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Laz's Path Micro > Immunology > Flashcards

Flashcards in Immunology Deck (270)
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1

What do sebaceous glands produce that has antibacterial effects?

Hydrophobic oils – repels water and microorganisms
Lysozyme – destroys the structural integrity of the bacterial cell wall
Ammonia and defensins – anti-bacterial properties

2

How do NK cells determine whether to lyse cells or not?

They have inhibitory receptors which recognise self HLA and they have activating receptors that recognise heparan sulphate proteoglycans
The balance of these signals determines the response
They kill ‘altered self’ cells (e.g. malignancy or virus-infected cells)

3

What does a dendritic cell do after phagocytosis?

Upregulate expression of HLA molecules
Express co-stimulatory molecules
Migrate via lymphatics to lymph nodes

4

Which receptor is involved in the migration of dendritic cells to lymph nodes?

CCR7

5

For each of the following subsets of CD4+ T cell, list their polarising factors and effector factors.
a. Th1
b. Th2
c. Th17
d. Follicular T cell
e. Treg

a. Th1
Polarising
 IL-12
 IFN-gamma
Effector
 IL-2
 IL-10
 IFN-gamma
 TNF-alpha
b. Th2
Polarising
 IL-4
 IL-6
Effector
 IL-4
 IL-5
 IL-10
 IL-13
c. Th17
Polarising
 IL-6
 TGF-beta
Effector
 IL-17
 IL-21
 IL-22
d. Follicular T cell
Polarising
 IL-6
 IL-1
 TNF-alpha
Effector
 IL-2
 IL-10
 IL-21
e. Treg
Polarising
 TGF-beta
Effector
 IL-10
 Foxp3
 CD25

6

Outline the mannose binding lectin pathway of complement activation.

Activated by the direct binding of MBL to microbial cell surface carbohydrates
This directly stimulates the classical pathway involving C4 and C2 (but NOT C1)
NOTE: this is NOT dependent on the adaptive immune response

7

What are the effects of complement fragments that are released during complement activation?

Increase vascular permeability
Opsonisation of immune complexes
Opsonisation of pathogens
Activation of phagocytes
Promotes mast cell/basophil degranulation
Punches holes in bacterial membranes

8

What are the ligands for the CCR7 receptors on dendritic cells?

CCL19
CCL21
This interaction is important in directing dendritic cells towards lymph nodes

9

Give three examples of failure of neutrophil production and outline their mechanism.

Reticular dysgenesis
 Autosomal recessive severe SCID with no production of lymphoid or myeloid cells
 Caused by failure of stem cells to differentiate along lymphoid or myeloid lineage
Kostmann syndrome
 Autosomal recessive congenital neutropaenia (mutation in HAX-1)
Cyclic neutropaenia
 Autosomal dominant episodic neutropaenia due to mutation in neutrophil elastase (ELA-2)
 Occurs every 4-6 weeks

10

Describe the pathophysiology of leucocyte adhesion deficiency.

Caused by deficiency of CD18
CD18 normally combined with CD11a to produce LFA-1
LFA-1 normally binds to ICAM-1 on endothelial cells to mediate neutrophil adhesions and transmigration
A lack of CD18 means a lack of LFA-1, so neutrophils cannot enter tissues
During an infection, neutrophils will be mobilised from the bone marrow (HIGH neutrophils in the blood) but they will not be able to cross into the site of infection (NO pus formation)

11

Outline the pathophysiology of chronic granulomatous disease.

Absent respiratory burst (deficiency of components of NADPH oxidase leads to inability to generate oxygen free radicals)
Excessive inflammation (persistent neutrophils and macrophage accumulation with failure to degrade antigens)
Granuloma formation
Lymphadenopathy and hepatosplenomegaly
Can be treated with IFN-gamma

12

Describe the cytokine cycle between macrophages and T cells.

