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MOL MED block 1 > 5.2. Innate Immune System: Cells > Flashcards

5.2. Innate Immune System: Cells Flashcards

1
Q

Macrophages

A

Phagocytosis
Inflammation
T-cell activation
Tissue repair

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2
Q

Neutrophil

A

Phagocytosis

Inflammation

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3
Q

Eosinophil

A

Defense against parasites

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4
Q

Basophil

A

Inflammation

Defense against parasites

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5
Q

Mast cells

A

Inflammation

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6
Q

Natural killer cell

A

Killing of infected or tumor cells

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7
Q

Dendritic cell

A

Phagocytosis

Activation of naive T cells

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8
Q

Macrophage:

Non activated phagocyte and antigen presenting cell (APC)

A

Engulfs dead and dying cells

  • generally removes debris after barriers penetrated
    1. First cells to respond as it is already present in the tissue under all the barriers
    2. Recognize
  • antigen Cos TLR and NLR and mannose receptors
  • opsonised antigen Cos CR and Fc receptors
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9
Q

Phagocyte

A

Phagocytose pathogen and degrade in phagolysosome

  1. Later in immune response newly synthesized monocytes (live for 1-3 days) leave blood, become macrophages and they predominate cell at 48-96 hrs
  2. Long lived cell
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10
Q

APC

A

Antigen presenting cell

  • have MHCII
  • secrete cytokines and chemokines
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11
Q

TNFalpha

A

Enhance endothelium permeability and expression of adhesion molecules and inflammation

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12
Q

IL6

A

Acts on liver to cause production of acute phase proteins
E.g. C reactive protein, mannose bonding lectin

Cause fever

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13
Q

IL1

A

Fever

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14
Q

CXCL8

A

Recruits neutrophils from bloodstream

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15
Q

IL12

A

Activates NK cells and production of TH1

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16
Q

GM CSF

A

Granulocyte macrophage colony stimulating factor stimulates proliferation of dendritic cell and macrophages

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17
Q

Steps of extravasation

A
  1. Rolling adhesion
  2. Right adhesion
  3. Transmigration
  4. Cells now follow chemokine gradient (5)
18
Q

Rolling adhesion

A

Carbohydrate ligands on the circulating leukocytes bind to P selectin molecules causing it to roll along endothelial surface (1)

19
Q

Tight adhesion

A

Integrins (activated by chemokine signaling = inside out signaling) on leukocyte surface are now able to bind to integrin receptors (ICAM) on endothelial cells causing cell to bind tightly but transiently and stop rolling (2)

20
Q

Transmigration

A

Occurs through the gaps between endothelial cells using PECAM proteins present on leukocytes and on junctions between endothelial cells (3)

Leukocyte now produces enzymes which break down the basement membrane (diapodesis) allowing entry into subendothelial tissue (4)

21
Q

Neutrophils

A

(Phagocyte)

  1. Move into tissues because of C3a and C5a and cytokines releases by epithelial cells and macrophages
    - predominant cell you’re enter damaged tissue from the blood in the first 0-48 hrs
22
Q

What do neutrophils recognize?

A
  1. Antigen via TLR

2. Opsonised antigen via CR and Fc receptors

23
Q

How do neutrophils kill pathogens?

A
  1. Phagocytosis
    - phagolysosome formed and antigens inside killed by oxygen dependent and independent mechanism
  2. Secretes toxic granules (anti-microbials e.g. defensins, lactoferrin)
    And chromatic (DNA and histones) forming neutrophil extracellular traps (NETs)
24
Q

What cytokines are released by neutrophils?

A

IFNgamma:

Macrophage activation, increased MHC proteins

25
Q

How long do neutrophils survive?

