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Advanced Immunology > Week 1 Study Questions > Flashcards

Week 1 Study Questions Flashcards

1
Q

Innate immunity cell mediators and its role

A
  • Provides early defense against microbes, cellular and molecular mechanisms are in place before infection – does not involve antibodies
  • NK cells, dendritic cells, neutrophils, phagocytes/macrophages, epithelial barriers, complement activation
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2
Q

Adaptive immunity cell mediators and its role

A
  • Specific defense system & ability to respond more
    vigorously to repeated exposures to the same microbe – memory
  • T cells, B cells, effector T cells, antibodies
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3
Q

Describe the cytokines involved in myelopoiesis and the differentiation pathway they control

A

Stem cells: secrete SCF, IL-6 and Flt3L to produce a common myeloid progenitor

Common myeloid progenitor:

  • driven by IL-5 to become an eosinophil
  • driven by G-CSF to become a neutrophil
  • driven by Flt3L to become a macrophage
  • driven by M-CSF to become a monocyte
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4
Q

What are M1 and M2 macrophages?

A
  • M1 macrophages stimulate Th1 cells and are involved in a fight response against pathogens
  • M2 macrophages stimulate Th2 cells and are involved in a healing response
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5
Q

Functions of M1 macrophages

A
  • Involved in classical complement activation
  • Anti-microbial and anti-tumour properties
  • Pro-inflammatory, and secrete IL-6
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6
Q

Functions of M2 macrophages

A
  • Involved in alternative complement function
  • Wound healing and tumour growth properties
  • Anti-inflammatory, and secrete IL-10
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7
Q

Name the different subsets of dendritic cells

A
  • Classical DCs (cDCs)
  • Plasmacytoid DCs (pDCs)
  • Inflammatory DCs (infDCs)
  • Langerhans cells (DCs of the skin)
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8
Q

How can NETosis contribute to disease?

A
  • NETosis is the release of intracellular proteins potentially giving rise to auto-antigens and release of DAMPs that amplify ongoing immune reaction (e.g. MPO, ROS, TF)
  • Lots of auto-antigens -> immune system doesn’t shut off or self-regulate -> excessive inflammation
  • NETs can damage the host.
  • NETosis has a role in variety of pathophysiological conditions (e.g. there are many NETs in the sputum of cystic fibrosis patients)
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9
Q

What are some of these diseases NETosis contributes to?

A
  • Some diseases NETosis contributes to includes SLE, rheumatoid arthritis, cystic fibrosis, thrombosis etc.
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10
Q

Naïve CD4+ T cells can be polarised into different effector subsets –what are they and what do they do?

A
  • T helper 1 (Th1): involved in driving cytotoxic CD8, secretes INFy
    • Th2: involved in allergy responses and parasites, secretes IL-4
    • Th17: maintain barrier immunity at mucosal surfaces, secretes IL-17
    • regulatory T (Treg) cells: maintenance of immune cell homeostasis, regulate immune cell activites, secrete TGFB
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11
Q

Explain how Treg cells are critical for the maintenance of self-tolerance and immune homeostasis

A
  • Treg cells suppress potentially harmful activities of several immune cells
  • Treg cells are activated via the TCR to become suppressive

-Treg-cell activation is antigen-specific; and the suppressive activity of Treg cells is triggered in an
antigen-specific fashion

  • Once they are activated, they do not require re-stimulation via the TCR to suppress and suppression is not MHC restricted
  • Secrete TGF-β, IL-4 and IL-10 which contribute to
    suppression
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12
Q

How do innate lymphoid cells differ from the various Th cell subsets?

A
  • Innate lymphoid cells are bone derived
  • Innate lymphoid cells do not express antigen receptors or undergo clonal expression
  • ILCs are earlier in their immune response comparing to other T helper cells
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13
Q

Describe some of the ways ILCs assist an immune response and describe how they can also be involved in immunopathology.

A

-Macrophage activation, mucous production, vasodilation, thermoregulation, phagocytosis etc.

