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22 spring: immunology > Test 1: lecture 4 DC cells > Flashcards

Test 1: lecture 4 DC cells Flashcards

1
Q

___ are the bridge between innate and adaptive immune system

A

dendritic cells

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2
Q

gives specific information about the kind of proteins a pathogen has

A

dendritic cells

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3
Q

Dendritic cells are the ___ that sense pathogen and danger to link innate and adaptive immunity

A

sentinels

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4
Q

•MHC II positive cells, such as ___ cells, are potent initiators of the Mixed Leukocyte Reaction

A

dendritic cells

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5
Q

three types of cells that present antigen

A

dendritic

macrophages

B cells

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6
Q

antigen presents ells express high amount of ___ as well as CD80, CD86

A

MHC class 1 and 2

(will stimulate a Tcell response)

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7
Q

___ integrin is found on the surface of dendritic cells

A

(integrins- tell where to go- binds sticky)

alphax beta2

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8
Q

how do myeloid cells sense pathogens

A

innate immunity

receptors- Pattern Recognition Receptors (PRRs) and
Pathogen Associated Molecular Patterns (PAMPs)

cell surface and intracellular toll like receptors detect distinct PAMPs

TLR is a type of PRR

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9
Q

TLR are a type of ___. where are they found

A

PRR

Pattern Recognition Receptors

intracellular or cell surface

they recognize specific PAMPs (Pathogen Associated Molecular Patterns)

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10
Q

how do dendritic cells sense pathogens

A

Pattern Recognition Receptors (PRRs)

each receptors is specialized from specific PAMPs (Pathogen Associated Molecular Patterns)

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11
Q

what kind of PRR detect

–Double stranded RNA

–Lipopolysaccharide (LPS)

–Unmethylated CpG DNA

–Flagellin

A

TLR-3 (ds RNA virus)

TLR-4 and MD-2 (detect gram - bacteria)

TLR-9 (DNA virus)

TLR-5 (motile bacteria)

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12
Q

what kind of danger does dendritic cells respond to?

A

•Conserved microbial motifs

–Double stranded RNA–Lipopolysaccharide (LPS)–Unmethylated CpG DNA–Flagellin

•Products of tissue damage

–HMGB1–S100B–Uric acid–ATP

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13
Q

TLR trigger signals such as adapter molecule ___ to allow new gene expression and generates cytoskeletal changes that allow for phagocytosis

A

MyD88

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14
Q

___ are types of phagocytes

A

dendritic cells

neutrophils

monophils/macrophages

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15
Q

___ cells do not “see” native antigen and need MHC to see

A

T cells

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16
Q

•T-cell Receptor responds to ___ cleaved from the antigen that are “presented” in the groove of an MHC molecule

A

peptides

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17
Q

Peptides from antigens obtained from ___sources are presented in MHC II, and from the ____ in MHC I

A

extracellular

cytosol

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18
Q

•DCs prepare the ___ for the T-cells and tell them whether to respond or not.

A

antigen

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19
Q
A

DC cells can recruit T cells faster and recruit more T cells then other antigen presenting cells like B cells and macrophages

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20
Q

how are DC developed?

A
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21
Q

4 kinds of DC cells

A

lymphoid side adaptive:

activated CD 8+ cDC

activated CD8- cDC

myeloid innate:

monocyte derived inflammatory DC

activated plasmaDC

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22
Q

types of lymphoid DC cells

A

lymphoid side adaptive:

activated plasmaDC

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23
Q

myeloid DC cells

A

myeloid innate:

monocyte derived inflammatory DC

activated CD 8+ cDC

activated CD8- cDC

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24
Q

IL-12

A

cytokine the recruits adaptive immune system to kill (reacts to intracellular pathogen)

cause CD4+ T cells → TH1 (organize kill response to pathogen→ produce IFN gamma make NK cells more deadly, induce rapid killing of virally infected cells)

enhanced CD8+ T cell effector response (kill cells)

