05b: Immunology 2

Question 1

Live vaccines induce (cell/humoral) immune response and are contraindicated in which populations?

Answer 1

Both cell and humoral;

Pregnant and immunodeficient patients

Question 2

BCG vaccine is (live/killed). Rabies vaccine is (live/killed). Rotavirus vaccine is (live/killed).

Answer 2

Live; killed; live

Question 3

Killed vaccines induce (cell/humoral) immune response. List some examples of killed vaccines.

Answer 3

“R.I.P. Always”

Rabies, Influenza (injection), Polio (salk), hep A

Question 4

List the four types of hypersensitivity reactions:

Answer 4

"ACID"
Type I: Anaphylactic/Atopic
Type II: Cytotoxic 
Type III: Immune complex
Type IV: Delayed

Question 5

Which hypersensitivity reactions are antibody-mediated.

Answer 5

I, II, and IIII

Question 6

Which key cells are playing role in anaphylactic reaction to bee sting?

Answer 6

Basophils and mast cells (releasing His) in response to IgE

Question 7

One mechanism of type (I/II/III/IV) hypersensitivity reaction is opsonization of cell by Ab, leading to:

Answer 7

II

1. Phagocytosis and/or complement activation
2. NK cell killing (cytotoxicity)

Question 8

(X)-mediated inflammation such as in Goodpasture syndrome is an example of type (I/II/III/IV) hypersensitivity reaction. List other examples like this.

Answer 8

X = Antibody;
II

Rheumatic fever, hyperacute transplant rejection

Question 9

List examples of Type II HS reaction in which Ab mediates abnormal cell function by binding its receptors.

Answer 9

MG and Grave’s

Question 10

Patient receives blood transfusion and 30 min later develops fever, chills, chest/flank pain. Urine is brown-colored. What type of hypersensitivity reaction?

Answer 10

Acute hemolytic transfusion reaction (ABO mismatch) is type II hypersensitivity (anti-ABO IgM bind donor RBCs and activate complement/lyse)

Question 11

Hemolytic disease of newborn is what type of hypersensitivity reaction?

Answer 11

Type II

Question 12

Serum sickness is Type (I/II/III/IV) hypersensitivity reaction and occurs (X) min/hour/days after (Y).

Answer 12

III (immune complex);
X = 5-10 days
Y = started drug (ex: infliximab)

Question 13

Classic histology findings in serum sickness

Answer 13

Fibrinoid necrosis, PMN infiltration of small blood vessels

Question 14

List the two mechanisms by which Type IV hypersensitivity reaction can be carried out.

Answer 14

1. Direct cytotoxicity (CD8 T cells kill target)

2. Delayed-type: sensitized CD4 helper T cells see Ag, release cytokines, activate macrophages

Question 15

List examples of Type IV hypersensitivity reactions.

Answer 15

3 T’s for the Th and Tc’s:

1. Transplant rejections
2. TB (and candida) skin tests
3. Touching (contact dermatitis like poison ivy)

Question 16

Patient that receives blood transfusion and has reaction (within 2-3 hours) involving urticaria, pruritus, and shock symptoms. Diagnosis must be:

Answer 16

Allergic/anaphylactic (can occur within minutes; Type I hypersensitivity)

Question 17

Transfusion-related acute lung injury occurs within (X) min/hours/days. What’s the mechanism behind this?

Answer 17

X = 6 hours

Donor Anti-leukocyte Ab attack recipient PMNs and pulmonary endothelial cells

Question 18

Anti glutamic acid decarboxylase Abs associated with which disease?

Answer 18

DM I

Question 19

Antisynthetase (anti-Jo), anti-SRP, and anti-helicase Abs associated with which disease?

Answer 19

Polymyositis, dermatomyositis

Question 20

Pt receives influenza injection vaccine. If exposed to virus through subsequent infection, (X) players of immune system will (stimulate/inhibit) viral (Y).

Answer 20

Killed vaccine:
X = neutralizing antibodies (humoral response) against hemagglutinin
Inhibit
Y = entry into cells

Question 21

Eosinophils fight off parasites via (X)-mediated cytotoxicity (degranulation).

Answer 21

X = antibody-dependent cell-mediated

IgG, IgE coat parasite and activate eos by binding Fc R

Question 22

T/F: Eosinophils play important role in Type I hypersensitivity reactions.

Answer 22

True, but in the LATE-PHASE type I HS (chronic allergic reactions)

Question 23

Bruton, aka (X), agammaglobulinemia: what’s the defect?

