratory tract)
    > sexual exposure (urogenital/ reproductive tracts)
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11
Q

How do most infectious agents enter the body?

A
  • mucosal routes > GI/ respiratory/ urogenital tracts
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12
Q

How are mucosal/ barrier infections typically controlled?

A

TH2 response

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13
Q

What cells sense pathogens via PRRs?

A
  • epithelial cells
  • APCs (macrophages/ DCs)
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14
Q

What is the response to helminths (parasitic worms)?

A

TH2 response > IL-4/ IL-5/ IL-13 cytokines

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15
Q

What immune effectors deal with pathogens in the GI tract?

A
  • antimicrobial proteins secreted by epithelial cells
  • innate lymphoid cells (ILCs)
  • MALT
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16
Q

What does the TH2 response involve?

  • how most barrier (surface)/ mucosal infections controlled
A
  • activation of ILC-2s
  • TH2 specific cytokines > IL-4/ IL-5/ IL-13
  • IgE capable of recognizing surface epitopes of pathogen
    > cells with high-affinity IgE receptor > basophils/ eosinophils/ mast cells
  • dimeric IgA at mucosal surfaces > neutralization (blocks pathogen binding to epithelial cells) > passive, so prevents dysbiosis from chronic inflammation
17
Q

What happens after pathogens breach epithelial barriers?

A
  • enter interstitial fluid (extracellular > can remain local/ spread through body via circulatory/ lymphatic systems
  • all pathogens that breach epithelial barriers will be found in extracellular space for all least part of their lifetime in host
  • some can enter host cells (intracellular)
18
Q

What are the immune mediators in extracellular spaces?

A
  • PRRs on phagocytic cells
  • complement system
  • antimicrobial compounds
  • cytokines > activate immune cells
  • IgG/ IgM/ mIgA antibodies
  • TFH/ TH17/ TH2 cells
19
Q

What is one reason intracellular pathogens are most difficult to find/ destroy?

A
  • antibodies can not enter cells
20
Q

What are the immune mediators for infectious organisms within intracellular vesicles?

A
  • TH1 response > DTH
  • TH1 cytokine IFNγ activates macrophages to digest vesicle-bound agents (bacteria/ parasites)
21
Q

What is an example of an infectious organism that enters intracellular vesicles?

A

Mycobacterium
- includes agent that causes tuberculosis

22
Q

What are the immune mediators for infectious organisms within the cytosol?

A
  • all viruses/ some parasitic agents enter cytosol > TH1 response/ CTLs
  • can be detected by cytosolic PRRs > NLRs/ RLRs
    > leads to cytokine secretion/ inflammasome activation
    > ultimately induces cytotoxic cells that can kill infected host cells (NK cells/ CTLs)
  • NK cells kill infected host cells > detect cell-surface changes (signs of infection) ex-decreased MHC I expression > ADCC
  • CTLs are primary adaptive mediators of infected cell killing
23
Q

What is required for the eradication of cytosolic infections?

A
  • strong/ comprehensive cell-mediated immunity
    > TH1 CD4+ T cells that can license DCs for cross-presentation
    > cytotoxic CD8+ T cells (CTLs)
24
Q

What are the 2 major types of barrier immune systems to the microbiome?

A
  • Tolerogenic > response to commensal bacteria (homeostasis)
  • Inflammatory > response to pathogenic microorganisms
25
Q

What are the tolerogenic/ inflammatory barrier responses to the microbiome?

A
  • IL-10 from tolerogenic DCs activates FoxP3+ Tregs
    > tolerogenic cytokines (IL-10/ TGF-β) > dampen pro-inflammatory responses
    > IgA producing B-cells
  • proinflammatory response to pathogenic microorganisms
    > proinflammatory TH1/ TH17 CD4+ T-cells > proinflammatory cytokines (IFN-γ/ TNF-α/ IL-17)
26
Q

How are antigens delivered from intestinal lumen to APCs?
> across epithelial cells > APCs in lamina propria

A
  • M cells > transcytose antigen/ sometimes microbes from lumen
  • FcRs >antigen-antibody complexes carried across epithelial cells
  • Goblet cells > transcytose small antigens
  • Direct APC contact > APCs extend their processes into intestinal lumen
27
Q

What are the 2 types of IBD?

A
  • Crohn’s disease > can affect all areas of GI tract
  • Ulcerative colitis > only in large intestine
28
Q

What factors can compromise the integrity of the epithelium and alter the balance between beneficial/ harmful microorganisms?

  • homeostasis > inflammation
A
  • antibiotics/ diet/ pathogen ingestion can directly alter the commensal microbiome
  • pollutants/ invading microorganisms can trigger inflammatory responses by epithelium/ APCS
  • stress hormones have both direct/ indirect effects on microbiome and epithelial integrity
  • inherited mutations in immune molecules (IL-10/ IL-23 receptors)

PABI 6100 Immunobiology- Exam (6 decks)

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