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Micro and Immuno > Immunity to infections/microbes > Flashcards

Immunity to infections/microbes Flashcards

1
Q

General overview of protective immune response against microorganisms

A

At the site of infection, cellular innate immune response recognizes the infection and then migrate to the secondary lymphoid organ to activate T cells. T cells migrate back to the site of the infection.

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2
Q

What type of immune response is elicited by extracellular versus intracellular pathogen?

A

Extracellular: antibodies, complement activation, phagocytosis, neutralization. IgA and antimicrobial peptide at cell surface.

Intracellular: For cytoplasmic, CD8 T cells, NK cells. For vesicular, T-cell and NK-cell dependent macrophage activation (IFNg and CD40)

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3
Q

The nature of the microbial stimuli determines…

A

the type of T cells and Ig

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4
Q

Step-by-step immune response for Intracellular virus/bacteria/fungi/protozoa

A
  1. Intracellular virus/bacteria/fungi/protozoa picked up by DC, and start making IL-12
  2. Once in lymph node, IL-12 stimulates naive T cells to become Th1 cells that make IFNg
  3. IFNg conditions B cells to isotope switch (IgG1, IgG2, IgG3 in humans)
  4. Phagocytosis by macrophages and NK cells, complement fixation
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5
Q

Step-by-step immune response for helminths

A
  1. Mast cells or basophils at the site of the infection produce IL-4
  2. IL-4 initiates naive T-cells to become Th2 cells, which make IL-4 and IL-5
  3. IL-4 from Th2 cells induces isotope switching to IgE. IL-5 activates eosinophils
  4. IgE can bind on the surface of the helminth. Fc portion of IgE binds to Fce receptor on the surface of the eosinophil, causing granule release.
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6
Q

Extracellular bacteria/fungi step-by-step response

A
  1. IL-1, IL-6, IL-23, TGFb initiates naive T cells to differentiate into Th17 cells. TGFb also induces isotope switching to IgA type
  2. Th17 cells make IL-22 and IL-17 which impact epithelial cells
  3. epithelial cells make antimicrobial peptides, and chemokines (IL-8, CSF) which attract neutrophils.
  4. complement also plays a role
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7
Q

Extracellular bacteria are able of replicating…

A

outside of the host cells

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8
Q

Extracellular bacterial Disease is caused by two mechanisms:

A
  • induction of inflammation resulting in tissue destruction
  • production of toxins having various effects
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9
Q

toxins produced by bacteria

A
  • endotoxins (cell wall components like LPS)
  • exotoxins (secreted)
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10
Q

exotoxins

A
  • can be cytotoxic (kill cells)
  • can interfere with normal cellular functions (no killing. Ex: inhibit protein synthesis)
  • can induce cytokine production
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11
Q

Mechanisms of innate immunity to extracellular bacteria

A

complement activation (C3 converters generated, C3b and C3a generated. C3b binds to surface of the microbe, resulting in opsonization and phagocytosis by neutrophils and macrophage. C5a and C3a stimulate inflammatory reactions because they are anaphylatoxins and recruit leukocytes leading to more destruction of microbes

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12
Q

Humoral immunity response to extracellular bacteria

A

Humoral immunity eliminate microbes and neutralize their toxins via
antibodies that recognize cell wall antigens and secreted and cell-associated toxins.
Ig induce opsonization and phagocytosis of microbes and complement activation

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13
Q

Effector function of Ig

A
  • neutralization
  • opsonization and Fc-receptor mediated phagocytosis
  • phagocytosis of C3b-coated bacteria
  • inflammation
  • lysis of microbe
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14
Q

Cellular-mediated immunity to extracellular bacteria

A

Bacterial protein antigens processed by DC activate CD4 helper T cells for
- production of IL-17 and neutrophil recruitment
- production of IFNg and activation of macrophages
- B cell help via CD40L

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15
Q

Intracellular/extracellular: P. gingivalis

A

intracellular

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16
Q

characteristics of intracellular bacteria

A
  • Replicate within macrophages or epithelial cells
  • Have evolved to resist killing within macrophages
  • Their elimination requires cell-mediated immunity (CD8 cells, NK cells, T-Helper cells activating macrophage)
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17
Q

Pathological consequences of intracellular bacteria due to:

A
  • The host response (granulomatous inflammation)
  • Toxin that lyses cells
  • Ex. Porphorymonas gingivalis (anaerobic gram-) produces
    lipopolysaccharides, fimbriae and proteases that affect the host response and damage oral cells
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18
Q

Innate Immunity to intracellular bacteria

A
  • Phagocytes and complement before cells become infected
  • NK cells are activated directly or via IL-12 produced by macrophages (NK cells produce IFNg, which activates macrophages)
  • innate immunity helps to control the level of infection: adaptive immunity needed to really clear the infection
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19
Q

Adaptive immunity to intracellular bacteria

A
  • Cell-mediated immunity is crucial
  • CD4 T cells differentiate into TH1 effectors via IL-12
  • Macrophage activation by T cell-derived signals (IFN!)
  • Antibodies against TB (functions before it has infected inside cells)
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20
Q

What happens in mice in TB infection without IFNg or IL-12?

