Lecture 3: Innate immunity and antigen presentation Flashcards

1
Q

What are the immune defences (broadly)?

A

Innate (external): Physical barriers, microbiome, humoral factors i.e enzymes, mucus

Innate (Internal): Early responders, cellular and humoral
Interact with:
Adaptive immunity: Cellular and humoral
To produce inflammation

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2
Q

Where are neutrophils found?

A

Circulate in blood and infiltrate sites of infection

aka polymorphonuclear leukocytes

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3
Q

Describe phagocytosis:

A

1) Adherence
2) Membrane activation
3) Phagosome formation
4) Fusion and digestion
5) Release of degraded products

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4
Q

What triggers neutrophil phagocytosis?

A
  • Receptors for common bacterial cell wall components i.e PAMPS: Pathogen associated molecular patterns, DAMPS: Damage associated molecular patterns (weak interaction)
  • Receptors for C3b complement component (Complement mediated opsonisation)
  • Receptors for Fc region of antibodies
    (immune complex-mediated opsonisation)
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5
Q

What are three examples of DAMPS?

A

Common cell wall structures i.e LPS, peptidoglycans i.e mannans and mannoproteins

Bacterial metabolic products i.e N-formyl-methionine-peotides

Heat shock proteins - Released by stressed cells

These are all immune danger signals

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6
Q

Where are dendritic cells found?

A

Within the tissue, they have PAMP receptors

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7
Q

When do acute phase proteins peak in their time profile?

A

Around a week before declining

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8
Q

What are acute phase proteins?

A
  • Activated by tissue injury alarm systems ie danger signals i.e dendritic cells
  • Produced mostly by the liver i.e opsonins, coagulation factors, haem and iron binding proteins
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9
Q

What are the actions of acute phase proteins?

A
  • Promote resolution and repair of inflammatory lesions
  • Limit tissue injury
  • Enhance host resistance
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10
Q

Describe in broad terms the complement system:

A

Common cell wall components are bound by the first compliment which in turns activates the other compliments that can lead to:

  • Opsonisation (enhanced phagocytosis)
  • Chemotaxis
  • Increased vascular permeability
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11
Q

Describe lymphocyte circulation:

A

Bone marrow produces lymphocyte precursors and these travel to the thymus and mature. ~10% enter circulation and travel to the secondary lymphoid tissues such as lymph nodes, spleen, tonsils/adenoids/payers patches

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12
Q

The lymphocyte sub-population can be divided into effectors and regulators. Describe the effector cells:

A

Effectors - B lymphocytes (AB producing), Antigen-specific cytotoxicity (CD8 T cells) -> Subset; NK cells, and ADCC (K lymphcytes)

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13
Q

The lymphocyte sub-population can be divided into effectors and regulators. Describe the regulator cells:

A

Regulator cells:

  • Cytokine production (CD4 lymphocytes)
  • Th1 (viruses, bacteria, intracellular agents)
  • Th2 (parasites, allergies, MULTICELULLAR)
  • Treg (Supressor cells, down regulate)
  • TH17 (Mucosa and inflammation)
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14
Q

Dendritic cells are APC cells, what are some examples?

A
Langerhan cells (SKIN)
Alveolar macrophages (Lungs)
Kupffer cells (liver)
Monocytes (Blood)
Epithelial M cells (gut)
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15
Q

What are the APC functions?

A
  • Antigen collection and transport
  • Antigen concentration
  • Antigen processing
  • Present processed antigen to lymphocytes
  • Co-stimulation (accessory signals) needed; surface molecules, pro-inflam cytokines
  • Tolerance induction
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16
Q

What are the two antigen presenting pathways?

A

Endogenous and exogenous

17
Q

Describe the endogenous antigen presentation pathway:

A
  • Peptides derived from ingested material
  • Only specialised APCs (dendritic cells, B cells)
  • Presented by MHC class 2
18
Q

Describe the endogenous antigen presentation pathway:

A
  • Peptides derived from cytoplasmic proteins
  • Normal metabolism
    = viral peptides
    = modified self peptides (tumors)

= Presented by MHC 1

19
Q

What is cross priming?

A

Exogenous pathway but with MHC 1 activation