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IHO Week 1 > Innate Immune System > Flashcards

Innate Immune System Flashcards

1
Q

Functions of Innate IS:

A
  1. Complement Activation
  2. Inflammation
  3. Cell Activation
    • -cytokine & chemokine production
    • -phagocytosis
  4. Priming of adaptive immune response
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2
Q

Defensins and Cathelicidins functions/MOA

A

Antimicrobial peptides. (short) Associated with physical barriers. Expressed in epithelial cells

MOA: membrane destruction by integrating into microbial membrane, aggregating, and poking holes in membrane

  • chemokine role to bring in other IS cells to infection site.
  • slows down pathogen
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3
Q

Defensins

2 classes:
Alpha–
Beta–

A

Beta stand peptides connected by disulfide bonds

Alpha: in granules of PMNs and Paneth cells
Beta: secreted by mucosal surface epithelia

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4
Q

Cathelicidins

A

Alpha helical peptides

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5
Q

Defensins: Alpha

  • -Human neutrophil peptide (HNP):
  • -Human Definsins (HD):
A

–Human neutrophil peptide (HNP) 1-4 :
PMNs, monocytes, and lymphocytes

–Human Definsins (HD) 5-6: paneth cells of s. intestines

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6
Q

Defensins: Beta

–Human beta defensing (HBD):

A

epithelial tissues mostly

sometimes: monocytes, macrophages, and dendritic cells.

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7
Q

HSC–> Myeloid progenitor cells

A

GM-CSF

IL-3

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8
Q

Myeloid Pro–> basophil, eosinophil pro, granulocyte-macropahge pro?

A

GM-CSF

IL-3

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9
Q

Basophil pro –> basophil

A

GM-CSF
IL-3
IL-4

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10
Q

Eosinophil pro–> eosinophil

A

GM-CSF
IL-3
IL-5

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11
Q

granulocyte-macropahge pro –> Neutrophil

A

GM-CSF
IL-3
G-CSF

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12
Q

granulocyte-macropahge pro –> monocyte

A

GM-CSF
IL-3
M-CSF

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13
Q

Monocyte–> Dendritic cell

A

GM-CSF

IL-4

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14
Q

Monocyte –> Macrophage

A

GM-CSF

M-CSF

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15
Q

Monocyte –> Neutrophil

A

IL-8

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16
Q

Congenital neutropenia

A
  • Lack of GM-CSF–so you can’t produce any cells downstream of myeloid precursor
  • Frequent bacterial infections
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17
Q

Name the cells that form the bridge between innate and adaptive immunity.

A

APCs!

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18
Q

TLR1+

TLR2

A

PAMPS Recognized:

  • –Triacylated lipoproteins (PAM3CSK4)
  • –Peptidoglycans
  • –Lipopolysaccharides

Production: AP-1 & NF-kB Inflammatory Cytokines (IC)

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19
Q

TLR2+

TLR6

A

PAMPS Recognized: Diacylated lipoproteins (FSL-1)

Production: AP-1 & NF-kB –>IC

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20
Q

TLR3

A

PAMPS Recognized:

  • dsRNA (poly I:C)
  • tRNA
  • siRNA

Production: IC & IFN-beta

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21
Q

TLR4

A

PAMPS Recognized:

  • -Lipopolysaccharides (LPS)
  • -Paclitaxel

Production: IC & IFN-Beta

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22
Q

TLR5

A

PAMPS Recognized: Flagellin

Production: IC

23
Q

TLR7

A

PAMPS Recognized:

  • -ssRNA
  • -Imidazoquinolines (R8
  • -Guanosine analogs

Production: IC & IFN-alpha

24
Q

TLR8

A

PAMPS Recognized:

  • -ssRNA
  • -Imidazoquinolines

Production: IC & IFN-alpha

25
Q

TLR9

A

PAMPS Recognized:

  • -CpG DNA
  • -CPG ODNs

Production: IC & IFN-alpha

26
Q

TLR10

A

PAMPS Recognized: Profilin-like proteins

Production: IC

27
Q

TRLs that produce both IC and Type1 IFN?

A

3, 4, 7-9

Beta: 3-4
Alpha: 7-9

28
Q

“Mother of all immune system transcription factors”?