A

Infection cannot be cleared - thus it is crucial to have a T cell response

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21
Q

Describe the Cooperation of CD4 and CD8 T cells in defense against intracellular bacteria

A

Lysis of infected cells by cytotoxic CD8 cells (CTL), which receive help from CD4 cells via IL-2

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22
Q

characteristics of fungi infection

A
  • Fungal infection are: endemic (fungi in the environment) and opportunistic (immunodeficient: AIDS, cancer therapy, transplant rejection)
  • Fungi may live in extracellular tissue and within
    phagocytes: similar responses as to extracellular and
    intracellular bacteria
  • Antifungal immunity is not well characterized
23
Q

Innate immunity to fungi

A

Neutrophils & macrophages phagocytose fungi for intracellular killing

24
Q

Adaptive immunity to fungi

A
  • Th1 and Th17 responses are protective
  • Specific Ab responses (serological diagnosis) are protective
25
Q

characteristics of viruses

A
  • Viruses are obligatory intracellular
    microorganisms: replicate within cells and various cell types
  • Viral replication interferes with normal cell function
    (cytopathic infection) and/or results in cell death (HIV)
  • Innate and adaptive immune responses block infection and lead to elimination of infected cells
26
Q

Immune response against viruses

A
  • innate immunity: IFNa (makes cells more resistant to viral infection) and NK cell killing
  • Antibodies neutralize virus, activate complement and lead to opsonization of viral particles
  • CD8 T cells kill viro- infected cells
27
Q

Innate immune response against viruses

A
  • Type I IFN (IFNa/b) is specific to viruses because it induces an anti-viral state. Cells receive a signal to become more resistant to viral infection, thus virus can’t replicate as well in these cells
  • NK cells have an inhibitory receptor that binds MHC Class I, inhibiting the activating receptor signal. Some viruses may down regulate MHC Class I, thus this allows NK cells to kill the infected cell. They also increase activating receptor ligands.
28
Q

Adaptive immune response to viruses

A
  • Antibodies neutralize virus, activate complement and lead to opsonization of viral particles (virus will be outside of cells before infecting them)
  • CD8 T cells kill viro- infected cells (they are re-activated by infected cells at the site of the infection). This decreases the viral reservoir.
29
Q

describe immunity to COVID-19 (SARS-CoV-2)

A
  • SARS-CoV-2 use ACE2 to enter target cells
  • SARS-CoV-2 and SARS-CoV bind ACE2 with same affinity
  • antibodies can inhibit binding to target cells
30
Q

characteristics of parasitic infection

A
  • 30% of the worlds population suffers from parasitic infestations
  • Protozoa and helminths vary greatly
  • Infections are chronic
  • Prophylactic vaccines necessary
31
Q

Statistics on malaria infections

A

100 million people are infected with malaria.
1 million death/year from malaria

32
Q

How do Protozoa and helminths vary greatly?

A
  • structural and biochemical properties
  • life cycles (vertebrate, intermediate host such as insects or snails)
  • pathogenic mechanisms
33
Q

what makes parasitic infections chronic?

A
  • weak innate immunity: Many protozoa (intracellular) are resistant to phagocytic killing. Helminths (extracellular) have thick teguments and resist cytocidal mechanisms of

neutrophils/macrophages

  • ability to evade adaptive immune response
  • antibiotics are not effective
  • repeated chemotherapy not possible (expense, logistic problem)
34
Q

Adaptive immunity to protozoa (intracellular parasite)

A
  • Macrophage activation by TH1 cell-derived cytokines
  • Activation of TH2 cells results in increased protozoa survival

and exacerbation of lesions (because this inhibits activation of macrophage)

  • CTL responses against lytic protozoa (malaria)
35
Q

Adaptive immunity to helminths

A

Activation of TH2 cells results in killing of helminth:
- Production of IL-4 which induces isotope switching to IgE, binds to surface of helminth
- Production of IL-5 which stimulates eosinophil development and
activation. FceRI of eosinophil binds to Fc portion of IgE bound to helminth, sending degranulation signal
- Degranulation of eosinophils and killing of helminth via release of major cationic protein and major basic protein

36
Q

What is the consequence of microbe-induced immune response? (overview)

