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Immunology > L1: Innate Immunity > Flashcards

L1: Innate Immunity Flashcards

1
Q

List two arms of immunity. Describe in terms of specificity, peak response time, cells involved, cell receptors used, circulating molecules, soluble mediators, amplification, memory.

A
  1. ) Innate: non-specific, hours to 1-2 days, phagocytes / neutrophils / NK cells, Fc / complement / lectins / PR receptors, complement molecules, cytokines and other acute phase / inflammatory mediators, recruitment amplifies, no memory
  2. ) Specific: highly specific, 7-10 days to weeks, T and B cells, BCR/TCR, Igs, lymphocyte factors, clonal expansion amplifies, has memory
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2
Q

What are the components of innate immunity?

A
  1. ) Cell associated pattern recognition receptors (PRRs): eg. Toll-like and cytosolic receptors
  2. ) Cellular components: epithelial barriers, phagocytes, NK cells
  3. ) Soluble molecules: complement and cytokines
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3
Q

Classes of components that PRRs recognize?

A

1) PAMPs (pathogen-associated molecular patterns): ssRNA, dsRNA, flagellin, LPS/endotoxin on gram neg bacteria, lipoteichoic acid on gram pos bacteria
2) DAMPs (damage-associated molecular patterns): endogenous factors released from dying cells

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4
Q

What toll-like receptor recognizes LPS?

A
  • TLR4
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5
Q

Where are TLRs expressed?

A
  • Plasma membrane facing extracellular fluid – against extracellular microbes (bacterial cell wall)
  • In endosome and cytosol – against intracellular microbes (DNA/RNA, peptidoglycans)
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6
Q

Describe response(s) caused by PAMP/TLR interactions

A
  1. ) PAMP/TLR bind – NFkB (TFs) – result: acute inflammation, stimulation of adaptive immunity
  2. ) PAMP/TLR bind – IRFs (TFs) – result: antiviral state
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7
Q

What is the inflammasome? What does generation of this cause the activation/release of?

A
  • Inflammasome refers to the structure of an intracellular PRR called NLRP3 that when bound to pathogen, forms complex, leading to activation of caspase-1. This leads to release of IL-1beta (and IL-18) and acute inflammation
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8
Q

What is the effect of IL-1beta?

A
  • Acute inflammation
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9
Q

What does dysregulated activation of the inflammasome cause?

A
  • Gain-of-function mutations in inflammasome component leads to excess IL-1 production, which causes recurrent attacks of fever and localized inflammation (joints and intestines) – autoinflammatory syndromes
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10
Q

List and describe immunological barriers that are part of the innate immune system

A
  1. ) Mechanical: epithelial cells joined by tight junctions, flow of air or fluid, movement of mucus by cilia
  2. ) Chemical: fatty acids, low pH, enzymes, salivary enzymes (lysozyme), antibacterial peptides/antibiotics such as defensins/cathelicidins that are directly toxic and/or activate leukocyte response
  3. ) Microbiological: normal flora
  4. ) Cells resident in epithelium = intraepithelial lymphocytes (different to common lymphocytes)
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11
Q

Effect of lysozyme on pathogens

A
  • Chews up peptidoglycans that are common to most/all bacteria
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12
Q

Function of phagocytic cells

A
  • Initial step in generation of an immune response

- Required for development and maintenance of normal tissue homeostasis

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13
Q

List professional phagocytes

A
  1. ) PMNs/aka neutrophils
  2. ) Monocyte/macrophage
  3. ) Dendritic cells
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14
Q

Describe process of phagocytosis. Include mechanisms by which microbes are killed

A
  1. ) Microbe binds to phagocyte receptors (mannose, integrins, scavenger receptors)
  2. ) Phagocyte membrane zips up around microbe, ingested
  3. ) Fusion of phagosome with lysosome
  4. ) Activation of phagocyte
  5. ) Microbe killed by acidification, ROS products (most commonly superoxide o2-), NO and lysosomal enzymes
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15
Q

What are opsonins, what are their functions? Most common opsonins

A
  • Soluble proteins that recognize phagocytic targets, bind and cause increased range, higher efficiency and effectiveness of phagocytosis by phagocytes
  • Common opsonins: IgG and C3b
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16
Q

What is chronic granulomatous disease? What is the defect?

A
  • Patients that are more susceptible to bacterial infection as a result of a defective NADPH oxidase in endosomal membranes that synthesize superoxide precursor (o2-), a specific ROS used to kill microbes
17
Q

What is the most potent cytokine for activating macrophages? What cell type produces it?

A
  • IFN-gamma

- Produced by NK and T-cells

18
Q

Besides phagocytosis and killing of microbes, what are other functions of phagocytic cells?