A

NF-kappaB

29
Q

Stimulation of TLRs initiates cascades that lead to activation of…

A

AP-1
NF-kappaB
Interferon regulatory factors
–IRFs 3 and 7

30
Q

Proinflammatory cytokines?

A

TNF-alpha
IL-6
IL-12

31
Q

Pro-inflammatory cytokines?

A

TNF-alpha
IL-6
IL-12

32
Q

Activation of NF-kappaB:

A
  1. Expression of pro-inflammatory genes (TNF alpha)
  2. Increased phagocytosis
  3. Increased efficiency of antigen presentation
33
Q

C5b

A

byproduct of complement activation and opsonization

-acts as focal point for deposition of membrane attack complex

34
Q

Hallmarks of inflammation

A
  1. Influx of fluid (edema)
  2. Increased temp (hyperthermia)
  3. Decreased oxygenation
  4. Influx of WBCs
35
Q

Triggers of inflammation:

A
  • Complements C5a stimulation of basophils and mast cell degranulation
  • Macrophages
  • NK cells
36
Q

Changes in acute inflammation:

A
  1. increased blood supply to affected area
  2. Increase capillary permeability
  3. Increase in leukocyte migration into affected tissue.
37
Q

Pro-inflammatory cytokines?

A

TNF-alpha: produced by macs
IL-1
IFN-gamma

38
Q

Cells of acute vs chronic inflammation

A

Acute: Neutrophils and activated helper T cells

Chronic: macrophages, cytotoxic T cells, and B cells.

39
Q

granulocyte-macropahge pro –> Neutrophil

A

GM-CSF
IL-3
G-CSF

40
Q

PMNs

A
  • Granules
  • First responders (phagocytic)
  • Have FcR to bind antibodies

GM-CSF
IL-3
G-CSF

41
Q

Eosinophils

A

-bilobed nucleus
-phagocytic
-Granules contain Major Basic Protein
MBP is toxic to HELMINTHS

GM-CSF, IL3, IL5

42
Q

Basophils

A
  • Multilobed nucleus
  • Express FcR1 receptors for IgE so IgE is always on their surface
  • release histamine–>allergic response
  • activated by complement C5a and C3a

GM-CSF, IL3, IL4

43
Q

Monocytes:

A

Form macrophages
Horseshoe shaped nucleus
long lived

44
Q

Macrophages

A

Major producer of cytokines
Highly activated by IFNs
APC

45
Q

Dendritic Cells

Classical vs Follicular

A

Classical: process and present foreign protein antigens to T cells

Follicular: form immune complexes to B cells in LYMPHOID FOLLICLES

46
Q

Dendritic Cells

Classical vs Follicular

A

Classical: process and present foreign protein antigens to T cells

Follicular: form immune complexes to B cells in LYMPHOID FOLLICLES

*Take naive T cells and activate them

47
Q

DC1
Location?
Produces?

A

From myeloid precursor
Location? Diffuse
Produces: IL-8

48
Q

DC2
Location?
Produces?

A

Lymphoid precursor
Location? restricted to T cell areas of secondary lymphoid organs and tissues

Produces? mainly type I interferons

49
Q

NK Cells

A

Innate immunity

  • IFNs ramp up granule production in NKs
  • Look for missing MHC I molecules on cell surfaces

Lymphoid progenitor cell –> NK
IL-3 SCF and IL-2

50
Q

Chronic Granulomatous Disease

A
  • Inability to produce hydrogen peroxide and hypochlorous acid
  • Inability to kill phagocytosed bacteria
51
Q

Leukocyte Adhesion Deficiency (LAD)

A
  • Lack of INTEGRIN subunit, the common beta chain
  • Inability to RECRUIT innate immune cells to site of inflammation
  • Increased susceptibility to bacterial, fungal, and viral infections
52
Q

Complement Defects

A

Increased susceptibility to bacterial infections

-Reduced ability to remove immunocomplexes

53
Q

Chediak-Higashi Syndrome

A

Defect in gene LYST (CHS1), a lysosomal trafficking gene that affects lysosomes and meanosomes

-Increased susceptibility for bacterial infections.

IHO Week 1 (12 decks)

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