Lectures

Question 0

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

Answer 0

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

Question 1

Type 1 interferons produced by what cells?

Answer 1

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

Question 2

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

Answer 2

Perforin - form pore

Granzymes - enter cytoplasm of target cell and initiate apoptosis

Question 3

CD8 T Cell TCR binds to what?

Answer 3

MHC Class 1 with viral peptide

Question 4

How do CTLs kill virus infected cells?

Answer 4

1) perforin, granzymes

2) FasL - engages receptor FAS

Question 5

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

Answer 5

NK cells that can then produce IFN-gamma

Phagocytes- neutrophils and macrophages

Question 6

IL-12 function?

Answer 6

Killing of virus infected cells and…

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

Question 7

CD4 cells develop into what?

Answer 7

T Helper cells- Th1 and Th2

Question 8

CD8 cells develop into what?

Answer 8

CTL

Question 9

Th1 function?

Answer 9

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

Question 10

C3b on pathogen surface is useful why?

Answer 10

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

Question 11

C3a, C5a

Answer 11

Proinflammatory signals

Recruit additional phagocytes

Question 12

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

Answer 12

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

Question 13

Macrophage produced cytokines?

Answer 13

IL-1
IL-6
TNF-alpha

Question 14

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

Answer 14

Eosinophils and IgE

Question 15

Type IV:
Type of hypersensitivity
Pathologic immune mechanisms:
Cells
Timing

Answer 15

1)T cell Mediated

CD4 T Cells

Question 16

Type I-III are mediated by what response?

Answer 16

Humoral Responses

Question 17

Immediate Hypersensitivity (Type I) Reactions

Answer 17

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

Question 18

Type II

Answer 18

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

Question 19

Type III

Answer 19

Immune complex-mediated

Question 20

Mast cell stabilizers

Answer 20

Inhibition of mast cell activation, degranulation

chromolyn, nedocromil

Question 21

Leukotriene inhibitors

Answer 21

5-lipoxygenase inhibitor: zileuton

LTD4 receptor antagonists: montelukast, zafirlukast

Question 22

Bronchodilators

Answer 22

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

Question 23

Inhaled corticosteroids

Answer 23

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

Question 24

Omalizumab

Answer 24

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

Question 25

chemokine co-receptor on the cell with new infection

Answer 25

CCr5 | 32 pair base deletion -> resistant to HIV infection

Question 26

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

Answer 26

cytoplasm, then the DNA transfers to the nucleus

Question 27

What fluids do not transmit HIV

Answer 27

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

Question 28

Pathogenesis of TB

Answer 28

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

Question 29

Nosocomial infections: central line-associated bloodstream infection

Answer 29

MRSA

Question 30

Catheter associated UTI

Answer 30

ESBL E. coli

Question 31

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

Answer 31

Penicillins Cephalosporins Aztreonam