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IMI > Cells of the innate immune system > Flashcards

Cells of the innate immune system Flashcards

1
Q

who demonstrated bacteriolysis and hemolysis

A

Paul Ehrlich

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2
Q

roles of complement system

A

to opsonise foreign substances by marking to make them more visible, puncture the membrane of foreign substance and to signal the IS when there is foreign

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3
Q

describe the classical pathway

A

activated by antibodies, and C1 (Recognition C1q and proteases C1s and C1r) binds to antibody-antigen complexes to activate it. Once active, C1 triggers the cleavage of C2 into C2a and C2b, and C4 into C4a and C4b. C2a and C4b combine to form C3 convertase.

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4
Q

name the three pathways that initiate activation of C3 into C3b

A

classical pathway, lectin pathway, and alternative pathway

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5
Q

describe lectin pathway

A

triggered by PAMPs. Lectins bind specifically to carbohydrate molecules on the surfaces of pathogens. Mannose-Binding Lectins (MBLs) and ficolins (lectins) bound to the bacterial surface are opsonised by MBL-Associated Serine Proteases (MASPs). MASPs can cleave C4 into C4a and C4b. This promotes the cleavage of C2 into C2a and C2b. C2a and C4b combine to form C3 convertase.

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6
Q

describe the alternative pathway

A

C3 reacts with H20 to form C3H20 and binds to nearest exposed hydroxyl for activation and cleaves factor b into Bb. Bb binds to C3b to produce C3bBb - C3 convertase

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7
Q

function of factor p

A

stabilize C3 convertase and mediate C3 cleavage and responds to PAMPs

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8
Q

what does C3 convertase do

A

cleaves into C3a and C3b

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9
Q

describe the activation of C3

A

activation of c3 brings histidine residue into contact with thioester bond between cysteine and glutamine residue. This will react with any nearby hydroxyl group resulting in a covalent bond forming between activated C3 and macromolecule R on offending surface

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10
Q

what forms C5 convertase

A

C4bC2a3b and C3bBb3b

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11
Q

action of c5 convertase

A

cleaves C5 into C5a and C5b. C5a released and C5b covalently attached to surface

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12
Q

what does C3b and C5b do

A

immune cells bind to C3b or C5b on pathogen and trigger the phagocytosis and destruction of pathogen

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13
Q

Role of C3a and C5a

A

they are anaphylatoxins

they trigger inflammatory response to generate a chemotactic gradient for cells to find the source of infection.

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14
Q

Role of C3b and C4b

A

tell immune cells what to target and clear up the mess and identify bits of pathogen to be processed and presented

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15
Q

role of C5b

A

act as point of nucleation for pore that can peameabilize the membrane - disrupting osmotic balance and potentially lysing the cell

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16
Q

what produces the membrane attack complex

A

C5b recruits C6,7,8 and together catalyse the formation of a pore composed of ring of C9 molecules

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17
Q

role of MAC

A

to lyse cells which its components have been attached

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18
Q

what pathogens are resistant to MAC

A

pathogens with thick wall, MAC cannot penetrate

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19
Q

what inhibitors of the complements are soluble and what do they target

A

Factor I and Factor H, they target C4b, C3b and C3bBb respectively.

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20
Q

Function of membrane cofactor protein

A

recruits factor I to degrade C3b and C4b, prevent cells from being killed by alternative pathway

21
Q

Function of accelerating factor

A

dissociate subunit of C3 convertase

22
Q

function of CD59

A

bind C5b678 to prevent binding of C9 to prevent pore formation

23
Q

what makes up the myeloid lineage

A

granulocytes (neutrophils, basophils, eosinophils, mast cells) and monocytes that can differentiate into macrophage or dendritic cells

24
Q

adaptation of multi-lobed nucleus in granulocytes

A

allow granulocytes to easily squeeze through gaps between endothelial cells and rapidly migrate from blood or lymphatic vessels into tissue in response to an infection

25
Q

What can neutrophils do

A

phagocytosis, degranulation to release noxious substances and NETosis to release neutrophils extracellular traps which sacrifice themselves . nets immobilize bacteria and locally concentrate noxious substances to kill them

26
Q

What are the three types of granules and their function

A

Primary - contain proteases and denfensins, secondary which is the most abundant contain lysozymes and lactoferrin, tertiary contain metalloproteinases which degrades bacterial protein and breaking down ECM

27
Q

function of eosinophil

A

release granules containing lipids promoting inflammatory response

28
Q

function of basophils

A

cannot phagocytose, release granules containing histamine and heparin for anticoagulant

29
Q

function of mast cells

A

release histamine

30
Q

what are the two types of monocytes

A

patrolling monocytes to maintain homeostasis and phagocytosis, inflammatory monocytes which respond to pro-inflammatory cytokines and differentiate into macrophages and dendritic cells

31
Q

what are the two types of macrophages and their roles

A

tissue-resident macrophage which maintain homeostasis, to sense PAMPs and alert other cells by sending cytokines and also to remove and digest apoptotic cells.
monocyte -derive macrophages respond to pro-inflammatory cytokine and produce pro-inflammatory cytokines to recruit other immune cells

32
Q

Action of DCs

A

internalize pathogens by phagocytosis and load onto MHCII and migrate to secondary lymphoid organs to present to naive T cells

33
Q

Function of B cells

A
  • Naïve B cells express a membrane bound form of immunoglobulin - B cell receptor (BCR) and upon activation they also produce antibody in a secreted form
  • Effector B cells producing only antibodies and lacking a BCR- plasma cells
34
Q