Answer 23

X = X-linked

Defective BTK (tyrosine kinase gene) leads to no B cell maturation

Question 24

IL-12 receptor deficiency: low (X) cell response with frequent (Y) infections.

Answer 24

X = Th1
Y = disseminated mycobacterial/fungal infections

Question 25

IL-12 receptor deficiency: supplementation with (X) proves beneficial for these patients.

Answer 25

X = IFN-gamma

Question 26

Job, aka (X), syndrome is a deficiency of (Y).

Answer 26

``` X = Autosomal dominant Hyper-IgE Y = Th17 cell (STAT3 mutation) so impaired PMN recruitment ```

Question 27

What are the key characteristics/symptoms of Job syndrome?

Answer 27

"FATED" 1. course Face 2. cold/non-inflamed staph Abscesses 3. retained primary Teeth 4. high igE 5. Derm issues (eczema)

Question 28

SCID can be X-linked with defective (X) or AR with (Y) deficiency.

Answer 28

``` X = IL-2 receptor (most common) Y = adenosine deaminase ```

Question 29

Key issue/defect in Ataxia-telangiectasia, which is inherited in (X) fashion.

Answer 29

X = AR Defect in ATM gene causes failure to detect DNA damage/halt cell cycle (accumulated mutations)

Question 30

Ataxia telangiectasia triad:

Answer 30

3 A's 1. cerebellar Ataxia 2. spider Angiomas 4. low IgA (recurrent sinopulm infections); IgG and IgE also low

Question 31

Hyper-IgM syndrome due to defective:

Answer 31

CD40L on Th cells (X-linked R); class switching impaired

Question 32

Wiscott-Aldrich syndrome: mutation in (X) causes defective (Y).

Answer 32

``` X = WASp gene Y = Ag presentation (WBCs, platelets can't reorganize actin cytoskeleton) ```

Question 33

Wiscott-Aldrich syndrome is inherited in (X) fashion and presents with low levels of which Ig?

Answer 33

X = X-linked R IgG and IgM; high IgE, IgA

Question 34

Pt presents with recurrent skin/mucosal bacterial infections that are not purulent. Most likely diagnosis?

Answer 34

Leukocyte adhesion deficiency I

Question 35

Chédiak-Higashi syndrome is defect in (X) and is inherited in (Y) fashion.

Answer 35

``` X = LYST (lysosomal trafficking regulator) causing microtubule dysfunction in phagosome-lysosome fusion Y = AR ```

Question 36

Chédiak-Higashi syndrome: what would you expect to see on neuro/eye exam?

Answer 36

Nystagmus, peripheral neuropathy, neurodegeneration

Question 37

Chédiak-Higashi syndrome: what would you expect to see in histology?

Answer 37

Giant granules in granulocytes and platelets

Question 38

Chronic granulomatous disease is inherited in (X) fashion.

Answer 38

X = X-linked recessive

Question 39

Systemic candida infection is seen with low numbers of (X) cells whereas local candida infection is seen with low numbers of (Y) cells.

Answer 39

``` X = granulocytes (also other systemic fungal infections) Y = T cells ```

Question 40

Xenograft is graft from (X). Allograft is graft from (Y).

Answer 40

``` X = different species Y = same species, non-identical individual/twin ```

Question 41

Hyperacute transplant rejection is type (X) HS reaction

Answer 41

X = II (pre-existing Ab react to donor Ag)

Question 42

Patient develops chills, arthralgias a month after transplant. This is likely mediated by (X) cells.

Answer 42

X = CD8 (against donor MHCs; type IV HS) or by antibodies

Question 43

Chronic transplant rejection involves which components of immune response?

Answer 43

Both antibodies (type II HS) and CD4 T cells (type IV HS)

Question 44

Graft v host disease is type (X) HS reaction and occurs most commonly in which types of transplants?

Answer 44

X = IV Liver and bone marrow (rich in lymphocytes)

Question 45

(X) drugs are calcineurin inhibitors that have which mechanism of action?

Answer 45

X = Cyclosporine and Tacrolimus Immunosuppressants that block T cell activation by preventing IL2 transcription (in Th cell)

Question 46

Calcineurin inhibitors have which key side effect?

Answer 46

Nephrotoxicity

Question 47

Sirolimus is in (X) category of drugs and works by which mechanism?

Answer 47

``` Sirolimus = Rapamycin X = immunosuppressants (mTOR inhibitor) ``` Prevents IL-2 response in B and T cells

Question 48

Side effects of Sirolimus

Answer 48

Pancytopenia, insulin resistance, hyperlipidemia

Question 49

Basiliximab MOA

Answer 49

Blocks IL-2R (immunosuppressant)