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Immunology #2 > Effector Immunity- viruses, bacteria, parasites > Flashcards

Effector Immunity- viruses, bacteria, parasites Flashcards

1
Q

What type of effector response is needed?

A

Depends on the type of pathogen and the danger signals that are being detected by the innate immune system

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2
Q

Immune response for intracellular pathogens

A
  • Th1 type
  • Leads to cytotoxic T cells, IFN-gamma, NK cells
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3
Q

Immune response for extracellular pathogens

A
  • Th2 type
  • Leads to antibody response
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4
Q

Immune response for extracellular at mucosal surfaces

A
  • Th17 type
  • Leads to IL-17, IL-23, regulators of mucosal responses, tolerance
  • Can lead to autoimmune disease if response fails
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5
Q

Immune response to no danger signals (non-dangers)

A
  • Ex. foods, environmental
  • T regulatory response
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6
Q

What is an intracellular pathogen?

A
  • Viruses
  • Bacteria
  • Parasites
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7
Q

What is an extracellular pathogen?

A
  • Bacteria
  • Parasites
  • Fungi
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8
Q

Viruses

A
  • Intracellular pathogens. Basically proteins with some glycogen residues and a genome
  • Require cell machinery for replication (injects RNA or DNA into host cell for replication)
  • Have no metabolism
  • Lead to Th1 response and cytotoxic T cells
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9
Q

Viruses and evolution

A
  • Often share a close evolutionary relationship with their hosts. A symbiotic relationship would be best but not always possible

Ex. retroviral integration into the genome (HIV and SIV)

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10
Q

Virus shape and size

A
  • Highly organized but simple structure
  • Can be naked or enveloped
  • Small, 20-400nm
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11
Q

Smallest virus

A

Rhinovirus

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12
Q

Largest virus

A

smallpox

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13
Q

Recognition of viral PAMPs

A
  1. Virus enters the cells
  2. TLR or other pattern recognition receptor recognizes the viral genome in endosomes and cytoplasm of the cells
  3. Pro-inflammatory cytokines and type-1 interferons are produced
  4. Interferons alpha and beta establish an anti-viral state in all cells within the vicinity (interferons interfere with viral replication)
  5. Immune cells are recruited to site of infection
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14
Q

Purpose of Type 1 interferons

A
  • Includes interferons alpha and beta
  • They create an environment in which the virus cannot replicate preventing spread into blood and other organs

Ex. raising body temperature to make it more difficult to replicate
Ex. increase expression of ligands on infected cells for NK cell receptors
Ex. increase activation NK cells to kill virus-infected cells

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15
Q

Respiratory viral infection example

A
  • Virus enters the alveoli cells of the lungs
  • Macrophages phagocytose virus, and travel to lymph node an act as antigen presenting cells to activate T cells which move back to alveoli for
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16
Q

Effector cells in Th1 response

A
  • CD4+ T effectors
  • CD8+ T effectors
  • B cells
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17
Q

CD4+ T cells during Th1 response

A
  • Secrete interferon gamma to activate macrophages
  • Secrete interferon gamma to drive the Th1 response and enhance CD8+ T cell killing
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18
Q

CD8+ T cells during Th1 response

A
  • Recognize infected cells via MHC I and peptide
  • Kill via perforin/granzyme and Fas-FasL pathways
19
Q

B cells during Th1 response

A
  • IgG antibodies- used to neutralize virus that is leaving a cell and to opsonize viral antigen on the membrane of infected cells
  • Not as much of an antibody response compared to Th2
20
Q

Main mechanisms of Th1 response to overcome viral infection

A
  1. CD8 cytotoxicity
  2. Macrophage activation
  3. Antibody dependent cell-mediated cytotoxicity (NK cells have Fc-receptors which bind to specific antibodies found on the infected cells. Interaction causes release of granules to kill infected cells)
21
Q

Immune regulation by viruses

A

There are many ways in which viruses have evolved to avoid the immune response

22
Q

Example of viral immune suppression (viral evolution to avoid immune response)

A
  • HIV
  • Virus integrates into the genome of CD4+ T cells, and eventually re-emerges and depletes the T cell population leading to AIDS
23
Q

Example of a cytokine storm (viral evolution to avoid immune response)

A
  • COVID 19 or 1918 pandemic influenza
  • Hyperactivation of inflammatory cytokine response; completely out of control
24
Q

Bacteria

A
  • Gram negative, gram positive, acid fast
  • Cocci, bacilli, spiral shaped
  • Have conserved motifs (LPS, peptidoglycan, CpG DNA, etc.) that can be recognized by TLRs
25
Q

Bacteria mode of transmission

A
  • Infections at many different sites
  • Transmission includes contamination of food, instruments, fomites, direct contact, aerosols, etc.
26
Q

