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Medicine > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the TWO broad categories of autoimmune disease?

A
  1. Organ Specific

2. Non - organ Specific

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2
Q

What are Organ Specific Autoimmune diseases?

A

Where antigens on a specific organ are recognised by the immune system, triggering a response. This leads to damage and loss of function/ change in function of the organ

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3
Q

What are Non-Organ Specific Autoimmune diseases?

A

where there is wide spread/ systemic antigen recognition of the immune system leading to areas of damage wide spread. Examples are vessels and nucli

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4
Q

Give examples of organ specific autoimmune diseases

A

Graves disease

Diabetes Type I

MS

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5
Q

Give an examples of non-organ specific diseases

A

RA

Systemic Lupus

Sclerodema

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6
Q

What are the TWO types of immune-deficiency diseases?

A

Primary - congenital, genetic factors in some component of the immune system

Secondary - acquired immune-deficiency

  • HIV Infection
  • Nutritional defects
  • Immuno-suppressants therapies - Chemotherapy
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7
Q

What part of the immune system can be affected by immuno-deficiency diseases? and what is their percentage of these diseases?

A

ALL CAN BE.

B - lymphocyte/ Antibody production - 50%
T & B Cell combined - 20%
Phagocyte - 18%
T cell - 10% 
Compliment - 2%
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8
Q

What levels of deficiency are possible with Phagocytes?

A

Production
Interaction - don’t recognise pathogens
ability to kill - can engulf but unable to phagocytose

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9
Q

What is a common receptor the HIV virus uses to enter the T lympocyte cell?

A

CCR55 Receptor

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10
Q

What type of virus is HIV?

A

Retrovirus

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11
Q

What does HIV use to make its complimentary DNA that it incorporates into the host cell DNA to enable it to replicate its proteins?

A

Reverse Transciptase

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12
Q

What are stages of HIV progressing to AIDS and why is this?

A
  1. initial stage: Flu-like symptoms - initial drop in CD4 T -cells
  2. Asymptomatic Phase - T - level builds up enough to deal with majority of infections
  3. Symptomatic Phase - decline in T-cells
    AIDS - reduction in T-cell below certain level
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13
Q

What are the two responses of the innate immune system and give examples?

A

Cellular - phagocytes & Natural Killer cells

Chemical - cytokines & compliment

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14
Q

What is stimulated and released to trigger further inflammatory cells when a phagocyte encounters a pathogen?

A

NFkB

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15
Q

What stops phagocytes “recognising” self tissue?

A

Display of MHC -1

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16
Q

What do PRR recognise and give an example?

A

They recognise PAMP and Toll-like receptors as example

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17
Q

What do Natural Killer cells recognise?

A

Infected and stressed cells & non- self cells & tumours

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18
Q

What are the functions of compliment?

A

Recruitment of immune cells
opsonisation of pathogens
MAP - acting membrane punching holes in them

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19
Q

What needs to be activated in compliment to get the cascade? and what enzyme is involved?

A

C3 needs to be cleaved to C3a and C3b.

C3 convertase

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20
Q

What are the three main ways compliment can be activated?

A

Classical pathway - binding to Fc portion of antibodies
Alternative pathway - binds to pathogen directly
Manose - binding Lectin pathway

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21
Q

Cytokines are small messenger proteins used in signalling during inflammation. Give an example of same main types:

A

Interleukins,
Chemokines,
TNF,
Interferons

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22
Q

What does IL-1 do?

A

Induces fever

Activation of endothelial cells - inflammation and coagulation

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23
Q

What does IL- 6 do?

A

Induces fever
Promotes synthesis of proteins from liver such as CRP
Activates lymphocytes
induced B - cell production of antibodies

24
Q

What does IL-8 do?

A

Neutrophil Chemotaxis - works with IL-12

always activated by LPS

25
Q

What does IL - 12 do?

A

Activates THC-1 and NKC - this is important for intracellular infections

Increases the cyto-toxicity of the cells

26
Q

What IL’s are key regulators of type I hypersensitivity reactions?

A

IL -4, 5, 13

27
Q

What cytokine is important for viral response?

