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Immuno Exam 1 > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

what are resident cells in the innate immune system

A

macrophages
dendritic cells
mast cells

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2
Q

What is the common progenitor cell of the dendrititc cells?

A

Myeloid stem cell

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3
Q

where are dendritic cells found?

A

tissue and blood

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4
Q

what is a leukocyte (aka WBC)

A

a colorless cell that circulates in the blood and body fluids and is involved in counteracting foreign substances and disease; a white (blood) cell. There are several types, all amoeboid cells with a nucleus, including lymphocytes, granulocytes, monocytes, and macrophages.

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5
Q

What is the most abundant leukocyte in the blood

A

Neutrophil

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6
Q

Many of the functions of the cells of
the innate and adaptive immune
systems are mediated by the release
of cytokines…..WHAT does a cytokine do?

A

~A diverse collection of soluble proteins and peptides that modulate the behaviour of cells at nanomolar to picomolar concentrations

~Conceptually similar to hormones
~Act both locally and systemically
~Have highly pleiotropic effects (aka 1 can have multiple effects)

~Chemokines are a type of cytokine with chemotactic properties (attract other cells).
~The activities of cytokines and chemokines often overlap with other cytokines and chemokines

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7
Q

What is G-CSF

A

Granulocyte Colony Stimulating Factor (G-CSF) produced at site of infection increases production of neutrophils by bone marrow.

~Helps release more neutrophils from the bone marrow- bc the neutrophils have a really short lifespan

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8
Q

What is acute inflammation

A

recruitment of neutrophils, that occurs shortly after there is an infection.

the accumulation of leukocytes (wbc) at the site of infection with associated vascular dialation and increased leakage of fluid and proteins is inflammation

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9
Q

Define inflammation

A

The accumulation of leukocytes at sites of infection, with associated vascular dilation and increased leakage of fluid and proteins into the tissue is called inflammation

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10
Q

What is the cause of swelling

A

Fluid, proteins=swelling

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11
Q

What is the role of IL-1 and TNF-alpha

A

these are cytokines that are released and expressed bc PAMPS bind to TLR’s when there is a pathogen.

~they have lots of function and causes…

~cause endothelial cells to express E and P selectin

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12
Q

E and P selectin

A

expressed by endothelial cells, and cause a low affinity binding to the neutrophil—cause the neutophil to ROLL

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13
Q

CXCL8

A

IL-8

~A chemokine that is HIGHLY chemotactic for neutrophils

~ secreted from the MACROPHAGES!!

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14
Q

CXCL8

A

IL-8

~A chemokine that is HIGHLY chemotactic for neutrophils

~ secreted from the MACROPHAGES!!

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15
Q

What are the high affinitity integrins on the surface of neutrophils

A

Mac-1

LFA-1

VLA-4

high affinity integrins that undergo a confirmational change

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16
Q

INtegrins

A

adhesion molecules that integrate extrinsic signals into changes of the cytoskeleton

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17
Q

ICAM-1 & VCAM-1

A

Integrin ligand

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18
Q

CXCR1 & 2

A

IL-8 receptors

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19
Q

what conformational change occur because of the high affinity binding?

A

As a result of this high affinity binding between the

integrins and their ligands, neutrophils are held tight to the endothelium, and spread out on the endothelial surface.

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20
Q

What is the role of the chemokine IL-8 once the neutrophil has made it across the endothelial surface?

A

acts like breadcrumbs and helps the neutrophil find the site of infection

~the neutrophils will travel along the chemokine concenrtation

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21
Q

What is the end goal of having neutophils enter the site of infection?

A

The result is the influx of neutrophils and monocytes capable of phagocytosing microbes/debris and plasma proteins such as complement that also have antimicrobial properties.

~they will help to controlt he infection

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22
Q

transmigration

A

neutrophil squeezing between the endothelial cells and going to the site of infection

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23
Q

what causes the neutrophil to change to high affinity state?