A
  • Inflammation (cytokines)

- Enhanced adaptive immunity (chemokines)

19
Q

NK cells. Do they recognize specific antigens? What cells do they kill? How?

A
  • Don’t recognize specific antigen
  • Kills virus-infected cells and certain tumor cells. All nucleated cells express MHC class I. When virally infected or cancerous, class I MHC expression is downregulated or removed and this is recognized by NK cells via their inhibitor and activating receptors.
20
Q

Is downregulation of MHC 1 sufficient for NK cells to kill cells?

A
  • No, also require use of their activating / inhibitory receptors. One such activating receptor is the Fc receptor to see if antibody is bound to self cell via a process called ADCC: antibody-dependent cell-mediated cytotoxicity
21
Q

What cytokine causes highly activated NK cells?

A
  • IL-2
22
Q

Function of IL-5/IL-13

A
  • allergic inflammation (helminths)
23
Q

Function of IL-17/IL-22

A
  • intestinal barrier for lymphoid organogenesis
24
Q

What are the innate lymphoid cells? Describe their function

A
  • Gamma-delta T cells: less common T cells that reside in epithelial barriers
  • NKT cells: characteristic of T and NK cells, express TCRs with little diversity and some of these recognize lipid antigens
25
Q

Function of complement system?

A
  1. ) Punch pores causing death by osmotic lysis
  2. ) Opsonize antigen for promotion of phagocytosis
  3. ) Produce chemokines to promote inflammation and recruit lymphocytes
  4. ) Shuttle immune complexes out of body
26
Q

What chemokines are produced in the complement cascade? Function?

A
  • C5a and C3a

- Inflammation and recruitment of leukocytes

27
Q

3 complement pathways. What activates each of these pathways?

A
  1. ) Alternative: spontaneously activated by random cleavage of C3 on microbial surfaces
  2. ) Classical: activated by antibody such as IgG via Clq
  3. ) Lectin: activated by sugars such as mannose
28
Q

What is the central soluble mediator to all 3 complement pathways? Describe its use

A
  • C3 is central
  • Cleavage of C3 by C3 convertase generates C3a and C3b.
  • C3a is chemokine that triggers leukocyte recruitment
  • C3b is opsonin that stimulates phagocytosis
29
Q

What antibodies cause activation of classical complement pathway? Is single IgM and IgG sufficient? Which antibody is most efficient at activating this pathway?

A
  • Free antibody not sufficient. Require two IgGs:antigen appropriately space or one IgM pentamer
  • IgM is more efficient than IgG
30
Q

What is the MAC complex? Function?

A
  • C5b6789 = membrane attack complex that destroys cells via pores in cell membranes that causes osmotic cell lysis
31
Q

What is paroxysmal nocturnal hemoglobinuria?

A
  • DAF and CD59 are examples of regulators of complement. DAF dissociates C3 convertases and CD59 prevents binding of C9 to complete MAC formation
  • In this disorder, DAF and CD59 are lacking or defective and this leads to intravascular lysis of RBCs by complement
32
Q

What is hereditary angioneurotic edema (HAE)?

A
  • C1 inhibitor restricts spontaneous activation of C1 in plasma and regulates Hageman factor, molecule that functions in the coagulation cascade.
  • HAE is a deficiency in the C1 inhibitor. As a result of emotional stress or trauma, complement is activated and bradykinins are produced. Results in edema in skin and larynx, a potentially life-threatening disorder.
33
Q

Deficiency in what complement proteins leads to immune-complex diseases such as Lupus?

A
  • C1, C2, C4

- Sometimes C3 deficiency leads to immune-complex disease

34
Q

Deficiency in what proteins leads to bacterial infections mainly in childhood?

A
  • MBL, MASP1/2, C2 and C4
35
Q

Deficiency in what proteins leads to infection with pyogenic bacteria and Neisseria spp.?

A
  • Factor D and P
  • C3 deficiency leads to this, but sometimes also immune-complex disease
  • C5,6,7,8,9 leads to Neisseria spp infections only
36
Q

What does C5,6,7,8,9 deficiency lead to? Does it lead to pyogenic bacterial infections?

A
  • Leads to Neisseria spp. Infections only

- Not pyogenic bacterial infections

37
Q

What are cytokines? Effects?

A
  • Proteins that affect the behavior of other cells
    1. ) Local inflammation: adhesion molecules, increased permeability
    2. ) Systemic protective effects: fever, acute phase proteins, leukocyte production
    3. ) Systemic pathologic effects
38
Q

Actions of type 1 IFNs (alpha and beta)

A

Secreted by virus-infected host cells:

  • inhibit viral replication via paracrine action
  • enhance cytolytic capability of NK cells
  • increased cellular expression of class I MHC molecules

Immunology (18 decks)

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