Advanced Molecular > Immunology > Flashcards

Immunology Flashcards

(44 cards)

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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?

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A

due to the memory cells stored.

19
Q

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

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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?

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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?

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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?

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A

IgG, M, A, D, E

23
Q

Describe the structure of the classic IgG antibodies

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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

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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
Explain V(D)J recombination
- 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
How is somatic hypermutation involved in V(D)J recombination?
- 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
What is V(D)J junction diversification?
when nucleotides are lost/gained in recombining gene segments
28
What do the constant regions of antibodies determine?
The class of the antibody and effector functions
29
What is affinity maturation?
Over time after initial immunisation there is progressive increase in affinity of the antibodies
30
Why is it called 'hypermutation'
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
What is the role of activation-induced deaminase?
- 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
What is BCL-6?
- 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
How are degraded antigens displayed on the surface of antigen-presenting cells?
- 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
What is class-switch recombination?
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
What 3 membrane interactions do dendritic cells have to signal T-cells?
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
How do dendritic cells also tolerise T-cells?
By presenting self antigens on their MHCs- same as signalling but does not include to stimulatory ligand/protein
37
T cell structure
- immunoglobulins that have variable regions and hyper-variable loops - similar to antibodies - also generated by V(D)J recombination + junctional diversification
38
What happens in Candida albicans disease?
- 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
What happens in Staphylococcus aureus?
- 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
How does HIV work?
- 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
What happens in type 1 diabetes and multiple sclerosis?
Type 1 diabetes- Immune system attacks B cell islet of Langerhans MS- Immune system attacks myelin sheath of neurons in CNS
42
What diseases are caused by autoimmune atatcks as a result of a lack of self-tolerance?
Rheumatoid arthritis, psoriasis, Crohn's disease, UBD, ulcerative colitis
43
What is Immunosenescence
progressive decline of immune competence with age
44
What is the cancer immunoediting model?
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
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