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Infectious Disease > Week 1: Host-pathogen interactions > Flashcards

Week 1: Host-pathogen interactions Flashcards

1
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5
Q

Innate immunity effectors

A
  • Macrophages
  • Dendritic cells
  • Granulocytes
  • Antimicrobial peptides
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6
Q

Adaptive immunity effectors

A
  • B cells
  • CD4+ T cells
  • CD8+ T cells
  • Antibodies
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7
Q

Innate immunity Response/Specificity

A
  • Relatively non-specific
  • Recognition of broadly conserved microbial antigens or their effects
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8
Q

Adaptive immunity specificity

A
  • Specific
  • Recognition of microbial peptides in context of MHC I (CD8+ T cells), MHC II (CD4+ T cells) or sepcific antigens (antibodies/B cells
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9
Q

Innate immunity Response time

A

Constitutive and/or rapid (hours to days)

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10
Q

Adaptive immunity Response time

A

Delayed (days to weeks)

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11
Q

Innate immunity Memory

A

*Usually* no memory

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12
Q

Adaptive immunity memory

A

*Usually* has memory

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13
Q

What protects us from pathogens?

A

Physical barriers

  • skin
  • mucous membranes

pH

Iron hoarding

Innate immune response

Acquired immunity (adaptive)

beneficial bacteria and their products

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14
Q

Abnormal physiology that can increase risk of infection

A
  • Vesicoureteral reflux
  • Auto-splenectomy
  • Atopic dermatitis
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15
Q

Vesicoureteral reflux role in increased risk of infection

A

increased risk of pyelonephritis

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16
Q

Auto-splenectomy role in increased risk of infection

A
  • Splenic necrosis induced by sickle cell anemia, SLE
  • Prone to infections by encapsulated organisms (ie Streptococcus pneumoniae and Haemophilus influenzae)
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17
Q

Atopic dermatitis role in increased risk of infection

A

Increased risk of skin infections (Staph aureus, Strep pyogenes, HSV)

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18
Q

How does the innate immune system protect us from pathogens?

A
  • response is early or constitutive and non-specific
  • Essential for immune cells to go to the site of infection
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19
Q

How does the acquired immune system protect us from pathogens?

A

Delayed because cells and products need to be made - but high specificity and MEMORY! (usually)

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20
Q

Describe the role/mechanisms of normal flora in protecting us from pathogens

A
  • Occupy space
  • Angry neighbors
  • Assist in host function
  • Immunomodulation
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21
Q

Describe the mechanisms of COST of normal flora in protecting us from pathogens

A
  • Opportunistic pathogens
    • Staph infections
    • Dental caries
    • Gastritis
    • Sepsis
  • Nutrient competition
  • Can be passed on to susceptible individuals
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22
Q

What are the components of the microbiome

A
  • Bacteriome
  • Virome
  • Mycobiome
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23
Q

Adaptive immune cells

A
  • CD4+ T cells
  • CD8+ T cells
  • B cells
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24
Q

Basic function of CD4+ T cells

A
  • Direct immune responses
  • required for CD8+ T cell memory and Ig class switching
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25
Q

Basic function of CD8+ T cells

A

Kill infected cells

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26
Q

Basic function of B cells

A
  • Make antibody
    • M-A-D-G-E
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27
Q

Basic function of macrophages

A

big cells that eat things and present antigen

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28
Q

Basic function of monocytes

A

Like pre-macrophages in the blood

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29
Q

Basic function of granulocytes

A
  • Eosinophils - (cause allergies and kill worms)
  • Basophils - (allergies, worms, cytokines)
  • Neutrophils - (eat bacteria, then die and make pus)
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30
Q

Basic function of Dendritic cells

A
  • Great at antigen presentation and cytokine production
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31
Q

Basic function of NK cells

A
  • Kill infected cells and cancer cells
  • Produce cytokines
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32
Q

Basic function of cytokines and chemokines

A

Modulate immune responses

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33
Q

Pro-inflammatory cytokines and chemokines

4 listed

A
  • IL-6
  • TNF-α
  • IFN-γ
  • IL-17
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34
Q

Anti-inflammatory cytokines and chemokines

A

IL-10

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35
Q

Cytokines that inhibit intracellular pathogen replication

A
  • IFN-α
  • IFN-β
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36
Q

Basic functions of cytokines and chemokines

A
  • Modulate immune response
    • pro-inflammatory
    • anti-inflammatory
    • inhibit intracellular pathogen replication
  • Recruit immune cells
  • Activate immune cells
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37
Q

Describe the mechanisms of innate recognition of pathogens

A
  • Recognition of pathogen products (PAMPS-Pathogen Associated Molecular patternS) by host (PRR-Pathogen Recognition Receptors)
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38
Q

What are PAMPS?

