Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3rd year > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the innate immune cells?

A

Mast cells
Natural killer cells

Blood - basophil, neutrophil, eosiniphil, monocyte.

Tissues - Mast cell, macrophage, dendritic cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are 3 functions of the innate immune system?

A

Recruitment of immune cells.
Phagocytosis.
Oxidative Killing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is an antigen?

A

Molecule capable of inducing an immune response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is an antibody?

A

A glycoprotein produced by B lymphocytes that binds antigens with a high degree of specificity and affinity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do antigens present in MHC1?

A

Process and present intracellular antigens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do antigens present in MHC2?

A

Process and present extracellular antigens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens when T cells differentiate into naive T cells in the thymus?

A

Naive T cells move to the lymph node where they encounter antigen presentation by dendritic cells. If they recognise the antigen, they proliferate into T helper cells (CD4) of cytotoxic T cells (CD8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do Dendritic cells do?

A

Presents antigen via MHC II.
Sentinel for the immune system.
Excellent at activating adaptive immune system.
Internalises pathogen and processes it into peptides which it presents (antigen) .
T cells which have not seen antigen before are activated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where do T cells mature?

A

Bone marrow then the thymus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where do B cells mature?

A

Bone marrow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where do T and B cells go?

A

Migrate to secondary lymphoid organs, where they encounter antigen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What do Th1 cells do?

A

IgG production
Host defence against intracellular microbes.
Role in disease = Autoimmune diseases, tissue damage, associated with chronic infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do Th2 cells do?

A

IgE production
Host defence - helminthic parasites.
Role in disease - Allergic diseases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do Th17 do?

A

Neutrophilic inflammation.
Host defence - Extracellular bacteria/fungi.
Role in disease - autoimmune inflammatory diseases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why are cytokines important for T helper cells?

A

Release of cytokines, facilitates the activation and actions of the other immune cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the functions of cytokines?

A
  1. Large and heterogenous soluble proteins.
  2. Communication system.
  3. Regulate and co-ordinate the cells of innate and adaptive immunity.
  4. Produced during normal homeostasis.
  5. Produced in response to microbes, tissue damage or other antigens.
  6. Produced by many cells types - especially Macrophages and T helper cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do cytotoxic (CD8) T cells kill?

A

Inducing apoptosis in targeted cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do cytotoxic (CD8) T cells kill?

A

Inducing apoptosis in targeted cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What do NK cells do?

A

Important against intracellular pathogens.
Activate ligands on infective cells in TB.
Kill infected cells.
They produce IFN-g which helps stimulate macrophages, TH1 ells and CD8 T cells.
Important if T cells response is not optimal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the different immunoglobulin isotopes and what are there functions?

A

IgM pentamer - best at activating complement. (fetus)

IgG monomer - can cross the placenta. (birth)

Secretory IgA dimer - contained in secretions. (1-2 months after birth) (breast milk)

IgE monomer - parasitic infectons and allergies.

IgD monomer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is opsonization?

A

Tagging of a microbe so that it is phagocytosed more easily and efficiently.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How are antibodies produced?

A

Activation of B lymphocytes by antigens and other signal molecules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do memory B cells do?

A

Generate an accelerated and more potent antibody-mediated immune response in secondary immune responses.

Immunological memory.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do memory T cells do?

A

Express either CD4 or CD8, and respond if the host is re-exposed to a previously encountered antigen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is IgG?

A

Most abundant type of antibody, is found in all body fluids and protects against bacterial and viral infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is IgM?

A

Found mainly in the blood and lymph fluid, is the first antibody to be made by the body to fight a new infection.

27
Q

What is IgA?

A

Mucous membrane immunity.

28
Q

What is IgE?

A

Parasite immune response, hypersensitivity.

29
Q

What are the light chains?

A

Kappa or Lambda - random selection for each cell. 1 type with 1 specificity.

30
Q

What are the regions of the immunoglobulin?

A

Fab region - variable defines the target binding.

Fc region - constant and defines subclass.

31
Q

What is a paraprotein?

A

Monoclonal immunoglobulin present in the blood or urine.

32
Q

What does presence of paraprotein tell us?

A

There is monoclonal proliferation of a B lymphocyte / plasma cell somewhere in the body.

33
Q

What does electropheresis do?

A

Separates protein based on size and charge.

34
Q

What does total immunoglobulin levels show?

A

Measures the Ig subclasses by heavy chain / Fc section.

35
Q

What does electrophoresis do?

A

Assesses antibody diversity, identifies paraprotein.

36
Q

What does immunofixation do?

A

Identifies what class of paraprotein is present.

37
Q

What do light chains tell us?

A

Assesses imbalance / excess of light chains in urine / serum.

38
Q

In terms of disease what does IgM paraproteins indicate?

A

Lymphoma

- Maturing B-lymphocytes make IgM antibody at the start of the immune response.

39
Q

In terms of disease what does IgG, IgA paraproteins indicate?

A

Myeloma.

