L7 - immune response to ecxtracellular pathogens Flashcards

1
Q

structure of lymph node and role in inefction

A

small bean shaped structures

infected tissues drain fluid to lymh node - APCs proscess and present

in paracrotex APCs activate T-cells

in cortex B cells are activated and migrate to secondary folicles with germinal centres (areas of rapid proliferation)

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2
Q

name one of the chmeokines produced by lymph nodes to attract T and B cells

A

CCL21

binds to CCR7 receptor on Naive T-cells

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3
Q

how do lymphocytes enter lymph node - 4 steps- simple

A
  1. Rolling
  2. activation
  3. adhesion
  4. diapedesis
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4
Q

how do lymphocytes enter lymph nodes - detailed

A
  1. T-cell enters high-endothelial venule of lymph node
  2. weak bidning between L-selectins and
    addressins of epithelial cells

= rolling movement

  1. T-cell binds to chemokines changing comformation of integrins increasing affinity

= strong binding

  1. T-cell enters lymph node through epithelial cells via diapedesis
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5
Q

name the different molecules and receptors involved in the 4 key steps of lymph node entry - rolling,activation , adhesion , diapedises

A

rolling:
L-selectins

Activation:
chemokines

adhesion:
integrins

diapedesis:
chemokines

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6
Q

what happenes to T-cells that are activated by APCs in lymph node and what happenes if there not (where do they return to blood)

A

activated T-cells stay in nodes and proliferate

rejoin blood at thoraic duct due to S1P gradient

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7
Q

what is S1P and how does it affect movemt out of lymph nodes for T-cells

A

Shingosine 1-phosphate

lipid higher conc outisde than insde lymph nodes

on activation T-cells downregulate receptors for S1P

= no longer sensitive to conc gradient

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8
Q

describe how b-cells enter lymph nodes and what happenes

A
  1. Circulating B-cells enter via high endothelial venules
  2. travel towards primary follicle BUT are activated by T-cells on border
  3. form a primary focus (proliferating B-cells/somatic hypermutation) = light zone
  4. B-cells can migrate to nearby follicle to form germinal centre (affinity maturation) = dark zone

= undergoes somatic hypermutation and affinity maturation with help of Tfh cells

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9
Q

what organ deals with blood-borne infections

A

spleen

due to no contact with lymphatic system

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10
Q

3 main functions of antibodies

A

neutralisation

opsonisation

complement activation - classical pathway

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11
Q

what is Gut-ascociated lymphoid tissue (GALT)

A

found in instestines

scattered cells and organised peyers patch stuctures

both drained by lymph system

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12
Q

structure of peyers patch

A

Microfold (M) cells sit over the peyers patch

inbetween epithelial cells

allow movement of antigens into underlyming lymph tissue

antigesn proscessed by APCs

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13
Q

how are Immune cells sent to the lymh node folliwng activation and how do the ‘home’ back

A

On activation in peyers patch dendritc cells upregulate the ‘lymph node chemokine receptor’
= CCR7

binds to CCL21 - moves to lymph

on activation CCR7 is downregulated and tissue specifc chemokine receptors are upregulated

  • same theory works for all immune cells getting to lymph node and back into circulation
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14
Q

why is class switching of B-cells T-cell depndant

A

binding of CD40 to CD40L by T-cells activates class switching

additionally cytokines produced affect what antibody

= No T-cell = IgM produced

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15
Q

name the cytokine produced by T-cells to cause class switching to IgA B-cells for mucosal sites

A

TGF-b

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16
Q

Name the enzyme involved in class/isotype siwtching of antibodies

A

AID

activation-induced cytidine deaminase

17
Q

what form do IgA antibodies take

A

dimers

linked by J chain

18
Q

how do IgA dimers corss the intstinal epithelium to enter gut lumen

A

Poly-ig receptor

binds to Fc region and is transported through cell

19
Q

role of IgA in the gut and at mucosal sites

A

binds to mucous layer

neutralsies pathogens and toxins

20
Q
A