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Principles 2018 > Immunology Part 2 > Flashcards

Immunology Part 2 Flashcards

1
Q

Where are the cells of the immune system derived from?

A

From precursors in bone marrow

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2
Q

Where do lymphocytes mature?

A

In bone marrow or the thymus and then continually circulate in blood, seconday lymphoid tissues and lymph during life

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3
Q

Name the secondary lymphoid tissues

A

Lymph Nodes – stations for monitoring tissues infections

Spleen – monitoring blood-borne infections

Mucosal-associated lymphoid tissues

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4
Q

What is the lymphatic system?

A

Vessels draining fluid from body tissues

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5
Q

Where are lymph nodes?

A

Regularly along lymph vessels

  • trap pathogens and anitgens in lymph
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6
Q

Where does lymph drain to?

A

drains back to bloodstream via lymphatic vessels and the right subclavian vein

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7
Q

How does lymph move?

A

moves via valves and the movement of muscles

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8
Q

What are the causes of lymphoedema?

A

Inherited

Cancer treatments

Parasitic infections

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9
Q

What are the two arms of the immune system?

A

Innate immune system

Adaptive immune system

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10
Q

What is the inate immune system responsible for?

A

Rapid response within minutes-hours

Same generic response to different pathogens

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11
Q

What is the adaptive immune response responsible for?

A

Unique response to each individual pathogen within days.

Generating immunological memory

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12
Q

What mediates the adaptive immune response?

A

B cells and T cells

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13
Q

Describe acute, limited infection

A

Rapidly cleared by the immune sysrem

Lasting immunological memory

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14
Q
A
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15
Q

Descibe latent infection?

A

Controlled by the immune system

Periodic episoes of pathogen reactivation and replication

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16
Q

Describe chronic infection?

A

Immune response fails‘immunodeficiency’

On-going pathogen replication

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17
Q

What are the two mechanisms of communication between the innate and adaptive arms?

A
  1. direct contact
    * receptor:ligand interactions
  2. Indirect
    * production and secretion of cytokines
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18
Q

Give examples of receptor ligand interactions in direct contact?

A

Peptide/MHC : TCR

PAMP : PRR

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19
Q

What cells can produce and secrete cytokines?

A

Injured tissue cells and activated immune cells

20
Q

Give examples of mechanisma of indirect communication?

A
  • Interleukins
  • Interferons (aplha, ß, gamma)
  • Tumour necrosis factor a (TNFa)

Autocrine, paracrine and endocrine signalling

21
Q

Descibe the characeristics of interferons?

A

Produced by virally infected cells

Host specific but not virus specific: general anto-viral protection

22
Q

Describe the role of IFNs?

A
  • prevent virus replication, stop them replicating within an infected cell
  • signal to allow infected cells to warn nearby cells of virus, signalling makes neighbouring cells increase MHC I molecules so T cells and NK cells can identify and eliminate infection
23
Q

What are the three stages of innate immune cells recognising and responding to pathogens?

A
  1. recognition phase
  2. activation phase
  3. effector phase
25
What is involved in the recognition phase?
* pathogens express signature molecules not found on human cells * PAMPs * Innate immune cells express receptors for PAMPs * Pattern recognition receptors (PRRs)
26
Name some PRRs and the pathogens related to them
Toll like receptor 4 (cell surface) : Lipopolysaccharide LPS (gram negative bacteria) Dectin 1 (cell surface) : B-glucans (fungi) Toll like receptor 7 (intracellular) : ssRNA (viruses)
27
What happens when a cell initiated the apoptotic programme?
Releases soluble 'find-me' signals that attract phagocytes
28
What does an activated macrophage release?
Interleukins (antiinflammatory cytokines)
29
Which cells are capable of phagocytosis?
Macrophages Neutrophils Dendritic Cells
30
What happens in phagocytosis?
1. Receptor binding to ‘eat-me’ signals on apoptotic cell - formation of a phagocytic cup 2. Cup extends around the target and pinches off, forming a phagosome 3. Fusion with lysosomes to form a phagolysosome - degradation of contents (acidification, lysosomal hydrolases) 4. Debris (including antigens) is released into extracellular fluid
31
32
How is phagocytosis different in response to a pathogen and pro-inflammatory stimuli (LPS, IFNgamma) as opposed to an apoptotic body?
The macrohpage will kill the pathogen and them present its antigen on its surface It will release proinflammatory mediators
33
What is present inside the phagolysosome?
Acidification, lysosomal hydrolases, proteases
34
Which bacteria can evade phagolysosomal killing?
Salmonella Staph aureus Mycobacteria
35
What is the pathway of viral infection?
1. virus infects host cells 2. direct activation (loss of MHC-I), indirect activation IFNa/B 3. NK cells activated 4. Infected host cells killed
36
What is the pathway of bacterial infection?
Extracellular bacterium phagocytosed by macrophages and undergo pathogen killing
37
What does interferon gamma released from NK cells do to macrophages?
Increased pathogen killing Increased antigen presentation
38
What are the inflammatory mediators produced?
* NO * prostaglandins/leuktrienes * histamines * pro-inflammatory cytokines (TNFa)
39
What does the acute phase response involve?
Changes in plasma concentration of specific proteins in response to inflammation * driven by cytokines produced during localised inflammation * changes are due to altered protein synthesis in the liver
40
What does increased * CRP * SAP * complement indicate?
Biological prevention of spread of infection Diagnostic marker
41
What does increased **Fibrinogen** indicate?
Wound healing Coagulation
42
What does increased * CRP * Haptoglobin * Manganese superoxidase dismutase * proteinase inhibitors indicate?
Preventing systemic inflammation
43
What is the normal levels of CRP?
\<10mg/L
44
What levels of CRP indicate mild inflammation or viral infection?
10-40mg/L
45
What CRP concentrations indicate active inflammation or bacterial infection?
40-200mg/L
46
What concentration of CRP indicated severe bacterial infection or burn?
\>200mg/L
47
What is the biological role of CRP?
Enhance phagocytosis Complement system activation

Principles 2018 (34 decks)

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