A

Recognition of pathogen products (PAMPS-Pathogen Associated Molecular patternS)

  • Pathogen surface proteins
  • Pathogen-specific nucleic acid structures
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39
Q

What are PRRs?

A

(PRRs-Pathogen Recognition Receptors)

  • Host receptors (membrane or cytoplasmic)
  • Toll-like receptors (TLRs), C-type lectin receptors (CLRs), NOD-like receptors, RIG-I like receptors (RLRs)
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40
Q

What is the response of innate recognition of pathogens (PAMPS recognized by PRRs)

A
  • Induce cytokine/chemokine responses to recruit immune cells, limit pathogen replication and modulate the overall immune response
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41
Q

What are the major types of pathogens?

A
  • Pathogens that require intracellular infection
  • Pathogens that remain extracellular and can be phagocytosed
  • Pathogens that are extracellular but are so large they evade phagocytosis
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42
Q

What are some Intracellular only pathogens?

A
  • Viruses
  • intracellular bacteria
  • some fungi
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43
Q

Responses for Intracellular-only pathogens?

A
  • Th1 responses predominate
    • IFN-γ
    • CD8+ T cells
    • IgG antibody subtypes
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44
Q

What are some examples of extracellular pathogens that are susceptible to phagocytosis?

A
  • extracellular bacteria
  • some fungi
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45
Q

Responses of extracellular pathogens that are susceptible to phagocytosis

A
  • TH17 responses predominate (some overlap with Th1 responses)
    • IL-17/IFN-γ
    • Activated macrophages
46
Q

Examples of pathogens that are extracellular that are too large for phagocytosis?

A
  • Helminths
  • Parasites
47
Q

Responses pathogens that are extracellular that are too large for phagocytosis?

A

Th2 responses predominate

  • IL-4
  • IgE antibody
  • Eosinophils
48
Q

Broad categories of immune responses according to pathogen type

A
  • Intracellular (virus and some bacteria)
  • Extracellular bacteria
  • Parasites
  • Fungi
  • Toxins
49
Q

Mechanisms of toxin breakdown

A
  • Cytokine responses
  • Innate cellular responses
  • Adaptive responses
  • Pathogen evasion mechanisms
50
Q

Describe the basic mechanism of immune response to intracellular pathogens

51
Q

Intracellular pathogen evasion mechanisms: Innate responses

A
  • Block type I IFN
  • Downregulate MHC I
    • CMV
  • Hide PAMPS
  • Inhibit APC activation
  • Escape from/survival in phagosome
    • M. tuberculosis
52
Q

Intracellular pathogen evasion mechanisms:Adaptive responses

A
  • Immunodominance
    • Direct B cell responses to non-protective epitopes (HIV)
  • Mutation
  • Antigen shift/drift
    • influenza
  • Antibody-dependent enhancement
    • Dengue virus
  • Latency
    • HIV, CMV, EBV
53
Q

Describe the basic mechanism of the immune response for extracellular bacteria

54
Q

Extracellular bacterial evasion mechanisms of the innate response

A
  • Resist phagocytosis
    • capsule (Klebsiella pneumoniae)
  • Escape from/survival in phagosome
    • Salmonella
  • Inactivation of complement
    • S. aureus
  • Skewing cytokine response
    • Bordetella
55
Q

Extracellular bacterial evasion mechanisms of the adaptive response

A
  • Immunodominance
    • Direct B cell responses to non-protective epitopes
  • Mutation
  • Antigen shift/drift/variation
    • Neisseria
  • Antibody neutralization
    • S. aureus
  • Antibody degradation
    • Streptococci
56
Q

Describe the basic mechanism of the immune response for extracellular parasites

57
Q

Extracellular parasite evasion mechanisms of the innate response

A
  • Too dang big to phagocytose
  • Tegument
    • physical barrier
  • inactivation of complement
  • Protease inhibitors
58
Q

Extracellular parasite evasion mechanisms of the adaptive response

A
  • Neutralization of superoxide radicals
  • cleavage of antibodies
  • Antigen shift/drift/variation
59
Q