A

IFN - gamma

28
Q

What does IL - 10 do?

A

Has anti-inflammatory effects

29
Q

What are the BROAD main features of inflammation and why?

A

Phagocyte chemo-traction - to kills the pathogens

Vascular changes - to isolate the infection

30
Q

What kind of pathogen does the humoral adaptive system combat?

A

extra-cellular

31
Q

What activates B - cells?

A

T - helper type II cells

32
Q

What B cells become memory cells?

A

Only the B cells with the most specific antibody production to the pathogen are stored

33
Q

What are the functions of antibodies?

A 
Opsonisation 
Compliment activation 
Neutralise toxins 
Restricts access of pathogen
Effects the surrounding effector cells
34
Q

What can the two light chains of Ig be?

A

Kappa or Lambda

35
Q

What activates the T- cell immunity?

A

T helper cell type I

36
Q

What are activated by T helper cell type I?

A

APC * Cytotoxic T lymphocytes

37
Q

What do CTL target?

A

Intracellular infections - viruses, some bacteria & fungus

38
Q

What do cytotoxic T cells recognise the antigen on?

A

MCH - 1

39
Q

What is released to an infected cell when a CTL comes across one?

A

Perforin - puts a whole in the membrane

Granzymes & granulyzin are released into the cell

40
Q

What TWO things must be present for the T cell to be activated and why?

A

MHC -1 - which is recognised by CD8
B7 protein - which is recognised by CD28.

this is a back up to make sure the cell is meant to be stimulated.

41
Q

What is the fate of the CTL?

A

Destroyed

Memory T cells

42
Q

Typically what kind of a response would a bacteria infection trigger?

A

Humoral response

43
Q

What bacterial infections wouldn’t trigger a humoral response as they are intra-cellular infections?

A

Salmonella

Chlamydia

44
Q

In a typical viral response, what would be triggered?

A

Cell mediated

NKC are also stimulated

45
Q

What are primary lymphoid organs?

A

Bone & thymus

46
Q

What are secondary Lymphoid Organs?

A

Lymph nodes

Spleen

47
Q

What are the steps to leukocyte extravasion?

A
  1. Chemoattraction
  2. Rolling
  3. Tight binding
  4. Diapedisis
  5. Chemotaxis
48
Q

What molecule is involved in attracting guiding APC and other immune cells to the lymph nodes?

A

CCR7

49
Q

In Bruton’s Agammaglobulinaneamia what is effected and what is the result?

A

Bruton’s Tyrosine Kinase Gene

Prevents Pro B-cell becoming Pre-B-cell
= low antibody production

50
Q

In Hyper IgM Syndrome, what is affected and what is the result?

A

CD40 on the T-Cell.

Results in the inability for B-cell Activation by helper T-Cell

51
Q

In X-linked SCID, what is defected? and what is the result?

A

IL-2R- Gamma - the common gamma chain for cytokine receptors.

Cytokines are unable to activate the T-cells - which also result in no humoral response. - therefore there is no adaptive immunity.

52
Q

In granulomatous Disease what enzymes are defected and what is the result?

A

NADPH enzymes.

No formation of oxidative enzymes for phagocytes to use.

53
Q

In the compliment cascade, how is opozonisation augmented?

A

Binding of the the C3b on the pathogen is recognised by receptors CR1 on the marcophages inducing phagocytosis

54
Q

What are TLR expressed on?
What do they recognise?
What is the outcome of activation of them?

A

Expressed on innate cells in the body.
Recognise PAMPs
Induce inflammation via the NFkB route

55
Q

What is the Basic reproductive rate? (R0)

A

The theoretical amount of people that will become infected from one person getting infected. Therefore highly contagious disease will have higher R0

56
Q

What is the Effective reproductive rate? (R)

A

The real world R0. Some people are immune to the disease in question. Therefore it is the amount of people that will actually get infected by one person getting infected first.

R0 x the no. of people immune = R

57
Q

What is the critical vaccine threshold?

A

1 - (1/R0).

It tells us how many people we must vaccine in order to get herd immunity

Medicine (33 decks)

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