A

Short lived cells:

A couple of days

26
Q

Eosinophils

A
  1. Kill extracellular parasites too large to engulf (E.g. helminths) by releasing highly toxic granules and ROS
  2. Synthesize prostaglandins & cytokines which amplify the immune response - inflammation
  3. Levels increase when Th2 cells secrete IL5
  4. Can act as phagocytes
  5. Involved in allergic responses
27
Q

Basophils

A
  1. Have receptors for IgE
  2. Release histamine, IL4 when activated
  3. Promote Th2 development
  4. Involved in allergic responses and inflammation
28
Q

Mast cell

A
  1. Sentinel cells present in the skin, mucosal epithelium, and connective tissues that rapidly secrete proinflammatory cytokines & lipid mediators in response to infections and other stimuli
  2. Express receptors for IgE antibodies (Fc receptors) and TLR
  3. When activated they release histamine (cause vasodilation and increase capillary permeability) and lipid mediators e.g. prostaglandins
  4. Promote acute inflammation and provide defense against helminths
  5. Plays a role in allergic reactions
29
Q

Life span of mast cell

A

Weeks to months

30
Q

Helminths

31
Q

Natural killer cells

A

Lymphoid lineage cell important for killing cells infected with cytoplasmic pathogens and cancer cells

32
Q

How do natural killer cells recognize cells?

A
  1. Receptors for stress receptors (MICA) on infected cells
  2. Receptors which bind MHCl in cells e.g. KIRS
  3. Receptors for antibodies (FcR)
33
Q

How are natural killer cells activated?

A
  1. By IFNalpha (dendritic cells)
  2. IFNbeta (fibroblasts)
  3. IL12 (macrophages)
34
Q

How do natural killer cells kill infected cells?

A
  1. Apoptosis induction by perforin & granzyme
    - increase stress receptors on infected cells together with lack of MHCl on infected cells
    - infect cells coated in antibody (ADCC)
35
Q

Cytokines secreted by natural killer cells

A

IFNgamma:
Activates macrophages
Increase MHC expression and antigen processing
Suppresses TH2

36
Q

Lifespan of natural killer cells

37
Q

Dendritic cells

A

[Phagocytes and antigen presenting cells (APC)]

  1. Most important cell in activating naive T cells
    - link between innate and adaptive immune system
  2. Recognize pathogens via TLRs and mannose receptor & opsonised pathogen via CR
  3. Phagocytose pathogen and degrade in phagolysosome
  4. This activates dendritic cell to produce co-stimulatory proteins and chemokine receptors
  5. Further activated by IFNalpha and IFNbeta
  6. Moves via chemokine gradient in lymph to nearest lymph node
  7. Present antigen to naive T cells
38
Q

Cytokines produced by dendritic cells

A
  1. TNFalpha
    - enhances endothelium permeability & expression of adhesion molecules & inflammation
  2. IL6
    - acts on liver to cause production of acute phase proteins E.g. C reactive protein, mannose binding lectin and cause fever
  3. IL1
    - fever
  4. IL12
    - activates NK cells and production of Th1 cells
  5. IFNalpha
    - antiviral
    - increased MHCl
39
Q

Dendritic cell lifespan

A

Days to weeks

40
Q

Definition of Inflammation

A 
Calor (heat) 
Dolor (pain) 
Rubor (red) 
Tumor (swelling) 
Loss of function (immobility)
41
Q

Inflammation

A
  1. Initiated by injury to or infection in tissue
  2. Chemokines and cytokines releases by macrophages,
    Mast cells and damaged cells cause vasodilation resulting in increased local blood flow & permeability of endothelial cells resulting in increased leakage of fluids into tissues accounting for heat, redness and swelling
    - accumulation of complement and MBL in tissues which aid in host defence
  3. Increased neutrophils and monocytes move to the area
  4. Induces local blood clotting which provides a barrier to spread or infection
  5. Released mediators such as TNFalpha, bradykinin & histamine stimulate nerve endings, give rise to pain
  6. The loss of function due to swelling and pain
  7. Inflammation prevents spread of damaging agents, removes cell debris and pathogens, alerts adaptive immune system and sets the stage for repair

MOL MED block 1 (26 decks)

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