immunity to microbes part I Flashcards

1
Q

infections caused by pathogenic extracelular bacteria have 2 principal mechanisms:

  1. ____ causes tissue destruction at the site of infection
  2. bacteria produce ____ which have diverse pathlogic effects
A
  1. inflammation
  2. toxins
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2
Q

bacterial toxins are divided into 2 categories:

  1. ____ which are components of bacterial cell walls
  2. ____ whiuch are excreted by the bacteria
A
  1. endotoxins
  2. exotoxins
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3
Q

primary infection (extracellular bacteria) activation of complement pathways:

  1. alternative pathway caused by ____
  2. lectin pathway caused by ____
  3. classical pathway caused by ____
A
  1. LPS
  2. MBP
  3. C-Reactive Protein
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4
Q

complement causes:

  1. C3a and C5a →
  2. mast cells release →
  3. C3b →
A
  1. activate mast cells
  2. histamine and proteases that enhance blood flow
  3. opsonize the pathogen
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5
Q

upon extracellular bacteria primary infection:

local immune cell srelease chemokines/cytokines that activates endothelial cells and attracts neutrophils, especially through cytokine ____

A

IL-8

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6
Q

bacteria is opsonzied by C3b, promotes phagocytosis and killing by ____ and ____

A

neutrophils and macrophages

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7
Q

bacteria can be phagocytosed by DCs and processed to Ags → presented on ____

DC engulf and internalize bacteria and are activated by ____

A

MHC II

PRRs (e.g. TLRs)

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8
Q

mature DCs enter local LNs via ____ lymphatics and move to ____ cell zone

lymphocytes enter LNs via ____

DCs activate T cells (via Ag presented on MHC II) and begin ____

A

afferent T-cell

HEV

proliferation

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9
Q

naive T cells become differentitated towards ____ and ____ according to the DC signals

A

Th1 and Th2

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10
Q

Th cells migrate to germinal centers and interact with Ag-activated B cells resulting in ____ ____ and ____ maturatin

(early infections are characterized by ____ )

A

class switching (IgM → IgG/IgA)

affinity

IgM (low affinity with high avidity)

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11
Q

IgM is a very potent ____ complement activator that generates C3b opsonin

A

classical

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12
Q

some extracellular pathogens can evade immune responses:

  1. variation of surface ____ is key to evading humoral immunity
  2. inhibition of ____
  3. resistance to ____
  4. eliminate reactive oxygen species via ____
A
  1. Ags
  2. complement
  3. phagocytosis
  4. catalase
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13
Q

in the resolutioin of an infection, bacterial debris is removed by local ____ and ____ , or by ____ as soluble immune complexes

A

macrophages and neutrophils

antibodies

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14
Q

____ and ____ can independently (w/o MBL and CRP) actviate complement by the ____ pathway

A

alternative

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15
Q

the classical pathway is activated when ____ binds to Ab attached to Ag, activating ____ and ____ which cleave ____ and ____

A

C1q

C1r and C1s

C4 and C2

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16
Q

the lectin pathway is activated when ____ encounters conserved pathogenic ____ motifs, activating the ____ and cleaving ____ and ____

A

MBL

carbohydrate

MASPs

C4 and C2

17
Q

prevention of host bystander damage:

  1. factor I
  2. DAF, C4BP
  3. CD59
A
  1. inhibits assembly of C3 and C5 convertase → lack of inflammation and classical complement
  2. inhibit assembly of C3 convertase → inhibit classical (C4BP) and alternative pathway
  3. inhibit MAC assembly → inhibit lysis
18
Q

meutrophils and macrophages use surface TLRs, mannose receptors, and scavenger receptors to recognize extracellular bacteria. they use Fc receptors and complement receptors to recgonize intact bacteria or bacteria opsonized with Abs and/or C3b