Macrophages produce IL12 which stimulates T cells, which then produce IFN-gamma
IFN-gamma acts back on the macrophages and stimulates the production of TNF-alpha and free radicals
Deficiencies in IL12, IL12R, IFN-gamma or IFN-gamma receptor can cause immunodeficiency (inability to form granulomas - mycobacterial)

13

Name and describe the colour changes of two tests used to investigate chronic granulomatous disease.

Nitroblue Tetrazolium (NBT) – yellow to blue
Dihydrorhodamine (DHR) – fluorescent
NOTE: both of these tests are looking at the ability of neutrophils to produce hydrogen peroxide and oxidative stress

14

What is the main clinical consequence of complement deficiency?

Increased susceptibility to infection by encapsulated bacteria

NOTE: Properidin (P) deficiency will also lead to increased risk of meningococcal infection

15

Outline the clinical phenotype of complement deficiency.

SLE (if early components involved (e.g. C2)
Usually have severe skin disease
Increased risk of infection (common pathway deficiency)

16

What are nephritic factors?

Autoantibodies that are directed against components of the complement pathway
They stabilise C3 convertases (break down C3) resulting in C3 activation and consumption

17

What disease is associated with the presence of nephritic factors?

Membranoproliferative glomerulonephritis
It may also be associated with partial lipodystrophy

NOTE: it can cause a 'tram track' appearance on microscopy (immune complex and complement proteins deposit in the subendothelium

18

Outline the management of complement deficiencies.

Vaccination (especially against encapsulated organisms)
Prophylactic antibiotics
Treat infection aggressively
Screen family members

19

What is basophilic stippling?

Basophilic appearance of red blood cells caused by the presence of aggregated ribosomal material

20

In which conditions might you see target cells (codocytes)?

Iron deficiency
Thalassemia
Hyposplenism
Liver disease
NOTE: target cells have a high SA: V ratio

21

What are Howell-Jolly bodies? Which condition are they associated with?

Nuclear remnants present within red blood cells
Present in hyposplenism

22

Which deficiencies are typically seen in Coeliac disease?

Iron
B12
Folate
Fat
Calcium

23

Which HLA alleles are particularly common in patients with coeliac disease?

HLA-DQ2 (80%) – DQA1*0501 and DQB1*02 alleles
HLA-DQ8

24

Describe the T cell response to gluten in coeliac disease.

Peptides from gluten (gliadin) are deamidated by tissue transglutaminase
Deamidated gliadin is taken up by antigen-presenting cells and presented via HLA molecules to CD4+ T cells
CD4+ T cell activation results in secretion of IFN-gamma and may increase IL-15 secretion
These cytokines promote activation of intra-epithelial lymphocytes (gamma-delta T cells)
The intraepithelial lymphocytes will kill epithelial cells via the NKG2D receptor (normally recognises the stress protein MICA)

NOTE: anti-gliadin antibodies are the most persistent

25

List some other causes of high intraepithelial lymphocytes.

Dermatitis herpetiformis
Giardiasis
Cows’ milk protein sensitivity
IgA deficiency
Tropical sprue
Post-infective malabsorption
Drugs (NSAIDs)
Lymphoma

26

How often should a DEXA scan be performed in coeliac patients?

Every 3-5 years

27

Name a defect in stem cells that causes SCID and name the gene that is mutated.

Reticular dysgenesis – adenylate kinase 2 (AK2)
NOTE: this is a mitochondrial energy metabolism enzyme

28

Which mutation is responsible for X-linked SCID?

Mutation in common gamma chain on Xq13.1
This is a component of many cytokine receptors (in particular, IL2) leading to an inability to respond to cytokines, causing arrest in T and NK cell development and the production of immature B cells

29

Describe the typical cell counts you would expect to see in X-linked SCID.

Very low T cells
Very low NK cells
Normal or increased B cells
Low immunoglobulin

30

Describe the typical cell counts you would expect to see in ADA deficiency.

Very low T cells
Very low B cells
Very low NK cells