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Microimm 2500 > (I) Lecture 4: Innate Immunity Part III > Flashcards

(I) Lecture 4: Innate Immunity Part III Flashcards

1
Q

Immune Proteins

A

Cytokines
Complement Proteins (C3a and C3b)
Antibodies (Adaptive Immunity)

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2
Q

Types of Cytokines

A

Interleukins
Interferons
Tumor Necrosis Factors
Chemokines

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3
Q

Cytokines

A

Chemical messages (proteins that communicate w/ cells)

  • target cells can only respond if they have a receptor for it
  • cytokine receptors have HIGH AFFINITY = powerful biological responses
  • regulates hematopoiesis
  • have a role in BOTH innate and adaptive immunity
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4
Q

Responses induced from interaction btwn cytokines and their receptors

A
  • changes in expression
  • increase/decrease enzyme activity
  • induce differentiation
  • modulate effector functions
  • cell survival/death
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5
Q

Mode of action of cytokines

A

secreted cytokine binds SPECIFIC receptors

signal transduction pathway
- stimulus triggers cell to translate stimulus into expression of cytokine –> cytokine binds receptor –> biological response

Pleiotropy, redundancy, cascade induction

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6
Q

Pleiotropy

A

SAME cytokine act on DIFFERENT cells to evoke different responses

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7
Q

Redundancy

A

DIFFERENT cytokines evoke SAME response in cells

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8
Q

Cascade induction

A

action of a cytokine INDUCES PRODUCTION of one or more additional cytokines

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9
Q

Pro-inflammatory cytokines

A

Their presence triggers inflammation

Interleukins (IL): IL-1 and IL-6

Tumor Necrosis Factor (TNF): TNF alpha

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10
Q

Chemoattractant cytokines

A

Chemokines

cell recruitment to site of infection

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11
Q

Antiviral response cytokines

A

Interferons (IFN): Type I IFN

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12
Q

Homeostasis and cytokines

A

Cytokine networks moderate the cross-talk btwn epithelial cells w/ innate and adaptive immune cells to maintain homeostasis

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13
Q

Disruption of cytokine-guided cross-talk

A

Leads to initiation of inflammation (mostly by innate derived pro-inflammatory cytokines)

leads to IBD (inflammatory bowel disease)

If unresolved, it can lead to chronic inflammation since immune cells attack epithelia

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14
Q

Phagocytosis and inflammation

A

Phagocytosis results in inflammation

  1. Sensing PAMP/PRR (PAMP binding to PRR also triggers production of cytokines = inflammation)
  2. Phagocytosis
  3. Starvation/Intoxication
  4. Killing
  5. Signaling
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15
Q

Chemokines

A

chemoattractant cytokine

attracts immune cells to infected tissues

BOTH immune and epithelial cells secrete chemokines

immune cells w/ chemokine receptors are recruited from blood into specific tissue

inflammatory trigger causes release of chemokines = neutrophils go to site of infection

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16
Q

PAMP-PRR binding

A

Leads to phagocytosis and cytokine secretion

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17
Q

Signs of Inflammation

A

DOLOR: pain
RUBOR: redness
CALOR: heat
TUMOR: swelling
FUNCTIO LAESA: loss of function

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18
Q

Inflammation

A

dilation and increased permeability of endothelial cells

  • increased local blood flow
  • leakage of fluids and blood proteins into tissues
  • extravasation (leakage) of immune cells into tissues
  • results in heat, redness, and swelling

leads to increase in immune cells and enhanced clearance of pathogens

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19
Q

Neutrophils in the immune system

A
  1. Neutrophil sense bacteria
  2. Neutrophil slows and squeezes through blood vessel
  3. Neutrophil moves towards bacteria which have been marked by antibodies for ingestion
  4. Neutrophil engulfs and destroys marked bacteria
20
Q

Pathogens and inflammation

A
  1. bacteria/viruses trigger macrophages to release cytokines and chemokines
  2. vasodilation and increased vascular permeability cause redness, heat and swelling
  3. inflammatory cells migrate into tissue and release inflammatory mediators that cause pain
21
Q

Why is inflammation a good thing?