A

when the neutrophil detects IL-8 it will change from low to high affniity

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24
Q

Integrins that Monocytes express…

A

VLA-4

  • these are integrins that express and cause firm adhesion
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25
Q

Integrins that Neutrophils express…

A

LFA-1
Mac-1

Both use the Ligand ICAM-1 (CD54)

26
Q

“delayed separation of the umbillical cord…”

A

Leukocyte Adhesion Deficiency

~Rare autosomal recessive disorder characterized by decreased movement of leukocytes to inflammatory sites.

~Mechanism of Defect: Absent or deficient expression of the β2 integrins, LFA-1 and Mac-1 (which are heterodimers of CD18 and CD11) due to various mutations in the CD18 gene.

~Functional Outcome: prevention or decreased tight adhesion of leukocytes to the vascular endothelium.

27
Q

what is the functional defect in Leukocyte adhesion Def?

A

firm adhesion cant happen bc the CD-18 chain the in tegrins LFA-1 and Mac-1 is defective

28
Q

It is generally thought that a limited amount of inflammation at the site of vaccination helps to stimulate a strong adaptive immune response to the vaccine antigens. Which of the following substances, if introduced with the vaccine, would best serve the purpose of attracting a neutrophil infiltrate into the area?

A

IL-8

29
Q

TNF-alpha

A

a cytokine that will make the endothelial lining “sticky” via E and P selectin

30
Q

Polymorphonuclear Leukocytes [PMN]

A

neutrophil

31
Q

What do neutrophils contains?

A

Specific Granules: (most prevalent)
contain enzymes such as lysozyme, collagenase, and elastase which degrade bacteria.

Azurophilic granules:
contain enzymes and other microbicidal substances, including defensins and cathelicidins.

32
Q

‘neutrophil extracellular traps’(NETs).

A

~ additional mechanisms to destroy microbes that haven’t been phagocytosed.

  • Dying neutrophils release DNA which then form networks of chromatin called ‘neutrophil extracellular traps’(NETs).
  • NETs trap bacteria and fungi, which are then killed by extruded granule antimicrobials (lysozyme, elastase, and defensins).
33
Q

how can inflammation damage host tissue?

A

NETs
–> neutrophil extracellular traps’(NETs)

Granule enzymes and ROS can also damage host tissues when released by the cell. This is a prominent mechanism by which inflammation can damage host tissue.

34
Q

What is the role of G-CSF

A

A reserve pool of neutrophils is stored in the BM and released during an infection.

  • inc neutrophils from bone marrow
35
Q

What is the major component of pus?

A

dead neutrophils that have been engulfed and eaten by macrophages

36
Q

Where are tissue resident macrphages dervied from?

A

from the yolk sac and fetal liver

37
Q

tissue resident macrophage

A

Macrophages that are resident to the tissues are serve the function of sentinel cells at these sites, are derived from tissue macrophage precursors which originate from in the yolk sac and fetal liver

38
Q

Functions of macrphage

A

engulf
secrete
present

39
Q

Secretion function of macrophage

A

Secrete cytokines that act on endothelial cells to enhance recruitment of leukocytes from the blood

secrete IL-8 (chemotactic cytokine that will make the neutrophil follow to the site of infection)

40
Q

is a macrophage an APC?

A

yes!

it can engulf and present peptides to the T-cells

professional APC

41
Q

explain the steps that macrophages use to destroy microbes (slide 46)

A
  1. Receptor induced endocytosis
  2. microbe is ingested in a phagosome (floating inside the macrophage)
  3. phagosome will FUSE with a Lysozome that has ENZYMES!!
  4. microbes killed by lysosomal enzymes in the “phagolysosome”
  5. ROS and NO kill microbes
42
Q

What Antimicrobial Molecules are in the phagolysosome

A

Antimicrobial Molecules:

Reactive Oxygen Species
~NADPH Oxidase
~Myeloperoxidase

Reactive Nitrogen Species
~ iNOS

Proteolytic Enzymes
~ Lysozyme, others

43
Q

Phagocyte oxidase

slide 47 image

A

enzyme that changes hydrogen peroxide to ROS to kill bacteria:

44
Q

Chronic Granulomatous Disease (CGD)

A

Caused by mutation in NADPH phagocyte oxidase enzyme complex, disrupting production of ROS

The result is recurrent infection with catalase producing bacteria and fungi infections.