Virulence mechanisms of bacteria

A
  • There are different immune responses to different bacterial species

Includes:
- Endotoxins (inside) and exotoxins (secreted)
- Spores and biofilms (persistence in environment, on surgical tools)
- Granulomas (virus remains latent and evades immune system)
- Intracellular cell-cell replication (syncytia)

27
Q

Bacteria intracellular vs extracellular

A
  • Extracellular: Th2 response
  • Intracellular: Th1 response
28
Q

Virulence factors

A

Secretion systems export toxins and directly inject them into host cells

29
Q

Innate response to bacteria

A
  1. Breach of primary barrier
  2. Recognition of PAMPs by TLR. Triggers macrophages to release cytokines, chemokines, and anti-microbial peptides
  3. Results in vasodilation and increased vascular permeability permits neutrophil and macrophage/DC migration
  4. Combination of phagocyte recruitment to the site of infection, cytokines, and anti-microbial peptides. Causes swelling, pain, heat, and redness
30
Q

Alternative activation of complement (bacteria)

A
  1. Motifs of bacteria activate the complement through alternative pathway
  2. C3b can opsonize bacteria which promotes the phagocytosis by macrophages, neutrophils, dendritic cells
  3. C3a and C5a are anaphylatoxins, promoting inflammation and phagocyte recruitment
  4. Membrane attack complex (MAC) punches holes in bacterial cell walls
31
Q

Th2 immunity to extracellular bacteria

A
  • Antigen presenting cells present bacterial peptide to CD4+ Th cells. Results in CD4+ T cells producing Th2 cytokines, and results in the release of IL-4, IL-5, IL-13, and the activation of B cells to produce antibodies
  • B cells become plasma cells that produce the antibodies that are pumped into the blood
32
Q

Antibodies job during Th2 immunity response

A
  1. Neutralize toxins (endotoxins, and exotoxins)
  2. Opsonization (promote phagocytosis)
  3. Neutralize bacterial attachment to cells
  4. Activate complement (classical activation)
33
Q

Th1 immunity to intracellular bacteria

A
  1. Intracellular bacteria enters host cells, begins to replicate
  2. TLRs inside the cells will detect bacteria and drive a Th1 reponse
  3. Cell mediated immunity and the production of interferon gamma (activates macrophages and clears bacterial infection)
34
Q

Parasites

A

Well developed invaders. Developed to evade the immune responses of the host and to cause minimal reactions so that they can persist and use host resources for a long time

35
Q

Immune responses to parasites

A
  1. Protozoa (Th1 or Th2 response)
  2. Helminths (Th2 response)
  3. Arthropods (Th1 or Th2 response)
36
Q

Extracellular protozoa with intracellular replication

A
  • Ex. Toxoplasma
  • Immune response is generally Th1 and involves the activation of macrophages through interferon gamma which clear the infection
  • Extracellular activation will result in antibodies (opsonization , agglutination, and complement activation)
37
Q

Extracellular protozoan

A
  • Ex. African trypanosomes
  • Present in tissues and blood and transmitted through tsetse flies. Devastates cattle population
  • Immune response is typically through antibody production
  • Effective immune response avoidance by switching and shuffling gene expression makes it nearly impossible for the antibody response to keep up because the surface structure (glycoproteins) changes so much and antibodies can’t bind
    » Results in waves of different trypanosomes. When immune response applies pressure, parasite changes
38
Q

Helminths

A

The immune system is not well equipped to control helminth infections since these organisms often are very well adapted and cause little inflammation or disease

39
Q

What makes helminths hard to destroy?

A
  • Too big to be phagocytosed
  • Have thick extracellular cuticle that protects worm from attack by the MAC of the complement system
40
Q

Th2 immunity of Helminths

A

Immune response results in the production of IgE which cause mast cell degranulation that act to expel the worms
- Basically an allergic response to salivary antigens of the helminth causing worms to detach from the intestinal wall and pass out in feces

41
Q

Eosinophils and helminths

A
  • Eosinophils have Fc receptors and will bind to antibody-coated helminths, degranulate and release their granule contents onto the worm cuticle
  • Most efficient way to kill larvae in tissues and important in controlling helminth numbers
42
Q

Immune response against Arthropods

A
  • Immune response against arthropods is mainly directed at salivary proteins (carrier molecules- haptens and collagen)
  • Local inflammation and secretion of antimicrobial peptides and cytokines can make it difficult for attachment and adherence of the arthropod.
    o Restricted blood flow from inflammation inhibits the arthropod feeding
43
Q

Arthropod immune invasion

A

Saliva has immune modulators that suppress inflammation and the establishment of an innate response. Helps with attachment to host and transmission of pathogens

44
Q

Potential vaccine strategies for arthropods

A
  1. Target immune modulators in the saliva of arthropods (host more capable to launch an immune response)
  2. Target midgut antigens of the arthropods (antibodies from the host enter the blood meal of arthropods, disrupt the function of the arthropod)

Immunology #2 (17 decks)

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