Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IHO Week 5 AJL > Regulation of the Immune Response- Diebel > Flashcards

Regulation of the Immune Response- Diebel Flashcards

1
Q

What happens at the end of an immune response when there is reduced antigen exposure or increased CTLA-4/B7 interactions?

A

Results in reduced expression of IL-2 and it’s receptor—>

Apoptosis of antigen specific T cells……some survive to become memory cells

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

Intracellular organisms elicit what type of immune response?

A

Cell Mediated Immune Response

NK Cells, CD8+ cells, etc

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

Extracellular organisms elicit what type of immune response?

A

Humoral Immune Response

Complement, antibodies

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

What neat interleukin is produced with the CD28/B7 interaction?

A

Inc. in IL-2

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

Important molecules necessary for tolerogenic DC:T Cell interactions?

A

CD152 (CTLA-4)
IL-10
TGF-beta

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

What is a tolerogenic DC? What makes it tolerogenic?

A

Tolerogenic DC lead to clonal deletion or anergy of antigen-specific T-cells

They express low levels of CD86, MHCII, CD40, and CCR7……they’re sittin around being bums

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

What percent of CD4+ T cells are Tregs?

A

10%

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

What do Tregs do? What is the inborn lack of Treg cells called?

A

Limit autoimmune responses, dampen responses against microbial and viral antigens, allergens, and allografts, and protect fetuses during pregnancy.

IPEX (Immunodysregulation, polyendocrinopathy, enteropathy, X-linked) Syndrome….whew!

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

What are the different Treg effector mechanisms?

A
  • Immunosuppressive cytokines (IL-10, TGF-beta, IL-35)
  • IL-2 consumption
  • Cytolysis (granzyme mediated)
  • Modulation of DC maturation and function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

IL-10 and TGF-beta induce what in B cells?

A

Proliferation and class switch recombination

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

What are the 3 different ways you can have issues with Tregs?

A
  • Complete absence of Tregs (IPEX)
  • Insufficient Treg effector functions
  • Resistance of effector T cells to Treg effector functions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens when you have a B cell that recognizes self antigen?

A
  • VDJ recombination to avoid self reactivity
  • Clonal deletion—–>apoptosis
  • Anergy, downregulate BCR, upregulate CD5
  • Lack of T cell help or survival factors—–>apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens with antigens administered subcutaneously or intradermally?

A

Evokes an active immune response (TH1 response)

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

What happens with antigens administered IV, orally, or aerosol?

A

May cause tolerance or an immune deviation from one type of CD4+ T cell response to another (TH2 response)

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

Th1 cytokines (IFNγ, TNFβ, IL-2) promote?

A

Cell Mediated stuff……
Macrophage activation
Antibody-dependent cell-mediated cytotoxicity
Delayed-type hypersensitivity

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

Th2 cytokine (IL-4, IL-5, IL-9, IL-10, and IL-13) promote?

A 
Humoral Immunity Stuff....... 
IgG1 and IgE isotype switching
Mucosal immunity
Stimulation of mast cells, eosinophil growth and differentiation
IgA synthesis
17
Q

How can antibodies cause B Cell Suppression?

A

The antibodies bind up all the antigen so the plasma cells aren’t being stimulated….can also get receptor cross-linking that results in a (-) growth signal

***Can also get a pro-proliferative signals with big immune complexes (B cell, IgM, complement, follicular DC)

18
Q

TH1, TH2, and TH17 chemotactic signals?

A

TH1- CXCR3 and CCR5
TH2- CCR3, CCR4, and CCR8
TH17- CCR6

19
Q

What is special about the anterior chamber of the eyes and the testes?

A

They are immune privileged….normally immune responses don’t take place here

20
Q

Individuals with defects in C1q, C1r, and C1s are predisposed to what?

A

SLE and lupus nephritis

21
Q

Individuals with dificiency in C3 have increased susceptibility to what?

A

Bacterial infections ——> immune complex disease

22
Q

TLR4 is an important sensor for what?

A

Gram (-) bacterial infections

23
Q

what happens to individuals with a mutation in the IL-7R alpha?

A

Reduced number of T cells

24
Q

what happens to individuals with mutations in the common cytokine receptor γ chain (γc)?

A

reduced numbers of T and NK cells and impaired B cell function, in part attributable to the lack of T cell help

25
Q

What happens to individuals with mutations in the IFNγ receptor (IFNγR) or IL-12 receptor (IL-12R)?

A

They have an increased susceptibility to mycobacterial infection

26
Q

What is CCR5 and why do we care about it?

A

CCR5 is a co-receptor used in the entry of macrophage-tropic strains of HIV-1 into cells.

A mutation that inactivates this receptor is found in some individuals of European origin, but is rare in populations of Asian or sub-Saharan African descent.

Individuals homozygous for this CCR5 mutation are very resistant to HIV-1 infection.

In this case resistance is related to the reduced primary spread of the virus rather than an enhanced immune response against it.

27
Q

What is the connection between increased levels of IgE and eosinophils?

A

IL-5 increases both IgE production and eosinophils

28
Q

What is the classic presentation of IPEX?

A

Intractable watery diarrhea, leading to failure to thrive, dermatitis, and autoimmune diabetes developing in infancy

29
Q

What causes IPEX?

A

Missense or frameshift mutations in FOXP3 result in loss of function of Treg cells and uninhibited T-cell activation

30
Q

Why is IVIg therapy a decent treatment option for IPEX?

A

It provides humoral immunity protection so you don’t elicit a cell mediated T cell response…….because if you have a T cell response in IPEX it goes crazy because there are no Tregs to check it

31
Q

So you better vaccinate those IPEX babies so they don’t get sick right?

A

Wrong! If you vaccinate them they’ll elicit a T cell response that goes nuts because they don’t have Tregs….if you do a BM transplant first then they can be vaccinated.

32
Q

Is a total BM transplant necessary in IPEX?

A

No, you just need a little bit to get some Tregs going. It’s not like you need to wipe out all the old BM and replace it…..you just need some Tregs to settle things down.

33
Q

What is AIRE? Why is it important?

A

I don’t know…..I spaced out during this…..whoops…..

IHO Week 5 AJL (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions