2.5.10 infection process Flashcards

1
Q

which has a greater SA, outer skin or mucosal surfaces?

A

mucosal

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2
Q

which are the encapsulated organs with both diffuse lymphatic tissue and lymphatic nodules?

A

Lymph nodes, thymus, spleen

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3
Q

describe discrete lymphatic tissue

A
  • can be 2-3 cells, nodule, or germinal center
  • can be nodular (has germinal centers) or non-nodular
    -HIGH ratio of lymphocytes to other cells
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4
Q

describe Diffuse lymphatic tissue

A
  • LOW ratio of lymphocytes to other cells
  • in GI or upper respiratory
  • 2 or 3 lymphocytes interacting with each other
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5
Q

what category do MALT, GALT and BALT fall into?

A

secondary lymphoid tissue

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6
Q

_____ are very diffuse and transient (come and go as infection does)

A

MALTs

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7
Q

what are examples of discrete lymphoid tissue? are they temporary or permanent?

A

GALTs and BALTS
Permanent

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8
Q

_____ allow liquids to remain inside and also carry agglutinated molecules away

A

Mucin molecules

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9
Q

the tonsils and adenoids form a ring of lymphoid tissues called _______ around the entrance of the gut and airway

A

Waldeyers ring

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10
Q

what does the GI tract consist of?

A

Commensals, s-IgA, Mucus

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11
Q

what are some of the things that commensal micro-organisms can do? (5)

A
  1. synthesize essential metabolites like Vitamin K
  2. break down plant fibers in food
  3. inactivate toxic substances in food or from pathogens
  4. prevent pathogens from benefitting from resources of human gut
  5. trigger immune response across epithelial border
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12
Q

In peyers patches, what cell brings in bacteria from gut lumen to GALTs?

A

M cell

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13
Q

Once antigens are brought into peyers patches, what happens?

A

dendritic cells and lymphocytes are waiting, B-cells and T-cells look for interactions so they can differentiate into effector T-cells or plasma cells

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14
Q

______ can extend processes across the epithelial later to capture antigen from the lumen of the gut

A

dendritic cells

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15
Q

Native lymphocytes that are activated in Peyers patch give rise to _____ that travel in the _____ and go out to the ________

A
  • effector cells
  • lymph/blood
  • mucosal tisssue
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16
Q

what are cells found in mucosal tissue?

A

effector leulocytes, CD8, CD4, plasma cells, dendritic cells, mast cells, dendrites

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17
Q

do we want to produce inflammation in the bowel?

A

NO

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18
Q

from blood vessels, effector T-cells bind to intestinal vascular endothelium and enter the _________. Here the T- cells bind to _______

A
  • lamina propria
  • chemokines expressed by intestinal epithelium (CCL25)
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19
Q

s-IgA has multiple mechanisms and they are all _______

A

non-inflammatory

20
Q

what are s-IgAs different mechanisms?

A
  1. export toxins and pathogens from lamina propria while being secreted
    2.bind and neutralize antigens in endosomes
  2. can bind and neutralize pathogens and toxins on gut surface
  3. secreted IgA can bind pathogen on M-cell and take it to lymphoid tissue
  4. Lymphoid IgA picks up antigen in endosomes and takes it to lymphoid tissue
21
Q

____ has a long fold region that is subject to proteases, _____ has a short fold region that wont get proteased.

A

IgA1
IgA2

22
Q

If there is a lack of ability to produce IgA, more what is produced?

A

IgM

23
Q

Secretory _______ (2) protects mucosal surfaces from microbial invasion

A

IgM, IgA

24
Q

IgG being transported from the blood —> lamina –> gut lumen by ______ is considered ______ (passive or active)

A

FcRn
- passive NOT active

25
Q

what is an example of innate immunity on mucosal surface cells?

A

NOD2 proteins in cytosol of RBC

26
Q

NOD2 proteins in cytosol of RBC respond to bacterial products by activating _______ ( just like TLRs)

A

NFkappaB

27
Q

Bacteria are recognized by _______ on cell surface or intracellular vesicles, while _______ recognize bacteria entering the cytosol

A

TLR
NOD1, NOD2

28
Q

what kind of response do we want against worms? why?

A

antibody, cellular response can damage the host

29
Q

______ triggers protective antibody responses against worms while _____ triggers a harmful cellular response

A

TH2
TH1

30
Q

the secondary response is ________ than primary response

A

stronger, more specific

31
Q

the majority of T-cell and B-cells that are activated become _________, but the minority becomes ________

A
  1. short lived effector cells ( effector T and plasma )
  2. long lived memory cells
32
Q

______ antibody amount increases with each infection. _____ antibody increases exponentially, while ______ affinity doesnt change much at all

A

IgG
IgG
IgM

33
Q

In primary response _____ binds to pathogen and there is production of ______

A

-Naive B cell
-low affinity IgM antibodies

34
Q

In secondary response _____ binds to pathogen coated with antibody and there is production of ______

A
  • naive b cell (activation prevented) and Memory B cell
  • production of high affinity IgG, IgA, IgE
35
Q

what is an example of how memory response can be detrimental?

A

If a Rh- mother carries an Rh+ fetus, then becomes pregnant with another RH+ fetus

36
Q

how can B-cell memory response be evaded?

A

antigen changes epitopes

37
Q

_____ remains around longer than an antibody molecule

A

T-cell memory

38
Q

_______ affects memory surface markers

A

mRNA splicing

39
Q

how do you recognize a naive CD4 T cell?

A

it has CD45RA that has ABC in gene transcript

40
Q

how do you recognize a memory/effector CD4 T cell?

A

it has CD45RO that excludes ABC (have been spliced out)

41
Q

when memory cells are directly activated from naive T-cells _____ turns into ______. these cells go on to be _____ & _____

A

CD45RA –> CD45RO
-central memory cells that express CCR7 and effector memory cells that LACK CCR7

42
Q

where do central memory cells with CCR7 go?

A

remin in lymphoid tissue

43
Q

where do effector memory cells without CCR7 go?

A

migrate to tissues

44
Q

some effector cells become _______ and most effector cells ____

A

-quiescent memory cells
-die after a few days

45
Q

where are gamma/delta T-cells located?

A

near epithelial tissue

46
Q

____ are MHC class 1-like molecules that bind gamma/delta receptors and induce infected cell to die from apoptosis

A

MICs

47
Q

how do MIC and NK cells work together to kill infected cells?

A
  • MHC1 + NK cell = no killing of cell
    -MIC + NK cell = killing of cell