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Immunology Jenny > 9. Regulation of immune response > Flashcards

9. Regulation of immune response Flashcards

1
Q

Regulation by antigen

A
  • Chemical (polysaccharide vs protein)
  • Soluble vs intracellular
  • Large vs small doses
  • Competition between antigens and peptides
  • The route and administration of Ag
  • Role of adjuvants
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2
Q

Adjuvant definition

A

Wiki: betegner en substans, oftest farmakologisk eller immunologisk, som modifiserer og forsterker effekten av andre substanser (f.eks virkesoff i vaksiner), mens et adjuvant i seg selv har få, om noen, direkte virkning gitt alene.

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3
Q

Response depending on dose of antigen exposure

A

Low virus dose (0.3)
= high antiviral cytotoxicity (+++)
= mainly Th1 (IFNγ) response

High virus dose (1000)
= low antiviral cytotoxicity (+)
= Mainly Th2 (IL-4) response (?)

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4
Q

Significance of APC

A
  • Professional vs non-professional APC
  • CD40L (T-cell) - CD40 (APC) interaction
  • CD28 or CTLA4 (T cells) - CD80/CD86 (APC)
  • The level of expression of MHC on antigen presenting cell
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5
Q

CD80/86

A
  • On APCs

- Bind to CD28 (pos) or CTLA4 (neg) on T cells

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6
Q

PD-L1/2

A

“Programmed death ligand 1/2”

  • On APCs
  • Bind to PD-1 on T cells
  • Inhibits TCR-mediated activation of IL-2 production and T cell proliferation
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7
Q

MHC receptor binding

A
  • On APCs

- Bind to TCR, (Lag-3) and (CD160)

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8
Q

Ab blocking

A
  • Kind of regulation by Ab’s
  • Ab competes with B cells for Ag
  • > B cell suppression
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9
Q

Receptor cross-linking

A
  • Kind of regulation by Ab’s
  • Ag-Ab complexes bind to Fc receptors and send inhibitory signal to B cell
  • > B cell negative costimulation
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10
Q

B cell positive costimulation

A
  • Kind of regulation by Ab’s
  • Costimulation of B cells is by complement receptors
  • B cells express CR2 which can bind C3d
    Ag-Ab complexes bind C3d and localize to APC via CR2 -> positive costimulation
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11
Q

CD4+ further differentiation

A

In thymus

1) foxp3+ => Treg
2) foxp3- => Th

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12
Q

Features of Treg cells (Quantity, surface markers, cytokine expression/secretion, suppression mechanism)

A
  • Quantity: 5-10 % of Th
  • Surface markers: CD25, CD103, Foxp3 (!), GITR
  • Cytokine: IL-10, IFN-γ, TGF-β (and CTLA-4?)
  • Suppression:
    a) contact with activated target CD8+/CD4+ T cells
    b) secretion of cytokines: IL-10, IFN-γ, TGF-β
    c) secretion of non-specific inhibition (“bystander effect”)
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13
Q

Treg’s inhibit initial T activation?

A

No, they inhibit sustained response, and thus prevent chronic and potentially damaging responses
- Suppress Th1 and Th2 responses

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14
Q

iNK T cell

A

“Invariant NK T cell”

  • Express semi-invariant (semi-constant) TCR α chain (Vα14-Jα18)
  • Recognize lipid (glycolipid) antigens presented by CD1d on APCs
  • Cytokines: INFγ, IL-4, GMCSF ++
  • Wiki: respond rapidly to danger signals and pro-inflammatory cytokines
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15
Q

Breg cells mechanism

A

Main mechanism: production of anti-inflammatory cytokine interleukin 10 (IL-10)

  • Suppresses inflammatory reactions by T cells, especially Th1 reactions (maybe also Th17 and Treg)
  • Promotes maturation to adaptive Treg cell?
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16
Q

Breg cell receptors

A
  • TLR4 (binds to LPS)
  • BCR (binds to antigen)
  • CD80/86 (binds to CD28/CTLA4 on T cells)
  • CD40 (binds to CD40L on T cells)
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17
Q

Types of cytokines

A
  • Interleukins
  • Chemokines
  • Colony stimulating factors (CSF)
  • Interferons
  • Tumor necrosis factors
  • Adipokines
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18
Q

Stimulatory cytokines

A
  • Most cytokines can be both stim and inhib
  • IL-1
  • IL-2
  • IL-4-6
  • IL- 8
  • IL-12
  • IL-17
  • IL-18
  • IL-26
  • IL-27
  • IFNγ
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19
Q

Inhibitory cytokines

A
  • Most cytokines can be both stim and inhib
  • IL-4
  • IL-10
  • IL-11
  • IL-13
  • IL-22
  • IL-23
  • IL-33
  • IL-35
  • TGF-β
  • IFN-α/β
  • IFN-γ
20
Q

Regulation by cytokines

A
  • Can be positive or negative regulators
  • Dependent on milieu (other cytokines+receptors)
  • Regulate the type and extent of immune response generated
  • Soluble cytokine receptors could be agonists and antagonists
21
Q

Th1/Th2 paradigm

A
  • Th1 secretes IFNγ which inhibits Th2
  • Th2 secretes IL-4, IL-10, TGF-β which inhibits Th1
  • Th1 has to do with cell-mediated immunity, Th2 has to do with humoral immunity
22
Q

Peptide-binding groove of APC is formed by the most polymorphic residues in MHC molecules

