Lectures Flashcards

0
Q

What does the inhibitory receptor on a NK cell bind to?

A

MHC Class 1
In a virus infected cell, MHC Class 1 expression is inhibited, so only the activated pathway for killing the cell is activated

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

Type 1 interferons produced by what cells?

A

INF- alpha - mononuclear phagocytes “leukocyte interferon”
INF-beta - fibroblast interferon
Similar effect
Produced by virus-infected cells!

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

How does NK cell kill a virus infected cell? What is released?

A

Perforin - form pore

Granzymes - enter cytoplasm of target cell and initiate apoptosis

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

CD8 T Cell TCR binds to what?

A

MHC Class 1 with viral peptide

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

How do CTLs kill virus infected cells?

A

1) perforin, granzymes

2) FasL - engages receptor FAS

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

IL-12 acts on what cells? What cells produce it?

A

NK cells that can then produce IFN-gamma

Phagocytes- neutrophils and macrophages

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

IL-12 function?

A

Killing of virus infected cells and…

As a source of IFN-gamma for activation of phagocytes, especially macrophages

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

CD4 cells develop into what?

A

T Helper cells- Th1 and Th2

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

CD8 cells develop into what?

A

CTL

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

Th1 function?

A

Adaptive immune substitute for NK cell. Take over function of producing INF-gamma, allowing for a more robust source of INF-gamma.

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

C3b on pathogen surface is useful why?

A

Acts as tag that allows pathogen to be recognized by phagocytes…
Opsonization and phagocytosis

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

C3a, C5a

A

Proinflammatory signals

Recruit additional phagocytes

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

Binding of c3b to microbe and activation of late components of complement leads to what?

A

Formation of membrane attack complex (MAC) -> osmotic lysis of microbe.

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

Macrophage produced cytokines?

A

IL-1
IL-6
TNF-alpha

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

What are the body’s primary defense mechanisms against helminths?

A

Eosinophils and IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
Type IV:
Type of hypersensitivity
Pathologic immune mechanisms:
Cells
Timing
A

1)T cell Mediated

CD4 T Cells

16
Q

Type I-III are mediated by what response?

A

Humoral Responses

17
Q

Immediate Hypersensitivity (Type I) Reactions

A

Classic T cell-dependent antibody-mediated response
IgE mediated
allergic rhinitis, asthma, anaphylaxis

18
Q

Type II

A

IgG-mediated
Ab to fixed tissue to Ag
Diseases: blood transfusions,

19
Q

Type III

A

Immune complex-mediated

20
Q

Mast cell stabilizers

A

Inhibition of mast cell activation, degranulation

chromolyn, nedocromil

21
Q

Leukotriene inhibitors

A

5-lipoxygenase inhibitor: zileuton

LTD4 receptor antagonists: montelukast, zafirlukast

22
Q

Bronchodilators

A

B2 selective agonists: albuterol, terbulatine, metaproterenol, pirbuterol… long acting: salmeterol, formoterol
Methylzanthine drugs: PDE inhibition maybe?… theophilline
Muscarinic receptor antagonist: ipratropium

23
Q

Inhaled corticosteroids

A

Anti-inflammatory: beclomethasone, budesonide, ciclesonide, flunisolide, fluticasone…

24
Q

Omalizumab

A

anti-IgE mAb: blocks binding of IgE onto the mast cell surface
Expensive!

25
Q

chemokine co-receptor on the cell with new infection

A

CCr5

32 pair base deletion -> resistant to HIV infection

26
Q

Reverse transcriptase with HIV acts in what part of the cell?

A

cytoplasm, then the DNA transfers to the nucleus

27
Q

What fluids do not transmit HIV

A

Tears, saliva urine and stool unless they are mixed with a lot of blood.

28
Q

Pathogenesis of TB

A
  1. Bacilli implant and multiply in alveolar spaces, alveolar macrophages
  2. An area of inflammation develops and center undergoes caseous necrosis.
  3. bacilli, free or within phagocytes transit to regional lymph nodes =The Ghon complex (primary lesion + infected adjoining lymph node)
  4. During the first few weeks there is dissemination in blood and lymph to other parts of the body.
  5. In approximately 95% of cases, development of CMI controls the infection.
  6. The Ghon complex heals and becomes fibrotic. It may calcify (visible on X-Ray) Bacteria within can be eradicated OR persist contained (tubercle) or progress.
  7. Reactivation later in life may occur
29
Q

Nosocomial infections: central line-associated bloodstream infection

A

MRSA

30
Q

Catheter associated UTI

A

ESBL E. coli

31
Q

Extended spectrum B-lactamases (ESBLs) confer resistance to…

A

Penicillins
Cephalosporins
Aztreonam