  1. TLRs activate ____ activities of phagocytes
  2. mannose and scavenger recptors promote ____ of the microbes
  3. Fc and complement receptors promote both ____ and ____ of the phagocytes
A
  1. mimcrobicidial
  2. phagocytosis
  3. phagocytosis and activation
19
Q
  1. TLR1 and TLR2 recognize bacterial ____
  2. TLR4 detects ____
  3. TLR5 recgonizes ____
A
  1. lipoprotein
  2. LPS
  3. flagellin

these TLRs mediate NFkB activation which requires adaptor protein MyD88

20
Q

humoral effector mechanisms for extracellular microbes

  1. toxin ____
  2. opsonization and ____
  3. ____ activation
A
  1. neutralization
  2. phagocytosis
  3. complement
21
Q

cell-mediated immunity for extracellular microbes:

  1. protein Ag of extracellular bacteria activates ____ T cells
  2. Th17 recruit neutrophils and monocytes promoting ____
  3. Th1 releases IFN-gamma that activates ____
  4. Th2 assists with ____ responses
A
  1. CD4+ helper
  2. inflammation
  3. macrophages (resulting in phagocytosis and killing)
  4. antibody
22
Q

principal injurious consequences of host responses to extracelular bacteria are ____ and ____ ____

A

inflammation and septic shock

23
Q

septic shock:

characterized by:

A

circulatory collapse → drop in blood pressure

IV coagulation

24
Q

early phase of septic shock:

  1. caused by cytokines produced by ____ causing a cytokine ____
  2. TNF-alpha upregulates iNOS , IL-18 → futher activation of ____
A
  1. macrophges storm
  2. macrophages
25
Q

late phase of septic shock: systemic

  1. cytokines stimulate production of ____ ____ ____ from liver
  2. leading to ____ activation
A
  1. acute phase proteins
  2. complement
26
Q

cytokine ____ is a global suppressor of macrophage function

A

IL-10

27
Q

certain bacteria (superantigens) bind MHC II to ____ subunit of TCR without Ag present in peptide binding groove

cause unregulated release of cytokines → ____ shock

can lead to polyclonal ____ cell activation

A

beta

septic

T-cell

28
Q

red flags for superantigens:

  1. staphylococcus
  2. S. aureus
  3. S. pyogenes
A
  1. common in food poisening
  2. toxic shock syndrome
  3. streptococcal Tss or acute rheumatic fever)
29
Q

____ protrude through the capsular surface, enabling the adhesions to bind to host receptors yet keeping the bactyerial surface hidden

A

PILI

30
Q

the major mechanism used by bacteria to evade humoral immunity is variation of surface ____

A

Ags

31
Q

the innate immunity is mediated by phagocytes and NK cells interactions among which are mediated by ____ and ____. may control bacterial growth, but elimination of the bacteria requries adaptive immunity.

A

IL-12 and IFN-gamma

(IL-12 activates NK cells to release IFN-gamme to macrophages so they can kill ingested bacteria)

32
Q

the adaptive immunity is cell-mediated immunity in which ____ cells activate phagocytes to eliminate the microbes

A

T-cells

33
Q

M. Tuberculosis (an intracellular bacteria):

  1. this bacteria invades macrophages and prevents lysosome from fusing with ____ → no phagolyosome
  2. activates macrophages to produce ____ and activates T cells
  3. CD4 T cells release ____ which recurits more macrophages and kills intracellular bacteria
  4. CD8 respond to MHC I through cross-presentation and ____ the infected cells
A
  1. phagosome
  2. IL-12
  3. IFN-gamma
  4. kill
34
Q

intracellular bacteria evasion mechanisms:

  1. inhibition of ____ formation
  2. inactivation of ____ and ____
  3. disruption of phagosome ____
A
  1. phagolysosome
  2. ROS and NOS
  3. membrane
35
Q

role of Th1/Th2 cells in infection outcome:

  1. Th1 cells:
  2. Th2 cells:
A
  1. activate phagocytes to kill ingeted microbes (classical macrophage activation)
  2. which inhibit this classical pathway of macrophage activation (alternative macrophage activation)