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Immunology Flashcards

1
Q

How does the body get rid of pathogens that enter through areas not covered by skin?

A

Eyes: tears containing lysozymes
Airway: mucas, moves by cilia to oesophagus to be swallowed into stomach acid
Urine: flushing out pathogens
Friendly bacteria: mouth, gut, vagina

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2
Q

What are the 3 ways pathogens are idnetified?

A
  1. Pathogen-associated molecular patterns (PAMPs)
  2. Damage associated molecular patterns (DAMPs)
  3. Toll like receptors (TLRs)
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3
Q

What are PAMPs

A

Certain properties the body uses to identify potentially harmful things
e.g. LPS in bacteria cell wall

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4
Q

What do DAMPs do?

A

Released by damaged/stressed cells signalling the presence of harmful events such as infection or tissue injury
- Signalling to destroy

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5
Q

What are TLRs?

A
  • Expressed on dendritic cells/macrophages, theses are what detect PAMPs and DAMPs
  • When PAMP/DAMP is identified these cells activate inflammatory actions to eliminate the pathogens
  • They also recruit other immune cells.
  • Responsible for dendritic cells presenting pathogen components, important in initiating the adaptive immune response
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6
Q

How many new cells are made in the bone marrow each day?

A

500 billion

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7
Q

What are the two lineages of multipotential hematopoietic stem cells?

A
  1. Myeloid lineage= Immune cells of the innate response i.e. neutrophils, macrophages etc
  2. Lymphoid lineage= Adaptive immunity i.e. B cells and T cells
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8
Q

Give some properties of neutrophils

A
  • Short lived
  • Respond and migrate to detection site
  • Phagocytose
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9
Q

Give some properties of Eosinophils

A

-Target molecules too large to engulf e.g. a splinter

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10
Q

Give some properties of macrophages

A
  • Long-lived phagocytes
  • Abundant in areas likely exposed to pathogens
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11
Q

What is the inflammatory response once a DAMP/PAMP has been identified by TLR?

A
  1. Blood vessels dilate and become permeable, endothelial cells become sticky to catch white blood cells and facilitate their access
  2. Pro-inflammatory cytokines released (e.g. prostaglandins)
  3. Fever induces as part of a complement cascade when PAMPs are identified, inhibits pathogen proliferation and speeds chemical reaction used by antimicrobial peptides
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12
Q

How does the body respond to sepsis?

A

Loss of plasma volume
Crash of blood pressure
Clotting
Cytokine storm

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13
Q

How do dendritic cells link the adaptive and immune response?

A
  1. Are phagocytic and express TLRs (plus other recognition receptors too)
  2. Present fragments of digested pathogen
  3. Migrate to lymphoid tissues to activate and stimulate T-cells of the active immune system
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14
Q

What is adaptive immunity?

A

Specific response to a specific pathogen

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15
Q

Where are B cells and T cells made and where do they go?

A

B cells = Bone marrow
T cells = Thymus

  • Migrate to lymph tissue for foreign antigen exposure
    (letters relate to name)
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16
Q

What are the different types of T cells?

A

Cytotoxic = Kills infected host cell
Helper = Activates B cells, other T cells etc
Regulatory= tells immune cells to ‘stand down’

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17
Q

Explain the activation of the adaptive immune system

A
  • Body has a library of ‘dormant’ lymphocytes
  • If the dendritic cell presents antigens for one of these dormant lymphocytes it will be activated
  • Stronger fit= stronger activation
  • Plasma cells then produced
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18
Q

Why is the second response stronger and faster than the primary response?

A

due to the memory cells stored.

19
Q

How can the immune system not respond to a ‘self-protein’?

A
  • Can ‘forget’ if its not seen it for a while
  • Experiments where proteins are knocked out and reintroduced but the immune system attacks because it didnt learn to recognise
20
Q

What does self-tolerance mean?

A

The immune system’s ability to recognize and tolerate the body’s own cells and tissues while still effectively responding to foreign substances
- Avoids autoimmune reactions

21
Q

What are 4 ways that self tolerance is developed?

A
  1. Receptor editing
    - Developing lymphocytes that recognise self molecules (self-reactive lymphocytes) change their antigen receptors so that they no longer recognise self antigens.
  2. Clonal deletion
    Self-reactive lymphocytes die by apoptosis when they bind their self antigen.
  3. Clonal inactivation
    - (also called clonal anergy), self-reactive lymphocytes become functionally inactivated when they encounter their self antigen.
  4. Clonal suppression, regulatory T cells suppress the activity of self-reactive lymphocytes
22
Q

What are the 5 classes of antibodies?

