Immunology

Question 1

What is the half life of IgM?
What is the first antibody produced in response to an infection?
Which antibody is present in breast milk?

Answer 1

7 DAYS
IgM
IgA

Question 1

Is mannose binding lectin (MBL) a part of the adaptive or innate immune system?
What pathway is it in?
How does it function?

Answer 1

Innate
Lectin pathway / complement cascade
It binds to MBL-associated serine protease in the blood, than binds to infected cells. The serine protease than starts the breakdown of complement (C2+4) which starts the complement cascade

Question 2

What do deficiencies in the following complement cause?
C1-Inhibitor - HOW?
C1q/r/s + C2 + C4
C3
C5
C5-9
C9

Answer 2

C1 inhibitor = hereditary angioedema. A probable mechanism is the uncontrolled release of bradykinin resulting in tissue oedema
C1q, C1r,C1s, C2, C4 deficiency (classical pathway components) predisposes to immune complex disease e.g. SLE, Vasculitis and GN.
C3 deficiency causes recurrent bacterial/pyogenic infections.
C5 deficiency predisposes to Leiner disease which usually manifests as recurrent diarrhoea, wasting and seborrhoeic dermatitis.
C5-9 deficiency encodes the membrane attack complex (MAC) and is particularly prone to disseminated Neisseria meningitidis infection.
C9 – no clinical syndrome.

Question 3

How do the following drugs affect the immune system?
Cyclosporin and Tacrolimus?
Rapamycin/Sirolimus?

Answer 3

Cyclosporin / Tacrolimus = inhibits calcineurin, a protein essential for activating T-lymphocytes, which in turn reduces IL-2 production.

Rapamycin / Sirolimus) = inhibits the mammalian target of rapamycin (mTOR), a key regulator of cell growth and proliferation. It particularly affects IL-2-driven T-cell proliferation.

Question 4

What cytokines do Th1 vs Th2 produce?
What type of response does this promote?

Answer 4

Th1 - IL-2 + Interferon Gamma -> T-Cell proliferation + cell-mediated immunity
Th2 - IL-4/5/13 -> eosinophilic/allergic response

Question 5

The most common clinical picture associated with Immunoglobulin G (IgG) subclass deficiency is?

Answer 5

recurrent bacterial sinopulmonary infections.

Question 6

What disease does a lack of beta 2-integrin adhesion molecules on neutrophils cause?

Answer 6

leukocyte adhesion deficiency (LAD)

Question 7

What immune reaction is activated in each hypersensitivity immune response?
Type 1-4
Example of each

Answer 7

Type 1: Specific IgE on mast cell ie: anaphylactic reaction to penicillin.
Type 2: IgG cytotoxic ie: hemolytic anemia
Type 3: Immune complex ie: serum sickness, GN, SLE
Type 4: T cell mediated ie: contact dermatitis

Question 8

What are the mechanisms of action of the follow drugs?
Diseases used for?
And which one has the highest risk of Hep B reactivation?
Infliximab -
Rituximab -
Natalizumab -

Answer 8

Infliximab - TNF-alpha inhibitor - Crohn’s + Ulcerative colitis
Rituximab - CD20 inhibitor - RA/NHL/CLL/GPA
Natalizumab - Prevents leucocyte migration - MS

Rituximab = highest risk of Hep B reactivation`

Question 9

Where do each part of B cell development occurs?
A. Direct antigen activation
B. Positive selection
C. Somatic hypermutation
D. T-cell-directed activation

Answer 9

A - Lymph nodes
B - Thymus
C - germinal centre (lymph node OR spleen)
D - peripheral blood

Question 10

What ligand is involved in T-cell directed activation of B-cells?

Answer 10

Helper T-cells bind to B-cells via CD40L on T-cell to the CD40 on B-cell

Question 11

What is the most common auto-antibody in immune thrombocytopenia purpura?

Answer 11

GP IIB/IIIA