Mature plasma cells generate these types of immunoglobulin.

40
Q

What are the 2 broad classifications of immunodeficiency?

A

Primary, or congenital.

Secondary, or acquired.

41
Q

What is the major consequence of immunodeficiency?

A

Increased susceptibility to infection.
Susceptible to certain types of cancer.
Associated with increased incidence of autoimmunity.

42
Q

What are the key aspects of primary immunodeficiency?

A 
Genetic, congenital disorders. 
Part of immune system is either missing or functioning abnormally. 
Mainly caused by mutations. 
Some caused by autoimmunity. 
Predisposes to infections and tumours.
43
Q

Where can the abnormality lie in Primary Immuno?

A

Components of the innate immune system.
Stages of lymphocyte development.
Responses of mature lymphocytes to antigenic stimulation.

44
Q

What does the increased susceptibility to infection depend on?

A

The component of the immune system that is defective.

45
Q

What does the type of opportunistic infection tell us?

A

Clue to the degree and cause of immunodeficiency.

- repeated infection with encapsulated bacteria is a sign of defective antibody production.

46
Q

What do the following show:

  1. Antibody deficiency?
  2. infections with Staphylococci, gram-neg, fungi?
  3. Defects in T-cells or macrophages?
  4. Recurrent candida infection?
A
  1. Recurrent respiratory infection by pneumococcus or haemophilus.
  2. Associated with reduced number of function of phagocytes.
  3. Predispose to infection with intracellular organisms.
  4. Suggestive of defects in the TH17 pathway.
47
Q

What can cause primary immunodeficiency?

A 
Mutations 
Polymorphisms (variation of a single base pair) 
Polygenic disorders (some caused by autoimmunity)
48
Q

What do many mutations in severe combined immunodeficiency (SCID) affect?

A

Affect both T and B cells.

Infants with SCID die in the first few months of life unless treatment is given.

49
Q

How is SCID treated?

A

Stem cell transplant can cure it if done quickly enough. 90% survive, if delayed only 50% survive.
Screened for in many countries.

50
Q

What is HLA and what can happen in individuals with HLA problems?

A

Human leukocyte antigen - affect the outcome of infections.

Individuals that are unable to bind viral peptides have a worse outcome.

51
Q

What is MBL?

A

Mannan-binding lectin - collagen like protein that binds sugars in bacterial cell walls and activates classic complement pathway.

52
Q

What is CVID?

A

Common variable immunodeficiency, IgA deficiency and specific antibody deficiency.
Most common primary immunodeficiency requiring treatment.

53
Q

How is CVID picked up?

A

Low levels of total IgG. Levels of IgA and IgM and numbers of B and T cells are variable.
Causes recurrent resp infections.
Autoimunity common.

54
Q

How is Primary Immunodeficiency Clinical presentation.

A

Children with SCID have defective T cells and B cells and therefore develop infections in the first few weeks of life.
Unusual or recurrent infections.
Diarrhoea
Unusual rashes.
Fam history of neonatal death and consanguinity.

55
Q

Antibody deficiency Presentation

A

Later in life.
Chronic or recurrent bacterial respiratory infections.
Antibody levels - IgG, IgA and IgM should be measured.
Low levels - excludes secondary.

56
Q

Treatment of Primary immunodeficiency.

A

Prevent infection.
Mild immunodeficiency, prophylactic antibodies may be adequate.
If more severe antibody deficiency, immunoglobulin replacement therapy:
- antibodies against a wide range of pathogens.
- Ig pooled from thousands of normal donors.
- Ig replacement can be given IV.
Gene therapy - recombinanat technology to correct the defect.

57
Q

What is the criteria for gene therapy?

A

Genetic mutation for each patient must be identified, and must be evidence that it will improve condition.
Transfected gene must confer a proliferation/survival advantage.
Gene therapy not cause malignancy.

58
Q

When does secondary immunodeficiency occur?

A

Synthesis of key immune components is supressed.

59
Q

Whats the dominant clinical feature of aquired immune deficiency syndrome?

A

AIDS - oportunistic infections and tumours.

60
Q

What are the functions and properties of Helper T cells?

A

Involved in the cell-mediated immune response.
Recognises antigens presented by MHC class II molecules.
Expresses CD4
Also expresses CD3, TCR & CD28
Major source of IL-2
Mediates acute and chronic organ rejection.

61
Q

What are the functions and properties of Cytotoxic T cells?

A

Involved in cell-mediated immune response.
Recognises antigens presented by MCH class 1 molecules
Induce apoptosis in virally infected and tumour cells
Expresses CD8
Also expresses CD3, TCR
Mediates acute and chronic organ rejection.

62
Q

What are the function and properties of B cells?

A

Major cell of the humoral immune response.
Acts as antigen presenting cell
Mediates hyperacute organ rejection.

63
Q

What are the functions and properties of Plasma cells?

A

Differentiated from B cells

Produces large amounts of antibody specific to a particular antigen.

3rd year (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions