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VET 413: Infectious Disease/Immunology > Immune Response to Bacteria, Fungi, and Helminths > Flashcards

Immune Response to Bacteria, Fungi, and Helminths Flashcards

1
Q

what are the 4 classes of pathogens

A
  1. viruses
  2. intracellular bacteria, protozoa, parasites
  3. extracellular bacteria, parasites, fungi
  4. parasitic worms
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2
Q

what are the major determinants of what kind of effector response is used

A

size of pathogen
location of pathogen

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3
Q

what are the 4 main effector responses

A
  1. cytotoxicity
  2. intracellular immunity (type 1)
  3. mucosal and barrier immunity (type 2)
  4. extracellular immunity (type 3)
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4
Q

cytotoxicity

A

mediated by NK cells and CD8 T cells

used for viruses

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5
Q

intracellular immunity (type 1)

A

mediated by ILC1 and Th1 cells

induces macrophage activation

used for intracellular pathogens

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6
Q

mucosal and barrier immunity (type 2)

A

mediated by ILC2 and Th2 cells

induces eosinophil, basophil, and mast cell activation

used for parasites

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7
Q

extracellular immunity (type 3)

A

mediated by ILC3 and Th17 cells

induces neutrophil activation

used for extracellular bacteria and fungi

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8
Q

steps of detecting intracellular pathogen

A
  1. pathogen binds TLR on macrophage cell surface
  2. macrophage engulfs pathogen
  3. bacteria detect a change in pH once inside the phagosome
  4. bacteria injects proteins to prevent the macrophage from killing it
  5. macrophages unable to kill pathogen - requires clonal expansion of CD4 T cells
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9
Q

what type of T cells develop in order to combat intracellular pathogens

A

Th1 cells

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10
Q

main function of Th1 cells

A

produce IFN-y

also secretes other factors that promote the innate immune response (increase cell accumulation and extravasation)

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11
Q

IFN-y

A

activates macrophages to be able to kill intracellular pathogens

increases macrophage production of NO and superoxide

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12
Q

how are Th1 cells and CD8 T cells connected

A

CD4 Th1 cells can increase the ability of dendritic cells to activate CD8 T cells

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13
Q

what innate cells aid in combating intracellular pathogens

A

ILC-1
NK cells

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14
Q

ILC-1

A

innate lymphoid cell
- NO TCR

present in the tissues and act like Th1 cells by producing IFN-y before Th1 cells have differentiated

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15
Q

how do cells respond to extracellular pathogens

A

extracellular pathogens stimulate clinical expansion and differentiation of Th17 cells

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16
Q

main function of Th17 cells

A

produce IL-17 and IL-22 to increase phagocytosis in order to combat extracellular pathogens

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17
Q

IL-17 and IL-22 function

A

IL-17:
- recruit neutrophils
- stimulate neutrophil production in bone marrow

IL-22:
- promote antimicrobial peptide secretion at barrier surfaces
- increase epithelial cell turnover

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18
Q

how do neutrophils find the extracellular pathogens

A

respond to complement gradient (C5a)

19
Q

how do bacteria prevent detection by neutrophils

A

bacterial capsules can inhibit complement fixation (C3b) to prevent being detected

20
Q

what kind of response is required to combat capsulated bacteria

A

antibody response

21
Q

ILC-3

A

innate lymphoid cells
- NO TCR

present in the tissues and act like Th17 cells by producing IL-17 and IL-22

22
Q

are B cells able to become activated without T cell stimulation

A

yes - polysaccharide antigens can cross link so many BCRs that the B cell gets activated without T cells