Describe the basic mechanism of the immune response for fungi

60
Q

Fungal evasion mechanisms of the adaptive response

A
  • Antigen shedding
  • Induction of Tregs
61
Q

Fungal evasion mechanisms of the innate response

A
  • Escape from/survival in phagosome
  • Inhibition of complement
  • Elimination of ROS
  • Shielding of PAMPS
  • Size (morphotypes)
62
Q

Describe the Immune response to toxins

A
  • Targeting of pathogen doesn’t eliminate toxin
    • superantigen
    • LPS
  • Neutralizing antibody blocks toxin activity
    • need CD4+ T cells to generate potent antibody responses
      • class switching
    • Can induce with vaccination with toxoid (inactivated toxin)
63
Q

Immune response to Botulinum toxin

A

Clostridium botulinum

  • Inhibits acetylcholine release (induces muscle paralysis/weakness)
  • Passive administration of neutralizing antibody (vaccination with toxoid discontinued in 2011)
64
Q

Immune response to Diphtheria toxin

A

Corynebacterium diptheria

  • inhibits translation (myocarditis, paralysis)
  • PAssive administration of neutralizing antibody or vaccination (DTaP, Tdap)
65
Q

Immune response to Tetanus toxin

A

Clostridium tetani

  • Blocks inhibitory neurotransmitter GABA (muscle rigidity and spasms)
  • passive adminstration of neutralizing antibody or vaccination
66
Q

What are 3 ways a virus can evade the immune response?

67
Q

What are 3 ways extracellular bacteria can evade the immune response?

68
Q

What evasion mechanisms allow influenza virus to re-infect the population every year?

69
Q

List a cytokine and one cell type that plays a major role in immune responses to infection with

A
  • Virus
  • Extracellular bacteria
  • Nematode
70
Q

Summary of host-pathogen interactions

71
Q

Intracellular infection response cytokines

A
  • Type I IFN
    • IFN-α (13 subtypes)
    • IFN-β
  • IFN-γ
    • Drives TH1 response (generation of CD8+ T cells)
72
Q

Type I IFN mechanism

A
  • IFN-α (13 subtypes), IFN-β
  • Induce antiviral state in self and neighboring cells via interferon- stimulated genes (ISG)
    • inhibition of mRNA transcription and translation
    • Inhibit viral replication by binding to viral proteins
    • Dampen over-inflammatory responses
    • Activate APCs
    • Help induce CD4 and CD8 T cell responses
73
Q

IFN-γ mechanism against intracellular infection

A
  • drives Th1 response (generation of CD8+ T cells)
  • Macrophage activation for killing intracellular pathogens
74
Q

Macrophage mechanism against intracellular infection

A
  • Destruction of ingested pathogen
    • IFN-γ makes them really good at this
    • Oxidative/respiratory burst, lysozymes
75
Q

Macrophage and Dendritic cells mechanism against intracellular infection

A
  • Antigen processing/presentation
    • MHCI (presentation to CD8+ T cells)
    • MHCII (cross-presentation to CD4+ T cells)
  • Cytokines
    • Type I IFN
    • IFN-gamma
    • Inflammatory cytokines
76
Q

Natural killer (NK) cells mechanism against intracellular infection

A
  • Type I IFN
  • IFN-γ
  • Cytotoxicity (recognizes low/funky MHC I)
  • ADCC
77
Q

Infected non-immune cells mechanism against intracellular infection

A
  • Type I IFN
  • MHC I presentation
78
Q

CD8+ T cells mechanism in the adaptive immune response

A
  • Cytotoxicity
    • kills infected cells by inducing apoptosis
  • Cytokines
79
Q

CD4+ T cells mechanism in the adaptive immune response

A
  • Generation of CD8+ T cell memory
  • Induction of B cell antibody class switching (CD40/CD40L)
  • Direction of Th1 response through cytokine production IFN-gamma)
80
Q

B cells mechanism in the adaptive immune response

A
  • IgM
    • early response
  • IgG
    • Complement, opsonization, neutralization, ADCC
  • IgA
    • mucosal infections
    • ADCC, neutralization, immune exclusion
81
Q

Cytokines for Extracellular Bacterial Infection

A
  • IL-17
  • Type I IFN
82
Q

Mechanism of IL-17 against extracellular bacterial infection

A
  • Drives Th17 response (antibody)
  • Neutrophil, macrophage recruitment
83
Q