A

Encoded by different alleles

23
Q

What determines the accuracy of peptide binding/Ag presentation of APC

A

MHC dependent aminoacid sequences of the groove

24
Q

MHC-linked genes

A
  • Control response to several infections
  • Influences susceptibility to autoimmune diseases (Non-MHC-linked genes also affect susceptibility to several diseases)
  • Certain HLA haplotypes confer protection from malaria
  • Control response to infection (certain HLA haplotypes are associated with responders/nonresponders, susceptibility/resistance)
25
Q

Linkage disequilibrium

A

“Nonrandom association of alleles at different loci”

- Grouping of some genes that increase the risk of particular disease (ex: HLA-DR3/DR4 diabetes)

26
Q

Regulation cytokine and chemokine

A
  • Genetic polymorphism

- Primarily in receptor genes

27
Q

Non-MHC genes

A
  • E.g complement regulatory factors, regulation of macrophage activity
28
Q

Telomeres

A
  • Repeats of DNA sequence (GGGTTA) at end of chromosomes
  • Regulation of cell senescence (aging) by shortening (50-100 bp every cell division)
  • Provide stabilization and protect chromosomal ends from damage; regulate cell replication
29
Q

Aging by telomere shortening

A
  • When too short: Unstable chromosome -> DNA damage can occur -> cell die by apoptosis or enter cellular senescence (cell arrest)
  • Shorter telomeres: elderly, males, people with ageing syndromes
30
Q

Idiotype definition

A

Variations in variable region gives antibody/TCR its antigenic specificity

31
Q

Public idiotypes

A

Those found on other cells

32
Q

Private idiotypes

A

Unique for a given cell or cell clone

33
Q

Jerne’s idiotypic network

A

“Immune system seen as a network, components connected by variable- variable region interactions” (google bilde :) )

  • Idiotypic determinants are immunogenic
  • Anti-idiotypic Ab’s are formed following an anti-Ag Ab
  • Anti-idiotypic Ab induce anti-anti-idiotypic response (Ab3, bind to anti-idiotype Ab)
  • This leads to gradual fading of immune response against given antigen (damped oscillary motion)
34
Q

Anti-idiotypic antibodies (Ab2α)

A

May block antigen binding and thus regulate immune response (bind to variable region/Ag-binding region of Ab)

35
Q

Neuroendocrine modulation of immune responses

A
  • Lymphocytes express receptors for a variety of hormones, neurotransmitters and neuropeptides (steroids, catecholamines, encephalins, endorphins++)
  • Most are immunosuppressive when released during stress
    1) Sympatetic nervous system
  • NE to β2AR (on APC, B cell, Th1, naive T, CTL)
    2) Hypothalamus-pituitary-adrenal axis
  • IL-1 and IL-6
36
Q

IL-1 and IL-6 synthesis and function on neuroendocrine regulation

A 
Synthesis:
- Neurons and glial cells
- Pituitary cells
- Adrenal glands
Function:
- Stimulants of adrenal corticosteroid production
37
Q

Dysbiosis

A

Microbial imbalance or maladaption on or inside body

38
Q

Possible causes of dysbiosis

A

1) Host genetics (mutations in NOD2, IL23R, ATG16L, IGRM)
2) Lifestyle (diet, stress)
3) Early colonization (birth in hospitals, altered exposure to microbes)
4) Medical practices (vaccination, antibiotic, hygiene)

39
Q

Possible consequences of dysbiosis

A

1) Disease (Increased Th1, Th2, Th17)

2) Health (Increased Treg)

40
Q

Immune modulation

A

Manipulation of immune response

  • Vaccination (active+passive)
  • Cytokine application
  • Monoclonal antibodies application (!)
  • Suppression (by glucocorticoids or other immunosuppressive drugs)
  • Immune cell infusion
  • Extracellular vesicles-microvesicles (!)
  • Gene therapy
41
Q

Modification of monoclonal antibodies (Mabs)

A

V: varable part, C: constant part

  • Chimeric Mabs (V: mice, C: human)
  • Humanized Mabs (HyperV: mice, C: human)
  • Human Mabs (Human Ig expression in various biological carriers - bact.phages, transgenic animals, bacteria, plants)
  • Minibodies (mini-Mabs - better penetration)
  • Bispecific Mabs (specificity for 2 antigens)
42
Q

Examples of Mabs used in therapy + effect + disease

A
  • Infliximab: anti TNF (RA, Crohn)
  • Rytuksymab: anti CD20 (RA, B cell lymphomas/leukemias)
  • Efalizumab: antiCD11a (psoriasis)
  • Trastuzumab: anti-HER2/neu (breast carcinoma)
  • Cetuksymab: anti-EGFR (large bowel carcinoma)
  • Lambrolizumab: anti-PD-1 (melanoma?)
43
Q

iDC derived vesicles

A

Immunosuppressive

44
Q

mDC derived vesicles

A

Immunostimulant

45
Q

Immunosuppressive parts of immune system (?)

A

1) Cells: Treg, Th2, Breg, DCreg, Mreg (M2)
2) Inhibitory receptors: e.g NKG2A
3) Inhibitory cytokines: IL10, TGFβ
4) Microvesicles

46
Q

Immunogenic parts of immune system (?)

A

1) Cells: T cells (Th1, Th17), B cells, DC, Mφ, NK cell
2) Activating receptors: e.g NKG2D
3) Cytokines: e.g IFNγ
4) Microvesicles

Immunology Jenny (16 decks)

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