What are the types of T cells are their function

A

T helper cells with CD4 on their surface and cytotoxic T cells that release cytotoxic granules contains granzyme and perforin

35
Q

what is the difference between NK cells and T cells

A

NK cells cannot recognise repertoire of antigens as T cells do

36
Q

What is chemotaxis

A

Macrophages can be formed when monocytes migrate into infected tissues in response to cytokines (M-CSF)

37
Q

What is the function of phagocytosis

A

to destroy a pathogen and process material for presentation to the adaptive immune system

38
Q

What is the phagocytosis mechanis m

A
  1. Upon activation, the phagocytic receptors trigger actin filaments reorganization to form extension- pseodopodia that envelop and internalize the pathogen forming a phagosome
    1. Fusion of lysosomes with phagosome (phagolysosome)
    2. Material internalized in phagosome is then digested by proteolytic enzymes, modality vary on type of phagocytes
  2. Digested products are released from cell
39
Q

Describe the innate immune response

A
  1. During tissue injury, a message in the form of pro-inflammatory cytokine sent out by resident immune cells (eg. Resident macrophage, epithelial cells or mast cells
    1. Neutrophils cross rapidly from circulation and enter in the tissue to fight infection
    2. Neutrophils produce more inflammatory cytokines so monocytes get alerted
    3. Monocytes then respond by migrating from circulation into the tissue
    4. The pro-inflammatory cytokines (IL-6, IL-2 and TNF-a) present at site of infection promote monocyte differentiation into macrophage
      • Called inflammatory macrophages (M1)
      - Produce inflammatory cytokines that boost the infection-fighting ability and survival of other immune cells (neutrophils)
    5. To restore tissue homeostasis, macrophages scavenge and engulf all that has been left behind, as an after killing cleaning operation
40
Q

Describe tissue homeostasis

A
  • Apotosed neutrophils are tagged with ‘eat me’ signals such as phosphatidylcholine (PS) on their membrane
    • Signals recognised by macrophages that engulf neutrophils triggering stimulation of release of anti-inflammatory cytokines
    • Efferocytosis - phagocytosis of apotosed neutrophils
      • Helps to promote macrophages differentiate into non-inflammatory (M2 macrophage) capable of dampening inflammation (*similar to resident macrophage)
    • Low levels of TNF-a and IL-6 alongside increased levels of IL-10 and TGF-b provide molecular cues to re-establish tissue homeostasis and M1 to M2 transition
41
Q

Similarities between neutrophils and macrophages

A

both originate from bone marrow, • Both detect pathogens and produce inflammatory cytokines
• Both neutrophils and macrophages are phagocytes
• Both not only mediate inflammation, can also resolve or dampen inflammatory response
- Neutrophils sacrifice their life after fighting infection
- Macrophage remove them by efferocytosis initiating restoration of tissue homeostasis

42
Q

differences between neutrophils and macrophages

A

neutrophils have multilobed nucleus while macrophages have round nucleus. Neutrophils have granules filled with noxious substances while macrophages dont.
neutrophils mature in bone marrow, macrophages mature in tissues. Lifespan is much longer for macrophages. neutrophils is the first to attack bacteria while macrophages turn up later on

43
Q

Describe inflammation

A

Dilation of blood vessels to increase blood flow

  1. Structural changes in the blood vessels to allow extravasation of large plasma proteins (e.g. albumin) to form a provisional matrix within the tissue to allow attachment and survival of subsequently extravasated cells.
  2. Migration of leukocytes through endothelial wall and accumulation at the infection site
44
Q

What is the function of leucocyte adhesion cascade

A

allow effective migration of leucocyte from blood to tissue

45
Q

describe the leucocyte adhesion cascade

A
  1. Rolling
    • Selectins on leucocytes surface interacts with cell adhesion molecules (CAM) on the endothelial cell surface allowing capture of leucocytes by endothelium
    • Selectin/CAM interaction is relatively weak and leucocytes in this phase slow down their forward movement
    1. Activation
      • Interaction between chemokines and chemokine receptors
      • Trigger a signal that induces a conformational change in the integrins on leucocyte surface rendering them able to bind to their corresponding ligand on endothelial cells very tightly
    2. Arrest and adhesion
      • Altered integrins such as LFA-1 (lymphocyte function-associated antigen 1) now bind very tightly to adhesion molecules on endothelial cell surface - ICAM-1
    3. Diapedesis /Extravasation
      • The firm interaction between integrins and adhesion molecules triggers signals in the endothelial cells that loosen cell to cell interaction
      • Forming a breach that allows leucocyte to squeeze in the gap between cells and crawl into the inflamed tissue
46
Q

What happens after extravasation

A

cell migration follows a chemotactic gradient which guides the leucocyte to the site of infection- chemotaxis

47
Q

How macrophages kill the pathogen

A
  • Macrophages PRRs for example TLRs bind bacteria PAMPs and trigger signals that induce more inflammation (expression of pro-inflammatory cytokines)
    • Complement receptors (binding complement). Scavenger receptor (binding lipopeptides), C-type lectin receptor (binding sugars such as mannose), trigger phagocytosis
48
Q

What is the fate of the material digested by phagocytosis

A
  • The material digested can be expelled or assimilated
    • Macrophages and dendritic cells are also antigen presenting cells ; small portions or material digested is loaded into molecules called MHC II
    • These antigens loaded into MHC II are presented to T cells. This is a mechanism used by APCs and the innate immune system to alert the adaptive immune system
    • The adaptive immune system will help in the fight, if the innate immune system is unable to defeat the infection on its own

IMI (11 decks)

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