07 - Innate Immunity Flashcards

1
Q

What is immunology

A

study of the immune system and immune response (study of the body’s defense against infection)

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2
Q

What is the function of the immune system

A

prevent infection and eradicate established infections (maintain homeostasis)

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3
Q

What is immunity

A

resistance to disease

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4
Q

What is the immune system

A

functional system (rather than organ system)
- array of molecules and trillions of immune cells that inhibit lymphoid tissues and circulate in body fluids

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5
Q

What are primary lymphoid organs

A

where pluripotent stem cells divide and become immunocompetent (able to protect)
(where immune cells are born and develop)

red bone marrow and thymus

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6
Q

What are secondary lymphoid organs/tissues

A

sites where immune cells continue their maturation and can connect with one another to initiate adaptive immune responses
(where immune responses occur)

lymph nodes, spleen, lymphatic nodules/follicles

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7
Q

Describe red bone marrow
What does it do

A

in flat bones. epiphyses of long bones, bodies of vertebrae

pluripotent stem cells give rise to mature, immunocompetent B cells and immature (pre) T cells

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8
Q

Describe the thymus
What does it do

A

bilobed organ located in the anterior mediastinum

between the sternum and the aorta

where immature T cells go to develop into mature T cells
(early in life lots of T cells but then gland gets smaller and smaller – protection of new T cells reduce)

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9
Q

Describe the lymph nodes

A

small organs distributed throughout the body

along the lymphatic vessels - filters for lymph

places where cells of the adaptive immune system “meet up”
- site where innate immune cell that encountered a pathogen goes to alert adaptive immune system

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10
Q

Describe the spleen

A

largest secondary lymphoid organ

one of its important functions is the removal of damaged/defective RBC (contains phagocytes)

sequester platelets (releases)

lymphoid organ: has WBC will detect if there are any pathogens/toxins floating in the blood

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11
Q

Describe the lymphatic nodules

A

organized masses of lymphatic tissue
- aggregations of immune cells sitting right under the epithelial barrier waiting for something to come in

not surrounded by a capsule
- embedded in the walls of organs

commonly associated with mucosal surfaces (MALT)

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12
Q

Describe the innate immune system

A

non specific - responds to anything that injured tissue

1st and 2nd line of defence
- 1. skin and mucous membranes
(continuity, fluids/secretions/ microbiome)
- 2. internal defenses (antimicrobial proteins, NK cells/phagocytes, inflammation, fever)

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13
Q

Describe the adaptive immune system

A

highly specific (identifies a specific antigen)

3rd line of defence

specific cell types and/or proteins are generated that attack foreign substances
- has memory (conferring lifelong protection)
- humoral immunity (plasma cells)
- cellular immunity (T cells)

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14
Q

Describe the first layer of defense

A

skin and mucous membranes (intrinsic barriers)
- physical (b/c continuity), chemical, biological

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15
Q

What are the barriers of the first line of defense

A

skin

eye
- blinking, tears, lysozme

respiratory tract
- coughing, sneezing, mucus, haris, ciliary action, lysozyme

gastrointestinal tract
- stomach acid, peristalsis, normal flora (B - commensal bacteria that take up space on the epithelium that prevent nasties from attatching)

urogenital tract
- flushing action of urine (P), acidity of urine (C), lysozyme, normal flora, vaginal lactic acid

skin
- sloughing (generating new cells and getting rid of the old), structural barrier, sweat/sebum, lysozyme, normal flora

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16
Q

Describe the second layer of defense
What are the cells and factors

A

non specific line of defense when pathogens penetrate the surface barriers

cells & factors:
- antimicrobiral proteins
- natural killer cells
- phagocytes
- imflammation

17
Q

What are antimicrobial proteins

A

enhance innate defence by attacking microorganisms directly or hindering their ability to reproduce

  • interferons (small secreted proteins that interfere with viral replication –> secreted by host cells)
  • complement system (cascade (already present) of interacting plasma proteins that
    1. promote phagocytosis of phathogens
    2. cause cytolysis of bacteria (poke holes)
    3. enhance inflammation (vascular response – allows WBC to go out))
  • iron-binding proteins (inhibit bacterial growth by binding iron
  • antimicrobial proteins (short peptides with broad spectrum antimicrobial activity)
18
Q

What are natural killer cells

A

unique group of defensive cells

large, grandular lymphocytees

found in blood and tissues

can kill tumour and virally infected cells and dock with the cell and tell it to die using:
- perforin (make a hole in the cell)
- granzyme (promotes break down of DNA in the cell –> apoptosis)

attack cells that display activation receptors that lack inhibition receptors

from the same lineage as adaptive cells (lymphocytes) but part of the innate response
- no immunological memory, doesn’t get better every time

