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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
24
Q
A
25
Q

What is involved in the recognition phase?

A
  • pathogens express signature molecules not found on human cells
    • PAMPs
  • Innate immune cells express receptors for PAMPs
    • Pattern recognition receptors (PRRs)
26
Q

Name some PRRs and the pathogens related to them

A

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
Q

What happens when a cell initiated the apoptotic programme?

A

Releases soluble ‘find-me’ signals that attract phagocytes

28
Q

What does an activated macrophage release?

A

Interleukins (antiinflammatory cytokines)

29
Q

Which cells are capable of phagocytosis?

A

Macrophages

Neutrophils

Dendritic Cells

30
Q

What happens in phagocytosis?

A
  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
Q
A
32
Q

How is phagocytosis different in response to a pathogen and pro-inflammatory stimuli (LPS, IFNgamma) as opposed to an apoptotic body?

A

The macrohpage will kill the pathogen and them present its antigen on its surface

It will release proinflammatory mediators

33
Q

What is present inside the phagolysosome?

A

Acidification, lysosomal hydrolases, proteases

34
Q

Which bacteria can evade phagolysosomal killing?

A

Salmonella

Staph aureus

Mycobacteria

35
Q

What is the pathway of viral infection?

A
  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
Q

What is the pathway of bacterial infection?

A

Extracellular bacterium phagocytosed by macrophages and undergo pathogen killing

37
Q

What does interferon gamma released from NK cells do to macrophages?

A

Increased pathogen killing

Increased antigen presentation

38
Q

What are the inflammatory mediators produced?

A
  • NO
  • prostaglandins/leuktrienes
  • histamines
  • pro-inflammatory cytokines (TNFa)
39
Q

What does the acute phase response involve?

A

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
Q

What does increased

  • CRP
  • SAP
  • complement

indicate?

A

Biological prevention of spread of infection

Diagnostic marker

41
Q

What does increased

Fibrinogen

indicate?

A

Wound healing

Coagulation

42
Q

What does increased

  • CRP
  • Haptoglobin
  • Manganese superoxidase dismutase
  • proteinase inhibitors

indicate?

A

Preventing systemic inflammation

43
Q

What is the normal levels of CRP?

A

<10mg/L

44
Q

What levels of CRP indicate mild inflammation or viral infection?

A

10-40mg/L

45
Q

What CRP concentrations indicate active inflammation or bacterial infection?

A

40-200mg/L

46
Q

What concentration of CRP indicated severe bacterial infection or burn?

A

>200mg/L

47
Q

What is the biological role of CRP?

A

Enhance phagocytosis

Complement system activation

Principles 2018 (34 decks)

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