A

IgG, M, A, D, E

23
Q

Describe the structure of the classic IgG antibodies

A

Two light chain
Two heavy chain
Disulphide bridge
Variable region has 3 hypervariable regions making up the antigen-binding surface

24
Q

Stress fibre structure and function

A

Structure:
- Bundles of actin filaments arranged in parallel bundles
- Associated with myosin motor proteins
- Associated with focal adhesions, regions where the cell contacts the extracellular matrix (through proteins such as talin and vinculin)

Function:
- Contractile forces
- Cell adhesion to ECM
- Mechanical support
- Cellular tension

25
Q

Explain V(D)J recombination

A
  • In an antibody the V(h) and the V(l) (heavy and light chains) are the variable regions
  • They both have a different amount of V, D and J segments
  • variable (V), diversity (D), and joining (J) segments.
  • During B cell development, V, D, and J gene segments undergo V(D)J recombination- involves rearrangement and joining of these gene segments through splicing to generate a unique combination
  • The developing B-cell joins a V segment to a J segment (on the gene level, chooses just one allele - allelic exclusion)
  • Transcription starts at V segment and continues to fused J segment
  • VDJ recombinase is responsible, coded for by RAG1
  • Can mix and match which exons are spliced meaning high variability
26
Q

How is somatic hypermutation involved in V(D)J recombination?

A
  • After initial gene arrangement B cells somatic hypermutation introducing random mutations in the variable regions- increased diversity
  • B cells with antibody variants that exhibit higher affinity for the antigen are preferentially selected, contributing to the refinement of the antibody’s specificity
  • Every generation select for the B cell that binds best, then the cell mutates again
27
Q

What is V(D)J junction diversification?

A

when nucleotides are lost/gained in recombining gene segments

28
Q

What do the constant regions of antibodies determine?

A

The class of the antibody and effector functions

29
Q

What is affinity maturation?

A

Over time after initial immunisation there is progressive increase in affinity of the antibodies

30
Q

Why is it called ‘hypermutation’

A

B-cells mutate at the rate of about one mutation per V-region coding sequence per cell generation, so much faster than ‘background’ mutation rate
- IN-VIVO EVOLUTION

31
Q

What is the role of activation-induced deaminase?

A
  • AID is responsible for introducing mutations by deaminating cytosine bases in the DNA to uracil
  • It is expressed in the germinal centre B cells (clusters of B cells in secondary lymphoid tissue where B cells proliferate super fast)
32
Q

What is BCL-6?

A
  • transcriptional repressor expressed in germinal centres, binds to sites in the p53 promoter switching off expression
  • Means hypermutation is occuring without an activated apoptosis pathway, no p53 ‘watchkeeper’
  • Means antibodies can be readily made but can go wrong as lymphomas could arise if there are hypermutation problems and no apoptosis
33
Q

How are degraded antigens displayed on the surface of antigen-presenting cells?

A
  • Present foreign peptides through MHC proteins
  • MHC proteins bind to the peptide fragments and carry them to the cell surface so T-cells can recognise them
34
Q

What is class-switch recombination?

A

Class switch recombination is a process by which B cells change the class of the antibody they produce (e.g., from IgM to IgG, IgA, or IgE) while retaining the same antigen specificity.

35
Q

What 3 membrane interactions do dendritic cells have to signal T-cells?

A
  1. Material presented by MHC proteins
  2. stimulatory ligands to say ‘take us seriously’
  3. Cell-cell adhesion molecules to hold the T-cells in place long enough for them to ‘get the message’
36
Q

How do dendritic cells also tolerise T-cells?

A

By presenting self antigens on their MHCs- same as signalling but does not include to stimulatory ligand/protein

37
Q

T cell structure

A
  • immunoglobulins that have variable regions and hyper-variable loops - similar to antibodies
  • also generated by V(D)J recombination + junctional diversification
38
Q

What happens in Candida albicans disease?

A
  • Yeast that can exist in mouth, gut, vagina with no problem but can become pathogenic
  • When phagocytosed/engulfed, candida can burst out of the macrophages (killing them) and form hyphae
39
Q

What happens in Staphylococcus aureus?

A
  • Has protein A in cell wall
  • Its active site binds to constant region of igGs
  • covers itself in a ‘coat’ of IgGs, avoiding detection from immune system
40
Q

How does HIV work?

A
  • HIV infects T-cells etc (anything with CD4 receptor)
  • Survives aspects of immune system detection
  • Phagocytoses the cell and displays its parts, telling the immune system to kill its own cells
  • Immune deficiency
41
Q

What happens in type 1 diabetes and multiple sclerosis?

A

Type 1 diabetes- Immune system attacks B cell islet of Langerhans
MS- Immune system attacks myelin sheath of neurons in CNS

42
Q

What diseases are caused by autoimmune atatcks as a result of a lack of self-tolerance?

A

Rheumatoid arthritis, psoriasis, Crohn’s disease, UBD, ulcerative colitis

43
Q

What is Immunosenescence

A

progressive decline of immune competence with age

44
Q

What is the cancer immunoediting model?

A

Suggests immune cells control/manage cancer/tumours in three stages:
1. Elimination = tumours killed by natural killer cells etc…
2. Equilibrium = balanced state between immune and tumour cells (being ‘managed’)
3. Escape = Immune system can’t deal with it anymore, tumour cells escape and become ‘clinically detectable’

Potential issues = not being able to identify cancer cells, or eliciting a response not strong enough to kill all of them

Advanced Molecular (13 decks)

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