Immunology

Question 1

<p>What is a Type 1 hypersensitivity reaction?</p>

Answer 1

<p>Type 1 is the classic allergic response, involving IgE release leading to mast cell degranulation and histamine release. Histamine release results in vasodilation and increased vascular permeability. Examples include Asthma and Anaphylaxis. IL-4 has a central role in driving IgE production.</p>

Question 2

<p>What is a Type 2 hypersensitivity reaction?</p>

Answer 2

<p>Type 2 is antibody-mediated, with the formation of IgG and IgM against self-tissues. These attract leucocytes and cause local tissue damage or dysfunction. Examples include Graves’ disease, Goodpasture's syndrome, and Autoimmune Haemolytic Anaemia.</p>

Question 3

<p>What is a Type 3 hypersensitivity reaction?</p>

Answer 3

<p>Type 3 hypersensitivity describes tissue damage from the deposition of antigen-antibody complexes. Leucocytes and complement pathways are activated, leading to inflammation and necrotizing vasculitis. Examples include SLE, serum sickness, and Arthus reaction.</p>

Question 4

<p>What is a Type 4 hypersensitivity reaction?</p>

Answer 4

<p>Type 4 (cell-mediated) hypersensitivity arises from T cell activation against self-tissues and T cell-mediated cytotoxicity. Examples include MS, type 1 diabetes, TB, IBD, and Rheumatoid Arthritis.</p>

Question 5

What is the central complement protein?

Answer 5

C3 is the central complement protein, which can be activated by several pathways

Question 6

What is the ‘classic’ complement cascade?

Answer 6

The classical pathway involves C1q combining with IgM or IgG antibodies that have already bound to an antigen.

Question 7

What is the ‘alternative’ complement cascade?

Answer 7

The alternative (lectin) pathway involves the activation of C3 cleavage by endotoxins and other foreign antigens without requiring an antibody.

Question 8

How does C3 get to its active form?

Answer 8

Both pathways lead to the formation of C3 convertase, which converts inactive C3 into its active components, C3a and C3b.

Question 9

What happens in the alternative complement cascade?

Answer 9

The lectin pathway follows the same course as the classical pathway but with the opsonin mannose-binding lectin (MBL) instead of C1q.

Question 10

What is the result of activation of the complement cascade?

Answer 10

Activation of the complement pathway has multiple effects. C3a, 4a and 5a cause mast cell degranulation and histamine release. C3b fixes to foreign microbes and opsonises them for destruction by neutrophils and cytotoxic T cells.

Question 11

What are the major cytokines involved in triggering inflammation?

Answer 11

TNF and Il-1

Question 12

What makes TNF and IL-1?

Answer 12

They are secreted by macrophages and T-cells

Question 13

What do TNF and IL-1 do?

Answer 13

They have systemic effects, such as fever and mobilisation of energy stores, as well as upregulation of adhesion molecules and secretion of other cytokines

Question 14

What does IL-6 do?

Answer 14

Similar inflammation triggering things as IL-1 and TNF

Question 15

What do IL-4 and IL-10 do?

Answer 15

anti-inflammatory cytokines that work to terminate the inflammatory response.

Question 16

ARe IL-12 and IFN-gamma more common in acute or chronic inflamation?

Answer 16

Chronic

Question 17

What does IL-12 do?

Answer 17

IL-12 is released by dendritic cells and macrophages, and increases production of IFN-gamma by T cells and natural killer cells.

Question 18

What does IFN-gamma do?

Answer 18

IFN-gamma increases macrophage activity and bacterial destruction.

Question 19

What is Goodpasture’s syndrome?

Answer 19

Goodpasture syndrome (anti-glomerular basement membrane disease) is an autoimmune disease characterized by the development of autoantibodies against type IV collagen

Question 20

What are the symptoms of Goodpasture’s syndrome?

Answer 20

It primarily affects the kidneys and lungs, leading to hematuria and hemoptysis. The effects on the kidneys are usually aggressive, leading to rapidly progressive glomerulonephritis and, subsequently, renal failure.

Question 21

What is the most common cause of endogenous hyperthyroidism?

Answer 21

Graves’ disease

Question 22

What are lipoxins?

Answer 22

Lipoxins are anti-inflammatory products of arachidonic acid metabolism. They act to balance the pro-inflammatory effects of other arachidonic acid products, like prostaglandins and leukotrienes.

Question 23

What are epithelioid cells?

Answer 23

Activated macrophages that resemble epithelial cells
Ill-defined cell boundaries and abundant cytoplasm
Stain pale pink on light microscopy with haemotoxylin and eosin stain
Elongated or oval pale pink nuclei

Question 24

What are epithelioid cells characteristically associated with?

Answer 24

They are the characteristic tissue inflammation in granulomatous TB along with caseous necrosis.
They are associated with intense immunological activity

Question 25

In the process of apoptosis, what are the executor caspases?

Answer 25

Caspase 3 and 6

Question 26

What are the initiator caspases?

Answer 26

8 and 9

Question 27

What are lipoxins?

Answer 27

Lipoxins are endogenous anti-inflammatory molecules produced from arachidonic acid derivatives. Production of lipoxins requires both leukocytes and platelets. Aspirin also triggers the biosynthesis of lipoxins

Question 28

What are the mechanisms of lipoxins?

Answer 28

Lipoxins play a vital role in reducing excessive tissue injury and chronic inflammation. Mechanisms of action of lipoxins at the site of inflammation include inhibition of neutrophil chemotaxis and adhesion, as well as modulation of levels of various inflammatory transcription factors such as nuclear factor κB, activator protein-1, and peroxisome proliferator-activated receptor γ.