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Pathology (Immunology) > IMED4111 - Introduction to Immunology - Thurs Week 7 > Flashcards

IMED4111 - Introduction to Immunology - Thurs Week 7 Flashcards

1
Q

What is the innate immune response?

A

> RAPID response to infection
Relatively non-specific

> responds the same way each time a foreign substance is encountered
orientates the adaptive immune system
maintains tissue integrity and repair

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2
Q

What does the innate immune response consist of?

A

Physical barriers (skin, mucosal membranes, saliva, mucous)

  1. Soluble proteins (complement, acute phase proteins - interleukins IL1, IL6, IL8, TNF-alpha, anti-microbial peptides)
  2. Cellular components (neutrophils, macrophages, NK cells)
  3. Cytokines (IFN-gamma, TNF-alpha) - cell-cell communication
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3
Q

What is the acute phase response?

A

> immediate inflammatory response which is INITIATED by the recognition of pathogen (innate immunity)
release of acute phase proteins in response to inflammatory stimuli

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4
Q

What are the 4 STEPS of the acute phase response?

A

STEP 1 - Innate immunity senses non-self (conserved structures)

STEP 2 - cytokines produced

STEP 3 - acute phase reactants produced locally and by the LIVER

STEP 4 - measures to localise spread of infection and enhance systemic resistance to infection - RESPONDERS COME TO SITE OF INFECTION

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5
Q

What are pattern recognition receptors (PRRs)?

A

Pattern recognition receptors are a way that the innate immunity recognises non-self

  • they recognise, altered, oxidsed, damaged cells
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6
Q

What are Pathogen Associated Molecular Patterns (PAMPs)?

A

Pathogen associated molecular patterns (PAMPs) are conserved elements on pathogens (usually on-human cells) that Pattern recognition receptors (PRRs) recognise

> PAMPs include Lipopolysaccharide (LPS), Flagellin, dsRNA, unmethylated CpG DNA

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7
Q

What are Damage/Danger Associated Molecular Patterns (DAMPs)?

A

These are molecules that are normally sequestered within cells but are released as a result of tissue damage.

> e.g. tumour DNA, hsp, uric acid, heparin sulfate

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8
Q

What are two main types of Pattern Recognition Receptors (PRRs)?

A

Toll-like Receptors (TLR) and Nod-like Receptors (NLR)

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9
Q

What are Toll-Like Receptors (TLR)?

A

They are the most important Pattern Recognition Receptors (PRRs).

> highly conserved
recognise a range of PATHOGEN-ASSOCIATED molecules from bacteria and viruses

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10
Q

Where are Toll-Like Receptors (TLRs) located?

A

Toll-like Receptors (TLRs) are located:

> cell surface
walls of intracellular vesicles (PARTICULARLY in dendritic cells and macrophages)

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11
Q

What do Toll-Like Receptors (TLRs) activate?

A

> NFkB, AP-1
to induce pro-inflam cytokines & chemotactic factors

> Interferon Regulatory Factor (IRF) to induce antiviral type I interferons (IFN alpha and IFN beta)

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12
Q

What are NOD-like receptors (NLRs)?

A

Intracellular PROTEINS and a type of Pattern Recognition Receptors (PRRs), and are expressed in the cytoplasm of cells that are regularly exposed to bacteria

> GUT epithelial cells
dendritic cells
macrophages

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13
Q

What is NOD2?

A

NOD2 is a protein of the NOD-like Receptor (NLR) family.

NOD2 proteins recognise intracellular MDP (muramyl dipeptide), which is a peptidoglycan constituent of both Gram positive and Gram negative bacteria.

> activating the NF-κB protein and other pro-inflammatory genes

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14
Q

Where is NOD2 strongly expressed?

A

Paneth cells (epithelium of small intestine)

  • regulate potent antimicrobial peptides
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15
Q

What is an example of a disease associated with NOD2 loss of function?

A

Crohn’s disease

> type of Inflammatory Bowel Disease (IBD)

> Chronic inflammatory disorder, in which the body’s immune system attacks the gastrointestinal tract possibly directed at microbial antigens - NOT AUTOIMMUNE THO

> loss of antimicrobial activity results in heightened T-cell mediated inflammation

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16
Q

What are NALPs?