T cells can NOT respond directly to polysaccharide antigens

23
Q

effect of T independent B cell activation

A

low affinity antibody for the polysaccharide antigen
IgM only

24
Q

how can a high affinity receptor for polysaccharide antigens be generated

A

CD4 Tfh (follicular T helper cells) that help activate B cells specific for non-protein antigens

can ONLY do this if there is a protein component attached to the polysaccharide

25
Q

steps of generating a high affinity polysaccharide antibody

A
  1. B cell binds bacterial polysaccharide bound to protein component
  2. antigen gets internalized and processed
  3. peptides from the protein component get presented on MHC II to CD4 Tfh cells
  4. CD4 Tfh cell activates B cell to produce an antibody against the polysaccharide antigen
26
Q

are the T and B cells specific for the same antigen during the production of high affinity polysaccharide antibody

A

no - B cell is specific for the polysaccharide, T cell is specific for the protein component attached to the polysaccharide

27
Q

what cell type drives almost every aspect of the antibody response

A

CD4 Tfh cells

  • drives germinal center formation and somatic hypermutation of B cells
  • produces cytokines associated with Th1, 2, and 17 responses for antibody class switching
28
Q

how are Tfh cells produced

A

during clonal expansion of Th cells, each Th cell produced will have a complementary Tfh cell that will stay in the LN to activate B cells

Th cell goes to tissue
Tfh cell stays in LN

29
Q

what makes helminths different from other extracellular pathogens

A

too large to be controlled by phagocytosis

must be degraded by toxic mediators

30
Q

phases of allergic responses

A
  1. sensitization - NO allergic reaction
  2. elicitation - HAS allergic reaction
31
Q

allergen sensitization

A
  1. allergen binds DCs –> presented to T cells in LN
  2. T cells proliferate and differentiate into Th2 cells which enter circulation
  3. complementary Tfh cell stays in LN to activate B cells
  4. B cell proliferates and differentiates into plasma cell
  5. plasma cell releases IgE antibody which coats mast cells at the tissue site
  6. mast cells and Th2 cells are primed for next encounter with antigen
32
Q

allergen elicitation

A
  1. subsequent encounter with antigen leads to immediate binding to IgE on mast cell surface
  2. mast cells degranulate –> release mediators to degrade cuticle
  3. Th2 cells bind antigen and release IL-4, 5, and 13 to recruit eosinophils, increase peristalsis and epithelial turnover, and promote repair
  4. basophils bind antigen to release IL-4, histamine, and lipid mediator to degrade cuticle
  5. eosinophils bind antigen and release toxic mediators to degrade cuticle
33
Q

ILC-2

A

innate lymphoid cell that release IL-4, 5, and 13 in response to alarmins secreted by epithelial cells in response to helminth detection

34
Q

how do Th2 cells promote tissue repair

A

induce macrophage differentiation into M2 macrophages

35
Q

M2 macrophages

A

anti-inflammatory macrophages

release IL-10 and TGF-B to suppress inflammatory response

36
Q

do eosinophils have a pathogen specific or non-specific response

A

pathogen specific

express Fc receptors that bind to the back end of IgE antibodies
- pathogen antigen binds to the front end of IgE to cause eosinophil to degranulate

37
Q

antibody dependent cellular cytotoxicity

A

Fc receptors allow the eosinophils (some macrophages) to draw the parasite close and release toxic mediators

38
Q

asthma susceptibility loci

A

gene regions that are associated with allergies/asthma

involved in hypersensitivity via Th2 cells

39
Q

atopic hosts

A

hosts with asthma susceptibility loci

means that they are more likely to develop allergies/asthma

40
Q

what does a host’s degree of hypersensitivity depend on

A

amount of IL-4, 10, and IgE produced

more produce = greater hypersensitivity reaction BUT also greater resistance to helminths

41
Q

how does the environment affect atopy risk

A

increased exposure to allergens increases risk of developing atopy (hypersensitivity reactions to the allergen)

42
Q

function of Treg cells

A

induce tolerance by preventing other T cells from eliminating the pathogen

produce TGF-B and IL-10 to suppress Th1 and Th2 cell responses

43
Q

why is tolerance to pathogens required in some cases

A

sometimes a host’s inflammatory response causes more damage than the pathogen itself - Tregs allow the pathogen to exist in the body without immune response

VET 413: Infectious Disease/Immunology (38 decks)

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