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14
Q

Describe the different roles of ILC2 and ILC3

A

ILC2: are involved in mucous production, alternative macrophage activation and vasodilation, some examples of cytokines released include IL-4 and IL-5

ILC3: involved in phagocytosis and epithelium survival, some examples of cytokines they secrete are IL-17 and IL-22

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15
Q

True/False: In hydrodynamic focussing, sheath pressure is greater than sample pressure

A

False: the sample pressure is greater than the sheath pressure otherwise both will mix together -> you will not see single cells

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16
Q

True/False: Flow cytometry can be used for bacterial analysis

A

True: make sure instruments are very clean because particle size can be similar to the debris of WBCs

17
Q

True/False: Forward scatter measures granularity

A

False: forward scatter measures size, side scatter measures granularity

18
Q

True/False: Cytokine bead array works on a similar principle as an ELISA

A

True

19
Q

Explain the difference between a longpass filter and bandpass filter

A

Longpass: If filter is set to 500nm, then wavelengths of 500nm or more will pass through

Shortpass: If filter is set to 500nm, then wavelengths of 500nm or less will pass through

Bandpass: If filter is set to 500nm, then wavelengths of
+/- a certain amount will pass though (e.g. 500+/-50, then 475-525nm will pass through)

20
Q

Describe how you would correct for spectral spillover

A
  • Compensation by increasing the voltage values so that all the single stained cells
21
Q

Neutrophil killing of bacteria by release of phagolysosome

A
  • Neutrophils phagocytose microbes, which initiates the release of phagolysosome
  • This is an enzyme that breaks the bacterial wall, and cationic peptides and ROS help to kill the bacteria
22
Q

Neutrophil killing with NETS

A
  • Neutrophils release their content to trap microbes and stop their spread
  • NETS can include Neutrophil elastase (NE), cathepsin G, lysozyme, myeloperoxidase (MPO) and proteases
    Ion chelators and histones
  • These can kill GP and GN bacteria, parasites and fungi
23
Q

What are the differences between the effects of splenic and intestinal ILC3s

A
  • Splenic ILC3s: increased CD40 & CD80/86 after IL-1β
    stimulation and promote CD4+ Th cell responses
  • Intestinal ILC3s limit commensal bacteria specific
    pro-inflammatory CD4+ Th cell responses →
    maintain intestinal T cell tolerance
24
Q

Classical DCs

A
  • DCs are antigen presenting cells, activate naïve T cells, and link innate and adaptive immune responses
  • Matured by Flt3L
  • Classical DCs are found in blood, lymph nodes (LN), spleen, and non lymph tissues including skin, liver, lung & gut
25
Q

Langerhans cells:

A
  • Originate from precursors in the skin before birth (yolk sac progenitors & foetal
    liver–derived monocytes).
  • In steady-state, LCs self-renew in situ independent of bone marrow (no replacement by bone marrow precursors) and development is independent of Flt3L.
  • Express MHC-II and induce
    differentiation of Th2 cells
26
Q

Plasmacytoid DCs (pDCs)

A
  • Circulate in the blood and lymph node compartments
  • Secrete large amounts of Type I interferons in response to viral infections
  • In steady-state – poor capacity to stimulate CD4+ T cells (low MHC Class II & costimulatory receptor expression and limited phagocytosis of antigens)
  • When activated – dendritic morphology, up regulate HLA-DR & co-stimulatory
    receptors, differentiate into functional APC and activate naïve CD4+ T cells
27
Q

Inflammatory DCs (infDCs)

A
  • DCs derived from monocytes in an inflammatory setting
  • Recruited to sites of inflammation & produce TNFα and iNOS,
  • Promote early pathogen specific T cell responses, preferentially induce Th1-type responses
  • Initiate inflammation and support the function of cDCs
28
Q

Classic DC positioning

A
  • Strategically positioned at body barriers and organ entry points & migrate to T
    cell zones within lymphoid organs or towards tissue-draining LNs → efficient stimulation of naïve T cells
29
Q

Outcomes of T cell encounters with MHC-peptide on cDCs

A
  • T cell proliferation
  • Th cell polarisation (Induce differentiation of helper T cells)
  • Memory cell formation
30
Q

3 signals required from cDCs for T cell outcomes

A
  • MHC-peptide – T cells interact with cell associated Ag
  • Co-stimulatory signals (induced by microbes) – T cells respond to peptides from microbes and not harmless molecules
  • Instructing cytokines – direct
    polarisation
31
Q

Antigen presentation and half life of cDCs:

A
  • Short half life of ~ 3-6 days – constantly replenished from bone marrow precursors in a Flt3L-dependent manner
  • Specialised Ag processing cells – efficiently present endogenous & exogenous Ag in both MHC-I & -II contexts.
- Cross presentation (present acquired exogenous antigens on MHC class I to naïve CD8+ T-cells – ingested antigens
transported from vesicles to cytosol where peptides enter the class I pathway

Advanced Immunology (5 decks)

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