A

NALPs is a subfamily of NOD-like Receptors (NLRs)

NALP3 is best characterised (also known as cryopyrin or NLRP3) and has a pyrin domain

17
Q

What is NALP3?

A

> Best characterised NOD-like Receptor (NLR) from the NALP subfamily
also known as Cryopyrin or NLRP3

> has a pyrin domain
expressed primarily in macrophages as a component of the inflammasome

18
Q

What is the inflammasome?

A

> Multi-protein complex (3 components)

> It is expressed in myeloid cells and is a component of the innate immune system

> promotes maturation of the inflammatory cytokines IL-1β & IL-18

19
Q

What activates the inflammasome?

A

Urate Crystals

Causes Gout

20
Q

What disease are associated with mutations in NALP3?

A

Inappropriate increased activation of the inflammasome

Two types of HEREDITARY periodic fever syndromes
> Muckel-Wells

> Familial Cold inflammatory Syndrome

21
Q

What is C reactive Protein (CRP) and what does it do?

A

> pro-inflammatory acute phase protein
important opsonin

> binds to bacterial structures, damaged cell membranes, apoptotic cells and microorganisms
protection against gram negative bacteria strep. pneumoniae by mopping up dead cells

22
Q

Where is C Reactive Protein (CRP) produced and how?

A

> Produced by the Liver
production is influenced by IL-6
short half life (19h)
CRP levels rise rapidly

23
Q

What is C Reactive Protein useful for?

A

BEST MARKER FOR ACUTE PHASE RESPONSE

> organic disease screening
monitoring responses
diagnosis of infection in immunosuppressed patients
risk factor for CVD

BUT does not rise in Systemic Lupus Erythematosus (SLE), Sjogrens or UC

SO look for a cause in these patients if they have a raised CRP

24
Q

What is Systemic Lupus Erythematosus (SLE)?

A

Systemic lupus erythematosus is a systemic autoimmune disease -

  • body’s immune system mistakenly attacks healthy tissue.
25
Q

What is Sjogrens Syndrome?

A

> chronic autoimmune disease in which the body’s WBC destroy the moisture producing glands of the body

26
Q

What is Ulcerative Colitis (UC)?

A

Ulcerative colitis (UC) is a form of inflammatory bowel disease (IBD) that causes inflammation and ulcers in the colon.

27
Q

Describe the process of local recruitment including

  1. Rolling Adhesion,
  2. Tight Binding and
  3. Diapedesis & Migration
A
  1. Neutrophils normally roll along endothelial walls. E-selectin adhesion to Sialyl-Lewis x on leucocytes is too weak
  2. Inflammation causes the upregulation of adhesion molecules, allowing neutrophils to be anchored.

On Endothelial walls, TNF-alpha (inflammatory cytokine) causes the expression of ICAM-1 and ICAM-2.

On Neutrophil surfaces, Chemokine CXCL8 upregulates expression of integrins such as LFA-1.

  1. Neutrophils extravasate - squeeze between endothelial cells and traverse basement membrane
    - follow chemokine gradient to site of inflammation
28
Q

What is phagocytosis? What is the process

A

Internalisation of pathogen

  1. Receptors on phagocyte bind to components of microbe
  2. internalisation into a phagosome
  3. killing by two ways - phagosome acidification or fusion with a lysosome which contains hydrolytic enzymes to form a phagolysosome
  4. macrophages and neutrophils then also produce anti-microbial peptides
29
Q

What are the two ways that phagosomes kill microbes?

A

Phagosome acidification

Phagosome fusion with lysosome to form a phagolysosome

30
Q

What are the three major classes of innate phagocytes

A

Granulocytes (Polymorphonuclear leucocytes - PMNLs) - neutrophils, basophils, eosinophils

Macrophages

Immature Dendritic Cells

31
Q

How many neutrophils are produced in a day?

A

1x10 ^11

32
Q

How long do Neutrophils circulate in the blood for?

A

6 hours

33
Q

How are neutrophils removed from the body?

A

by Macrophages in the liver or spleen

34
Q

How long from detection of microbe until adaptive immunity kicks in?

A

Innate immunity is from about 0 to 12 hours. Then Adaptive Immunity is for days after the infection

35
Q

What are the two sub-types of Adaptive Immunity?

A

Humoral and Cell-mediated immunity

Pathology (Immunology) (1 decks)

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