Highlights lecture 4.2 Flashcards

1
Q

TNF, IL-1 is a function of what?

A

Cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

PRR connects to what?

A

PAMPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do PRR + PAMP do?

A

Initiate phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Involvement of B and T cells in antigen presentation is what creates the bridge from innate to _________ immune response

A

adaptive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 3 ways to grab a pathogen?

A

1) PRR + PAMP
2) C3b receptor + C3b complement
3) Antibody + FC receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

B & T cells:
1) Which produces antibodies?
2) Which develop from naive to effector with the help of an APC?
3) Which controls humoral immunity?

A

1) B cells
2) T cells
3) B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

B & T cells:
1) Which can be cytotoxic?
2) Which controls cellular immunity?

A

1) T cells
2) T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

MHC I: CD8 T-Cells go with what?

A

MHC I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List the main reasons for CD8 to release its cytokines that lead to apoptosis or it destroy the cell

A

Cancer, viral infection, or a cell that is not our own

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MHC II:
1) Where does the II protein exist?
2) What recognizes the foreign antigen?
3) It is our primary way of dealing with what 2 things?

A

1) Only exists on phagocytic APCs
2) CD4 cell
3) Bacteria and fungi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Inheritance of particular alleles can form harmful immunologic responses; give an example

A

HLA B27 causing JRA or ankylosing spondylitis just to name a few

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

“Somatic recombination” allows for what?

A

Variation [in B cells]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

1) What happens to a B cell as it makes its new IgM?
2) What happens next?

A

1) Tested for self-tolerance
2) It is given IgD and allowed to leave bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

If a B cell If it finds an antigen, it must be tested again to see if it’s “right”. What happens if it’s approved by a T-cell?

A

It can proliferate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe how a B cell is created and activated in 3 steps

A

1) B cell in the bone marrow
2) Leaves as a Mature Naive B cell
3) Activated B cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What occurs when B cells go from IgM to IgG?

A

Isotype switching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

A mature naïve B cell receives an antigen
It asks T cell for permission to react, what does it release if it says yes?

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

True or false: IgG is hyper specific

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What happens after a mature naive B cell releases IgM?

A

Clonal expansion > somatic mutation for affinity maturation > leads to hyper specific binding

20
Q

1) What do activated plasma cells release?
2) What abt activated memory cells?

A

1) IgM released as a pentamer
2) IgG released as a monomer

21
Q

It is important to remember that the surface antigens that are __________ lead to antibodies in the blood
This is because _________________ was never developed for them

A

absent; self-tolerance

22
Q

In some cases, mother-fetus incompatibility in the Rh system can cause maternal antibodies to destroy red blood cells of the fetus, resulting in what?

A

Hemolytic disease of the newborn (HDN)

23
Q

Hemolytic disease of the newborn can occur when _________ doesn’t have the antigen, but the _________ does

24
Q

What type of reaction is an allergy? What happens?

A

Type I hypersensitivity; B&T cells are activated

25
Q

Hypersensitivity:
1) What happens on first exposure?
2) What abt second? What 2 things does this cause?

A

1) Mast cells become coated with IgE
2) Mast cells burst open (degranulate) and release lots of Histamine
-vasodilation and bronchospasm

26
Q

IL-4 excreted by CD4 cells is what?

27
Q

Describe Type II (cytotoxic) hypersensitivity reactions

A

Ig attaches to self cell
-Opsonizes cell for phagocytosis
-Compliment further

28
Q

Antibodies develop against the self in what kind of hypersensitivity reactions?

A

Type II (cytotoxic)

29
Q

Type II (receptor) hypersensitivity rxn: what does Ig do?

A

Lands on a receptor and either turns it off or turns it up

30
Q

Immune deposition describes what kind of hypersensitivity? What causes this?

A

Type III hypersensitivity; agent bound to antibodies that get stuck in small vessels

31
Q

1) When will type III hypersensitivity occur?
2) What does it do to the body? Give 3 examples

A

1) Systemic disease; lupus
2) Destroys good tissue; vasculitis, arthritis, kidney dz

32
Q

Destruction of articular cartilage and bone causing disabling arthritis is characteristic of what?

A

Rheumatoid arthritis

33
Q

1) Is RA systemic or local? Explain
2) What causes the disabling arthritis?

A

1) Systemic; mainly joints
2) Destruction of articular cartilage and bone

34
Q

Rheumatoid arthritis is and example of Type _______ hypersensitivity

35
Q

Name a systemic autoimmune disease that is mainly caused by nuclear antigens

A

Systemic Lupus Erythematosus

36
Q

1) What condition has inherited susceptibility in Class II MHC and complement genes
2) What type of hypersensitivity is it?

A

1) Systemic Lupus Erythematosus
2) Type III Hypersensitivity

37
Q

True or false: AIDS is just a collection of disorders associated w HIV

38
Q

Name a retrovirus that kills helper T cells

39
Q

List the 3 ways to contract HIV

A

1) Sexual contact (75%)
2) Parenteral inoculation (IV drug users, blood transfusions)
3) Vertical

40
Q

Acute phase of HIV infection:
1) What is infected?
2) Are there Sx?
3) Define seroconversion

A

1) Memory T cells
2) Signs of systemic infection
3) Immune system responds and antibodies against HIV appear (1-6 months)

41
Q

Acute phase of HIV infection: What happens toward the end of this stage?

A

T cell numbers return to nearly normal; replicates in CD4+ T cells and macrophages

42
Q

Chronic phase (clinical latency) of HIV infection:
1) What is the virus doing?
2) Are there Sx?
3) What is happening w the CD4 cells?

A

1) Replicating
2) Minor [infections]
3) # of CD4+ cells begin to decline; greater numbers of surviving CD4+ cells are infected

43
Q

When do immune defenses diminish with HIV?

A

Toward the end of chronic phase (clinical latency)

44
Q

Rejection of solid organ transplants:
1) What initiates it?
2) Treatment of graft rejection relies on what?

A

1) Host T cells that recognize the foreign HLA antigens of the graft
2) Immunosuppressive drugs, which inhibit immune responses against the graft.

45
Q

Amyloidosis:
1) What is it?
2) What defines it?
3) How is definitive Dx made?

A

1) Group of conditions where extracellular deposits of fibrillar proteins are responsible for tissue damage and functional compromise.
2) Based on the physical properties of the fibers
3) Only by demonstrating amyloid in tissue, which requires biopsy

46
Q

List 5 traits of the adaptive immune system

A

1) Specific chemical responses
2) More effective
3) Memory component
4) Lymphocytes
5) Deficiencies in immune defenses and inappropriate activation both cause disease