19
Q

What do phagocytes do
What are the phases

A

engulf foreign microbes and/or debris

phases:
1. chemotaxis: follow chemical trail to site of damage/infection
2. adherance: attachment to pathogen/debris
3. Ingestion: phagosome interalizes pathogen/debris
4. Digestion: phagosome fuses with lysosome that contains enzymes to break down proteins, lipids,… (H2O2, O2-, OCl-)
5. Killing/elimination
washed away by lymphatics

20
Q

What are the types of phagocytes

A

neutrophils
- most abundant leukocyte (WBC) in blood
- major component of pus (short life span)
- 1st phagocyte to move from blood to tissue during an inflammatory response (not present in healthy tissues - normally in blood sleeping, only activates when needed) –> do collateral damage

macrophages
- begin as monocytes in the blood
- move into tissues and mature into macrophages (big eaters)
- long life span
- reside in tissues, wander tissues looking for debris/invaders –> release cytocines to signal other things to come in or tell adaptive tissues to help)

dendritic cells
- tissue-resident (long lifespan)
- antigen-presenting cell (take whatever they encounter and take it to t-cells and b-cells to tell to kill)
- bridge gap between innate and adaptive immunity)

21
Q

How do phagocytes recognize the pathogens they need to kill

A
  • use pattern recognition receptors (PRRs) to “see” pathogen-associated molecular patterns (PAMPs) –> encoded in our DNA
  • PRR binds to PAMP –> generates a signal that stimulates the phagocyte
  • signals through some receptors causes the secretion of pro-inflammatory cytokins (talk to other immune cells, blood vessels, endothelial cells…)
22
Q

What is inflammation

A

non-sepcific, defensive response to any tissue damage (Doesn’t have to be a pathogen)

delivers effector molecules and cells to the site of infection to assist in killing microbes
- stimulates and assists the immune systen
- prepare site for tissue repare
- very localized

23
Q

What are the three stages of inflammation

A
  1. vasodilation and increased permeability of blood vessels (vascular response)
  2. emigration of phagocytes from blood to the infected site (cellular response)
  3. tissue repair (healing)
24
Q

What is the intial response of inflammation

A

damaged cells signal that something is wrong “chemical alarm”
- inflammatory mediators released into the extracellular fluid

resident macrophages become activated (PRRs)
- phagocytose pathogens
- release cytokines and chemokins –> signal the kind of help needed as well as directions

resident mast cells release potent inflammatory mediators
- histamine (major product)
- contribute to many aspects of the inflammatory response (vasodilation and increased vascular permeability)

within the first hour, see an influx of neutrophils and monocytes (immature macrophages)

25
Q

What are the signs and symptoms of inflammation

A

inflmmation usually localized and self-limiting (turn off by itself)

  1. redness (rubor/erythema) - due to increased blood flow
  2. heat (calor) - due to increased localized blood flow and cellular activity
  3. swelling (tumor/edema) - due to increased vascular permeability - cells/fluids/prtoeins collect in the tissue
  4. pain (dolor) - due to the swelling (stretching) and the release of neurotramitters and other chemical mediators (bradycardin..)
  5. loss of fucntion (funcio laesa) - due to swelling and the release of neurotransmitteres and other chemical mediators
26
Q

What happens to blood vessels during inflammation

A

released mediators change local blood vessels
- increased vascular diameter: increased local blood flow
- reduction in blood flow velocity: gives cells a change to bind
- increased vascular permeability: cells leave blood and enter site of injury
- blood and fluid exit into the tissues: cause of edema
- immune cells emigrate/migrate/extravasate from the blood vessels to the tissue to help eliminate injurious agents

clotting of micro-vessels prevents spread of infection (trapping)

27
Q

What is fever

What is the cause

A

abnormally high body temperature
- systemic response to invading microorganisms

body’s response to infection is more widespread

many cytokines (pyrogens) that they spill into the blood and get to hypothalamus and signals massive infection
- hypothalamus raises set point for temperature

28
Q

How does fever help

A

mild to moderate fevers are useful adaptation to infection
- immune cells work harder and faster
- sequestration of iron and zinc by the liver and spleen
- bacteria need these minerals to multiply

pathogens and viruses can’t replicate in conditions

(excess heat denatures proteisn and enzymes can lead to brain lesions)