cellular immunity

25
Langerhans Cells
skin specific macrophages/dendritic cells express CD1a
26
CD8- DC cells express \_\_\_
CD11b migrate from tissues to lymph nodes tolerogenic properties
27
CD103 DC
intestinal DC cells tells gut to not react to normal food things → **oral tolerance** express TLR 5 and TLR 9
28
pDCs
produce type 1 interferons→ help with killing virus → **antiviral** –TLR 7,8,9 can be lymphoid(adaptive) or myeloid (innate) lineage
29
In the intestine, DC can activate Transforming growth factor beta and retinoic acid to promote\_\_\_through expanding T regulatory cell function mice these are further divided into CD8a+ and CD8a-
immunosuppression **tolerate normal things, tells immune system to calm down**
30
In the lung, DC can promote tolerance to inhaled antigens by producing immunosuppressive \_\_\_
cytokines
31
mucosal DC in the lungs and gut \_\_\_
keep things quiet **immunosuppression** keep areas from reacting to normal things
32
immature vs mature DC
**immature:** low surface MHC-II, found in peripheral and lymphoid, highly endocytic → **antigen accumulation** **mature**: high surface MHC-II and costimulators, found in lymphoid tissues, endocytosis reduced → **T cell stimulation**
33
mature DC will have ___ on their surface
high amounts of MCH II costimulators (CD80, CD86)
34
\_\_\_ are types of pattern recognition receptors used by DC to detect pathogens
toll like nod like other cytosolic receptors
35
mature DC cells will increase the expression of costimulatory molecules \_\_\_
CD80, CD86
36
what happens during DC maturation
* Decreased macropinocytosis * Increased expression of costimulatory molecules -CD80, CD86 * Upregulation of cytokines (IL-12) * Mediate T lymphocyte differentiation Change expression of chemokines
37
chemokine vs cytokines
**chemokine**- molecule that **attract cells** to itself **cytokines-** small molecules/ proteins that communicate to other immune cells
38
3 signal of DC cell to T cell
* Signal 1 – antigen presented in MHC – *“What should I respond to?”* * Signal 2 – costimulation (CD80, CD86)– *“Is is dangerous?”* * Signal 3 – Cytokine milleu – *“What type of response should I make?”***PRR tell it what kind of antigen is there and tells it how to respond→ virus, bacteria ect**
39
signal 1 of DC cells to T cells
*"What should I respond to?”* * extracellular antigens are broken down and presented in **MHC II to CD4+ T-cells** * intracellular antigens are broken down and are presented in **MHC I to CD8+ T-cells** * The amount of any specific amount of a Signal 1 is proportional to: –The amount of available antigen (increased with increased pathogens) –The amount of MHC sent to the plasma membrane (increased upon maturation)
40
•extracellular antigens are broken down and presented in **\_\_\_**
**MHC II to CD4+ T-cells**
41
intracellular antigens are broken down and are presented in
**MHC I to CD8+ T-cells**
42
what controls the amount of signal 1 from CD to Tcell
What should I respond to→ pathogen on MHC –The amount of available antigen (increased with increased pathogens) –The amount of MHC sent to the plasma membrane (increased upon maturation)
43
•CD4+ T-cells bind to \_\_\_
MHC II cells extracellular antigens
44
CD8+ T-cells bind to \_\_\_
MHC class 1 intracellular antigens
45
•Upon maturation, DCs stop \_\_\_, and send most of their MHC II to the plasma membrane, optimizing the amount of displayed antigen that was being acquired at the time danger is sensed
phagocytosing push everything to the outside to attract T cells
46
Signal 2 of DC to T cells
Is it dangerous? * costimulation: **CD80 and CD86** – bind to CD28 on T-cell and provide extra signals to enhance TCR signals * OX40L – binds to OX40 on T-cells, promotes Th2 skewing * 4-1BBL – binds to 4-1BB and activates NFkB in T-cells Upregulated upon maturation
47
**CD80 and CD86** – bind to \_\_\_
CD28 on T-cell signal 2 of DC cells to T cells → is it dangerous
48
what bind to CD28 on T-cell
costimultatory CD80 and CD86 signal 2 of DC to Tcells → is it dangerous
49
signal 3 of DC to T Cell
what did I eat? what type of response should I have PRR on the DC cells produce specific cytokines based on what they eat those specific cytokines will tell the Tcell i ate a bacteria or I ate a virus and tell it what the next step is
50
IL-12 and IL-18 will cause T cell to become
TH1 cell ## Footnote **killing response**
51
IL-33 will cause T cell to become
Th2 cell
52
IL-1,6,23 and TGFbeta will cause T cell to become
TH17 cell kill bacteria and **fungus**
53
cytokines IL-12 will turn T cell into \_\_\_
* Heterodimer – p35 and p40 (p40 is shared with other “IL-12 family members”) * **Skews CD4+ T-cells toward Th1- killing response** **CD4+ react to MHC II → extracellular pathogen** •Enhanced CD8+ T-cell effector responses
54
cytokine IL-6 cause T cells to become \_\_\_
* Drives **fever,** inflammation, acute phase response * Helps in skewing **CD4+ T-cells toward Th17→ bacteria or fungus** **CD4+ react to MHC II → extracellular pathogen** •Helps with B-cell differentiation and antibody production
55
cytokine IL-10 cause T cells to become
**•****Anti-inflammatory cytokine** •Inhibits CD8+ T-cell effector responses CD8+ react to MHC 1 → intracellular •May help to skew **CD4+ T-cells toward Treg phenotype** **quieting cytokine**
56
\_\_ is the anti-inflammatory cytokine
cytokine IL-10
57
what cytokine drives fever and inflammation
IL-6
58
Can phagocytosed antigen be presented to CD8+ T cells?
CD8+ T cells react to MHC 1 → intracellular antigens **cross presentation** can allow for phagocytosed antigens to be seen by CD8+ T cells CTL responses require MHC class I on hematopoetic APCs: Cross-presentation

22 spring: immunology (23 decks)

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