A

inflammation quickly recruits circulating immune cells into infected tissue to enhance immune defenses

  1. cytokines produced by macrophages cause dilation of local small blood vessels
  2. leukocytes move to periphery of blood vessel as a result of higher expression of adhesion molecules
  3. WBCs extravasate at site of infection
22
Q

Fever

A

an early response to infection

pathogens activate phagocytes
phagocytes release cytokines
cytokines stimulate hypothalamus
hypothalamus produces prostaglandins
prostaglandins trigger fever

may help to combat infection by reducing growth rate of microbes (highly debated)

23
Q

Liver and infection

A

Cytokines can act on liver to promote release of acute phase proteins like CRP and Complement 3 protein

24
Q

CRP

A

C-reactive protein

used clinically to quantify inflammation

25
Q

Complement System

A

50-plus serum proteins that cooperates w/ both innate and adaptive immune systems to ELIMINATE PATHOGENS

26
Q

Complement proteins

A
  • directly kill microbes by forming the MAC (Membrane Attack Complex) = target pathogens for cell lysis and activation
  • decorate pathogens to promote phagocytosis (opsonization)
  • recruit immune cells/inflammation
27
Q

Complement Protein 3

A

Cleaved into C3a and C3b

28
Q

C3a

A

Maintains inflammation

  • recruits phagocytes to site
  • acts a cytokine
29
Q

C3b

A

helps w/ opsonization (coating of a surface of a pathogen with antibodies and complement proteins to promote PHAGOCYTOSIS)

  • bacterium is coated w/ C3b
  • when only C3b binds to CR1, bacteria are not phagocytosed
  • C5a can activate macrophages to phagocytose via CR1
  • helps phagocytes recognize pathogen faster and better
30
Q

Interferons

A

type of cytokine that are important in directing ANTIVIRAL responses

Type I Interferon: IFN alpha and IFN beta

  • critical to antiviral immune response
  • rapidly secreted by virus-infected cells
31
Q

Cytokine release and IFNs

A

Type I IFN is RAPIDLY secreted after a viral infection

after cytokine release, a wave of NKC follows

they control viral replication together

32
Q

Virus-infected cells and PRRs

A

Have PRRs expressed on the surface and inside of cells

Viruses have BOTH extracellular and intracellular phases

Endosomal PRRs recognize components released during intracellular viral replication/degradation (ex. nucleic acids)

Surface PRRs recognize components on the outside of the virus

Viral particles bind PRR and triggers rapid expression of IFN by infected cell

33
Q

IFNs and NKCs

A

Type I IFNs promote NK cell killing of virus-infected cell

Virus-infected cell secretes chemokines (attracts NKCs) and Type I IFN (activates NKCs)

NKCs release toxic enzymes (perforin and granzye) to target infected cell for apoptosis

34
Q

Viral Survival

A

some viruses can block IFN secretion and signaling

  • express effectors that act to suppress IFN expression (ex. hepatitis, polio, SARS-CoV2)
  • Need To cell immunity to fight them off

Type I IFN are used to treat SOME viral infections (ex. herpes and hep B)

35
Q

Cytokine Therapy

A

Cytokine inhibitor industry continues to grow

used for asthma, rheumatoid arthritis and some cancers to reduce inflammation

IFNs are used as therapy for MS

36
Q

Effector Function of Cytokines

A
  • phagocytosis (extracellular)
  • NK-mediated apoptosis (intracellular viruses)
  • inflammation
37
Q

Innate immunity response time

A

Rapid (seconds, minutes, hours)

38
Q

Innate immunity specificity

A

Broad (conserved molecular patterns only found in pathogens)

39
Q

Innate immunity diversity

A

Limited diversity

Germline-encoded receptors

40
Q

Innate immunity main cells

A

Phagocytes, NK cells, epithelial cells

41
Q

Innate immunity proteins

A

Proinflammatory cytokines, type I IFNs, tumor necrosis factors, chemokines

42
Q

Innate immunity mechanism of pathogen destruction/inactivation

A
  • Phagocytosis
  • Apoptosis
  • Chemical attack by antimicrobial peptides
43
Q

Innate immunity immune response

A

Non-adaptive = same response for every exposure to identical pathogen

44
Q

Innate immunity memory

A

NO memory is formed

45
Q

Innate immunity efficiency

A

Rarely malfunctions

46
Q

Innate immunity intracellular viruses

A

Microimm 2500 (29 decks)

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