Immunology

Question 1

Chronic Rejection of Transplant:

Timeframe?

Answer 1

Months - Years

antibodies form against graft cells AFTER transplantation

Question 2

Chronic Rejection of Transplant:

Mechanism of rejection?

Answer 2

• T-cell & Antibody mediated (antibodies form AFTER transplantation)
• Obliterative vascular smooth muscle fibrosis
• Fibrosis of graft tissue & blood vessels
• Class I-MHC(non-self) is perceived by CTLs as class I-MHC(self) presenting a non-self antigen

Question 3

Type of rejection?

Obliteration of intimal smooth muscle w/ fibrosis of graft tissue & blood vessels.

Answer 3

Chronic – occurs over months-years

Question 4

Hyperacute Transplant rejection:

Timeframe?

Answer 4

w/in minutes

Question 5

Hyperacute Transplant rejection:

Mechanism of rejection?

Answer 5

Antibody mediated (type II) b/c of the presence of PREFORMED anti-donor antibodies in the transplant recipient
- Occludes graft vessels, causing ischemia & necrosis

Question 6

Type of Transplant rejection?

Type II antibody mediated rejection due to presence of pre-formed antibodies in host.

Answer 6

Hyperacute – occurs w/in minutes

Question 7

Type of Transplant rejection?

Occludes graft vessels, causing ischemia & necrosis.

Answer 7

Hyperacute – occurs w/in minutes

Question 8

Acute Transplant rejection:

Timeframe?

Answer 8

Weeks later (or whenever immunosuppressive meds are removed)

Question 9

Acute Transplant Rejection:

Mechanism of rejection?

Answer 9

Cell-mediated due to CTLs reacting against foreign MHCs

• Reversible w/ immunosuppressants (e.g. cyclosporine, muromonab-CD3)
• Vasculitis of graft vessels w/ dense interstitial lymphocytic infiltrate

Question 10

Type of Transplant rejection?

Reversible w/ immunosuppressants (e.g. cyclosporine, muromonab-CD3).

Answer 10

Acute rejection

Question 11

Type of Transplant rejection?

Vasculitis of graft vessels w/ dense interstitial lymphocytic infiltrate.

Answer 11

Acute rejection

Question 12

Graft-versus-host transplant reaction:

Mechanism?

Answer 12

Grafted immunocompetent T-cells proliferate in the irradiated immunocompromised disease host & reject cells w/ “foreign” proteins, resulting in severe organ dysfunction

• Usually in bone marrow & liver transplants (organs rich in lymphocytes)
• Potentially beneficial in bone marrow transplant

Question 13

Graft-vs.-Host reaction - Clinical features?

Answer 13

• Maculopapular rash
• Jaundice
• Hepatosplenomegaly
• Diarrhea
• Usually in bone marrow & liver transplant (organs rich in lymphocytes)
• Potentially beneficial in bone marrow transplant

Question 14

Thymus Cortex & Medulla:
Which contains mature vs. immature T-cells?
Which is the site of positive selection (MHC restriction) vs. negative selection (nonreactive to self)?

Answer 14

Cortex is dense w/ immature T-cells & is the site of Positive selection.

Medulla is pale w/ mature T-cells & epithelial reticular cells containing Hassall’s corpuscles. Negative selection occurs here.

Question 15

Splenic dysfunction:
↓IgM → ↓complement activation → ↓C3b opsonization → ↑susceptibility to encapsulated organisms
What organisms are included in this?

Answer 15

• Streptococcus pneumoniae
• Haemophilus influenzae (type B)
• Neisseria meningitidis
• Salmonella
• Klebsiella pneumoniae
• Streptococci (Group B)

“SHiN SKiS”

Question 16

What cells & cytokines are the primary drivers of granuloma formation – as seen in Sarcoidosis, etc.?

Answer 16

Th1 type CD4 cells produce:

• IL-2 – stimulates Th1 cell proliferation
• IFN-γ – stimulates Macrophage activation

Question 17

What cells & cytokines are the primary drivers of the humoral immune response?

Answer 17

Th2 type CD4 cells produce:

• IL-4 – promotes IgE production by B-cells
• IL-5 – promotes production & activation of Eosinophils & B-cell synthesis of IgA