IM 2

Question 1

innate immune reponses

Answer 1

• 2nd line of defense ; defense without specific recognition
• recognize general molecular property marking invader as foreign (pathogen-associated molecular patterns)
• “identity” often carbohydrates or lipids on cell surface

-many cases innate response is to contain and limit spread of infection while adaptive mounts a more specific response

Question 2

toll-like receptors - innate immune response

Answer 2

• toll proteins on immune plasma membrane act as pattern-recognition receptors
• bind large numbers of pathogen-associated molecular patterns
• trigger cytokine secretion (cytokines : small proteins involved in cell signaling)
• generate an innate immune response

Question 3

interferon - “interfere” with viral replication

Answer 3

-cells infected with viruses produce proteins (interferons)

Question 4

type 1 interferon

Answer 4

• released from virus infected cells into extracellular fluid and bind non-infected cells
• non-infected cells start producing antiviral proteins that can prevent viral replication if become infected
• can target most cells in body (as long as have type 1 interferon receptor)

Question 5

type 11 interferon : interferon-gamma

Answer 5

• potentiates (increases effect of) type 1
• releases cytokines : proliferation some immune cells, secretion cytotoxic chemicals
• targets macrophages and NK cells (giving “activated” versions)

Question 6

phagocytosis

Answer 6

process where pathogens and cellular debris are engulfed and destroyed

Question 7

phagocyte

Answer 7

any cell that can do phagocytosis

Question 8

neutrophils and macrophages - best

Answer 8

• *neutrophils** - quick response
• *macrophages** - largest capacity

-migrate to damaged area as neutrophils and monocytes (convert to macrophages)

Question 9

4 phases of phagocytosis

Answer 9

adherence/ ingestion/ digestion/ killing

AIDK

aido is dumb kunt

-contact can also cause release of cytokines

Question 10

alternative complement pathway

Answer 10

• plasma proteins (at least 30) from liver, circulate inactive in blood
• C3 activation by contact with microbe surface leads to cascade of activations
• activated proteins “complement” or enhance immune reactions
• development of membrane attack complex (MAC) by proteins C5-9
• embeds itself in pathogen forming pore-like channels
• killed by inflow entering intracellular compartment
• C3b acts like an opsonin (marker) - phagocytosis enhancement
• see later: effect vasodilation, blood vessel permeability, chemotaxis during inflammation

Question 11

inflammation

Answer 11

local responses to tissue damage

Question 12

sources of inflammation

Answer 12

• pathogens
• abrasions
• chemical irritants
• cell distortion or disturbance
• extreme temperature
• inflammatory response is remarkably similar no matter triggering event

Question 13

characteristic symptoms of inflammation

Answer 13

• redness
• pain
• heat
• swelling
• can also be loss of tissue function in area sometimes

Question 14

inflammatory response

Answer 14

-often some resident immune cells (like fixed macrophages) at injury location but may not be enough to deal with damage

Question 15

goals of inflammatory response

Answer 15

• isolate, destroy or inactivate invader
• remove debris
• prepare for wound healing and tissue repair

example : a wood splinter has introduced bacteria through the skin defenses

Question 16

stage 1 inflammatory response

Answer 16

• vasodilation and increased permeability of blood vessels
• release of inflammatory mediators : histamine, kinins, prostaglandins, complement proteins, cytokines, etc.

Question 17

local effects inflammatory response stage 1

Answer 17

• vasodilation microcirculation : increases blood flow; delivery of leukocytes, plasma proteins, nutrients, oxygen (outward signs: local redness, heat)
• increased permeability : endothelial cells contract, opening spaces between them (will lead to chemotaxis into tissues from blood)

Question 18

non-local effects - inflammatory response stage 1

Answer 18

• inflammatory mediators in blood trigger proliferation new immune cells (bone marrow)
• mobilization of stored immune cells (spleen, lymph nodes)

Question 19

stage 2 - inflammatory response

Answer 19

movement by phagocytes into injury site from blood (within 1 hour)

• neutrophils early, later monocytes (mature into wandering macrophages)

Question 20

3 steps of stage 2

Answer 20

MDC My Dark Crayon

margination : phagocytes and local endothelium each form adhesion molecules for attachment to local area

diapedesis : phagocyte migration through blood vessels walls into interstitial fluid of tissue

chemotaxis : phagocyte migration to injury site guided by cytokines (chemoattraction)

• fluid follows; local distension (outward signs: some edema/swelling, pain)
• cytokine can come from a number of sources and attract other needed things (other cells, proteins)

Question 21

stage 3 -tissue repair

Answer 21

final stage of inflammation

• worn out, damaged, or dead cells replaced
• fibroblasts (connective tissue cells) divide rapidly producing large amounts of collagen
• new network blood vessels forms (angiogenesis): helps remove debris and delivers needed nutrients and oxygen
• local growth factors released from different cells control process
• remodelling may continue after initial repair
• depending on the tissue
• repair may leave no sign
• in other cases a scar (scar tissue: denser collagen fibers, decreased elasticity, fewer blood vessels)