A

Granuloma and immune complex deposit

37
Q

Describe how Granulomatous responses contribute to tissue injury

A
  • Immune system wall off foreign body that cannot be removed
  • Schistosoma mansoni eggs induces cirrhosis of liver
  • Filaria induces fibrosis of lymphatic vessels
  • Mycobacteria tuberculosis induces necrotizing granulomas and fibrosis in
    the lungs
  • Th1 responses to intracellular fungus infections (histoplasmosis) may elicit
38
Q

A consequence of persistent infection can be the formation of circulating immune complexes (microbe antigens and microbe- specific antibodies) that can be deposited in…

A

blood vessels and kidney (streptococcus, hepatitis B, malaria, Schistosoma)

39
Q

What are some of the Injurious consequences of host response

A
  • Cytokines produced by activated macrophages induce Inflammation (periodontitis) or Septic shock (TNF is the principal mediator)
  • Bacterial toxin result in non-specific activation of T cells. Induce subsequent systemic inflammatory syndrome called superantigens (Staph aureus)
  • CTL against viro-infected cells generate injury ex: LCMV and inflammation of meninge or hepatitis B and liver injury
40
Q

Cytokine storm in COVID-19

A
  • Elevated systemic chemokines (CXL8, CCL2, CXCL10) and cytokines (IL-1, TNF-!, IL-6, IL-12, IFN”) in COVID-19 patients
  • Insufficient type I interferon response (too little, too late)
  • Excessive immune response
41
Q

How do microbes evade the immune response?

A
  1. antigenic variation
  2. inhibition of complement activation
  3. resistance to phagocytosis
42
Q

Most Common evasion mechanism for bacteria, viruses and parasites

A

antigen variation

43
Q

what is antigenic variation?

A

When pathogens change their surface antigens due to changes in the genes of a pathogen; Generate variants with different antigenic composition that are not
recognized by Ig or T cells

44
Q

antigen variation in extracellular bacteria

A
  • pilin (gonococci and Escherichia coli)!
  • changes in glycosidase production leads to LPS and other
  • polysaccharide alteration (Haemophilus influenzae)
45
Q

antigenic variation in viruses

A
  • point mutations (antigenic drift), Also has potential not to cause any problem
  • reassortment of virus RNA genomes (antigenic shift) responsible for

influenza pandemics

  • produce antigenic changes in the hemagglutinin and neuraminidase of influenza virus and surface proteins of HIV
46
Q

antigenic variation in parasites

A

express different variant surface glycoproteins, e.g., trypanosome, plasmodium

47
Q

Describe antigenic shift

A
  • H1N1 is example
  • the process by which two or more different strains of a virus, or strains of two or more different viruses, combine to form a new subtype having a mixture of the surface antigens of the two or more original strains
  • host is doubly infected with different viruses which combine
  • immunity against original viruses is ineffective
  • often responsible for large-scale epidemics
48
Q

Describe the SARS-CoV-2 mutation in Europe and USA associated with enhanced infectivity

A

Increased viral loads in COVID-19 patients
Greater infectivity due to
less S1 shedding
greater level of S protein in the
virion

49
Q

Describe Trypanosomes and their ability to change surface antigen

A
  • > 100 waves of parasitemia can occur: B cells trying to keep up with surface antigens
  • Chronic infection
  • Vaccination difficult
50
Q

what are the ways pathogens can evade phagocytic machinery?

A
  • Blocking of the fusion of lysosome with
    phagocytic vacuole, e.g., Mycobacteria
  • Interference with acidification of the phagolysosomal
    vacuole, e.g., Histoplasma capsulatum
  • Disruption of phagosome membrane and escape into cytoplasm, i.e., Listeria monocytogenes via production of hemolysin protein
  • Resistance to C3b-mediated phagocytosis by bacteria with polysaccharide-rich capsules, e.g., Pneumococcus
  • Scavenging of reactive oxygen intermediates, e.g., catalase-positive Staphylococci, Mycobacterium Leprae via phenolic glycolipid
51
Q

describe the modulation of complement

A
  • Inhibition of complement activation: bacterial covered their surface with sialic acid (binds factor H), e.g.,
    Streptococcus pyogenes and Staphylococcus aureus & Adhesins bind complement factors, e.g., Staphylococcus aureus
  • Develop tegument that is resistant to damage by complement (schistosome)
52
Q

How does P. gingivalis manipulates the host response in periodontitis?

A
  • subverts complement
  • Inactivates antimicrobial peptides
  • Inhibits iNOS and NLRP3 inflammasome in macrophages
  • Favors Th17 differentiation
53
Q

How does P. gingivalis subvert complement?

A
  • gingipain generates C5a and degrade C5b & C3, now can’t bind as opsonin, but have C5a leading to inflammation
  • crosstalk between TLR2 and C5aR leads to blockade of neutrophil phagocytosis and inflammatory cytokines
  • leads to altered growth of microbial community
  • favors Th17 differentiation

Micro and Immuno (17 decks)

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