Mechanism of Type I IFN against extracellular bacterial infection

A
  • Activates phagocytes
  • Helps induce CD4 T cell responses
  • Can help, can hurt
84
Q

Mechanism of Macrophages against extracellular bacterial infection

A
  • Phagocytosis, killing
    • IFN-γ
  • Antigen processing for T cells
    • MHC II
  • Cytokines
85
Q

Mechanism of neutrophils against extracellular bacterial infection

A
  • Phagocytosis
  • Cytokines
  • Nets
86
Q

Mechanism of Dendritic cells against extracellular bacterial infection

A
  • Antigen processing for T cells
    • MHC II
  • Cytokines
87
Q

Mechanism of NK cells against extracellular bacterial infection

88
Q

Mechanism of Antimicrobial peptides against extracellular bacterial infection

89
Q

Mechanism of B cells against extracellular bacterial infection

A
  • IgM
    • early response; polysaccharides; opsonization
  • IgG
    • complement
    • opsonization
  • IgA
    • induction of B cell antibody class switching (CD40/CD40L)
    • Direction of Th17 response through cytokine production (IL-17)
90
Q

Features and Functions of IgM

A
  • Early response
  • Polysaccharides
  • Opsonization
91
Q

Features and functions of IgG

A
  • Complement
  • Opsonization
92
Q

Features and functions of IgA

A
  • Mucosal infections
  • Neutralization
93
Q

CD4+ T cells

A
  • Induction of B cell antibody class switching (CD40/CD40L)
  • Direction of Th17 response through cytokine production (IL-17)
94
Q

Cytokine response for Extracellular parasite infection

A

IL-4 (from CD4+ T cells) results in

  • IgE production
  • Alternatively activated macrophage activation
95
Q

Functions of alternatively activated macrophages

A
  • Anti-inflammatory
  • wound healing
  • Targeting of parastie, glucose transport, eosinophil recruitment
  • Antigen processing for t cells
    • MHC II
  • Cytokines
96
Q

Functions of eosinophils in an extracellular parasite infection

A

Parasite killing by

  • granule release
  • directed by IgE binding to parasites
97
Q

Functions of dendritic cells in an extracellular parasite infection

A
  • Antigen processing for T cells (from MHC II)
  • Cytokines
98
Q

Functions of NK cells in an extracellular parasite infection

99
Q

B cell function for an extracellular parasite infection

A

IgE from B cells allows for

  • Targeted degranulation by eosinophils
100
Q

CD4+ T cells function in an extracellular parasite infection

A
  • Induction of B cell antibody class switching (CD40/CD40L)
  • Direction of Th2 response through cytokine production (IL-4, 5, 13)
101
Q

Describe the cytokine response in a fungal infection

A

IFN-γ, IL-17

  • Drives Th1 and Th17 response
  • Neutrophil, macrophage recruitment
  • Acvtivation of CD8+ T cells
  • Activation of macrophages to kill phagocytized fungi
  • Release of anti-microbial peptides (AMPs)
102
Q

Macrophage function in a fungal infection

A
  • Phagocytosis/killing
  • Antigen processing for T cells
    • MHC II
  • Cytokines
103
Q

Neutrophils function in a fungal infection

A
  • Phagocytosis/killing
  • Cytokines
  • NET formation
104
Q

Dendritic cells function in a fungal infection

A
  • Antigen processing for T cells
    • MHC II
  • Cytokines
105
Q

Innate cellular immune response function in a fungal infection

A
  • Macrophages
  • Neutrophils
  • Dendritic cells
  • Iron and Zinc sequestration
  • γδ T cells making IL-17
  • Antimicrobial peptides
106
Q

Adaptive immune response in fungal infection

A

B cells

CD4+ T cells

107
Q

B cells in fungal infection

A
  • IgM
    • early response; polysaccharides; opsonization
  • IgG
    • Complement
  • IgA
    • Mucosal infections
    • Neutralization
108
Q

CD4+ T cells function in fungal infection

A

Induction of B cell antibody class switching (CD40/CD40L)

Direction of Th1 or Th17 response through cytokine production (IL-17, IFN-γ)

109
Q

Bacteria that can degrade antibodies

A

Streptococci

110
Q

Bacteria that can neutralize antibodies

111
Q

Bacteria that utilizes antigenic shift/drift

Infectious Disease (82 decks)

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