Form granulomas due to inability to kill phagocytosed bacteria

45
Q

what is a granuloma

A

the immune responses attempt to contain bacteria that it has eaten but cannot destroy

46
Q

a patient is found to have a catalase positive (+) bacteria—-what disease might they have?

A

Chronic Granulomatous Disease (CGD)

mechanism:
~catalase + bacteria do NOT allow the production of hydrogen peroxide (H202)
~causing there to be nothing to kill and destroy bacteria that has been engulfed

47
Q

when you can’t produce H2O2 you get…..

A

Chronic Granulomatous Disease (CGD)

The result is recurrent infection with catalase producing bacteria and fungi infections.

48
Q

M1

A

Clasically activate (PRO-inflammatory)

activated by IL-1 and TNF- alpha

49
Q

M2 (slide 52)

A

Alternative activated (REPAIR!!!)

~activated by IL-4 and IL-13
~TLR signals are absent

50
Q

Cytokines

A 
IL-6
IL-1
CXCL8 (IL-8)
TNF-alpha
IL-12
51
Q

Job of the immature dendritic cell =

A

Capture antigen in the periphery and bring to the draining lymph nodes to present to naïve T cells.

52
Q

Two types of dendritic cells (slide 55)

A

1) Conventional DC (cDC) (aka Myeloid): capture microbial protein antigens in peripheral tissues and present them to adaptive immune cells in the draining LN.
2) Plasmacytoid DC (pDC): circulating in peripheral blood. Recruited to sites of inflammation, where they become activated to produce large amounts of type I interferons. (***really important when you are responding to VIRUS/VIRAL infection)

53
Q

Type of dendritic cell important in the response to viral infection

A

Plasmacytoid DC (pDC): circulating in peripheral blood. Recruited to sites of inflammation, where they become activated to produce large amounts of type I interferons.

~Type 1 INTERFERON= ***really important when you are responding to VIRUS/VIRAL infection)

54
Q

Are NK cells Myeolid cells?

A

NO- They are derived from lympoid pregenitor cell- share a common origin with B and T cells

NK cells= large granular lymphocyte

55
Q

How do NK cells kill things? (slide 62)

A

Apoptosis is Important bc its controlled cell death!!

NK cells use two main pathways to induce apoptosis of target cells
Perforin (poke holes!!) /Granzyme (entrer thru the poked holes and kill things)
Fas/FasL (interaction between a receptor and a ligand)

Another way is  super high levels of TNF- alpha binding to receptors will cause apoptosis

56
Q

NK receptors

A

Killing is determined by a balance between the engagement of activating vs inhibitory receptors

Activating=
~The activating receptors recognize cell surface molecules expressed by infected cells, as well as cells “stressed” by DNA damage or malignant transformation.

Inactivating= 
~The inhibitory receptors recognize self MHC class I molecules, which are expressed on all healthy, nucleated cells.
57
Q

How do NK cells and macrophages function together to kill intracellular microbes

HULKING OUT

A

Activated macrophages produce IL-12, which activates NKs to produce IFNg, which in turn activates the macrophages to boost intracellular killing.

58
Q

INF-gamma (slide 69)

A

This is a STRONG activating signal that is secreted from the NK cell. It’s affect is to activate a macrophage and make it into a killing machine.

this is intersting bc the NK cell is stimulated to secrete INF-gamma only after the macrophage has phagocytosed microbes and produces IL-12

59
Q

Chemokines

A

are a type of cytokine

a cytokine is a :
A diverse collection of soluble proteins and peptides that modulate the behaviour of cells at nanomolar to picomolar concentrations

60
Q

Ecoli

A

gram - bacteria

TLR-4 will recognize the LPS on the bacteria

61
Q

IL-8 Receptor aka

A

CXCR 1 or CXCR 2

62
Q

il-15

A

importnat for the development and maturation of NK cells–> nk specific

Immuno Exam 1 (10 decks)

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