Immunology Flashcards

Part of ICS

1
Q

Haematopoiesis starting from haematocytoblast

A

splits to common myeloid progenitor and common lymphoid progenitor

Common myeloid progenitor—-> megakaryocyte, erythrocyte, mast cell, myeloblast

Myeloblast —->eosinophil, basophil, neutrophil, monocyte (—> macrophage)

Common lymphoid progenitor—> natural killer cell, lymphocyte (—> T cell, B cell—> plasma cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the primary lymphoid organs (where B cells and T cells come from)?

A

Both originate in bone marrow. B cells stay and mature in bone marrow but T cells move to the Thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is thymic tolerance?

A

Thymus ensures that T cells produced are good at recognising foreign antigens and the suppressing the attack on self antigens. Some T cells produced can want to attack self antigens but they are destroyed by thymus. Dysfunction of the thymus leads to autoimmune diseases such as Myasthenia Gravis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are secondary lymphoid organs (where does the actual immune fighting happen?

A

It is in these organs where the cells of the immune system do their actual job of fighting off germs and foreign substances.

-Lymph nodes - Site of Dendritic Cells (It is in these organs where the cells of the immune system do their actual job of fighting off germs and foreign substances) , B and T cell interactions
- Spleen - RBC recycling, encapsulated bacterial cell killing
-tonsils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the tertiary lymphoid structures?

A

Tertiary lymphoid structures (TLSs) are organized aggregates of immune cells that form postnatally in nonlymphoid tissues. TLSs are not found under physiological conditions but arise in the context or in response to chronic inflammation, such as in autoimmune disease, chronic infection, and cancer.

Pathological
- Germinal centres of rapidly proliferating lymphocytes

Lymphocyte proliferation is defined as the process whereby lymphocytes begin to synthesize DNA after cross-linking of their antigen receptor either following recognition of antigen or stimulation by a polyclonal activator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Qualities of innate immunity?

A

Non-specific
- Rapid
- Already active (little activation needed)
- No memory
- Short duration
- Killing usually via complement activation
- Mediated by neutrophils and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Complement activation?

A

At the basic level the broad functions of the complement system can be split into three areas: (1) the activation of inflammation; (2) the opsonization (labeling) of pathogens and cells for clearance/destruction; (3) the direct killing of target cells/microbes by lysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Qualities of adaptive immunity?

A
  • Specific
  • Slow
  • Needs activation
  • Have memory
  • Killing usually antibody mediated
  • Main cells are T, B and plasma cells
  • Long lasting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Examples of physical barriers

A
  • Skin
    Contains Chemical barriers (lysozymes in sebum and skin target microbes)
  • Mucus and cilia

Thick mucus secretions prevent pathogen entry

Antimicrobial substances (Protease + IgA ab)

mucociliary clearance in resp. tracts (waft away) mucosa lines Resp, GI and GU tracts

  • Also contains MALT (Mucosa-associated lymphoid tissue)
    (secondary lymphoid with lots of lymphocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Examples of chemical barriers

A
  • Lysozyme in tears
  • Stomach acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

complement pathways?

A
  • Classical
  • Lectin
  • Alternate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Complement system destroys foreign bodies by…

A
  • Direct lysis - Membrane attack complex formation
  • Opsonisation - Increased phagocytosis via protein C3b
  • Inflammation - Macrophage chemotaxis via proteins C3a and C5a
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

One of the innate cells- neutrophils?

A
  • Key mediator of acute inflammation - IL8 chemokine
  • 70% of all leukocytes
  • Act in hours-days
  • Express CD66 receptor (common for all granulocytes-neutrophils, eosinophils, and basophils)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Innate cells - macrophages?

A
  • Act over months-years (typically chronic)
  • Phagocytosis, antigen presenting and cytokine secreting (TNF-a, IL1 and IL12)
  • Express CD14+ and CD40+
  • Can be circulating or resident (eg: Kuppfer cells, alveolar macrophages)
  • Clear apoptotic debris
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Innate cells: eosinophils

A
  • Release major basic protein
  • Seen in parasitic infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Innate cells: basophils?

A
  • Circulate mast cells
  • Secrete serotonin and heparin and histamine
  • Important in asthma, anaphylaxis, atopic dermatitis and hay fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Innate cells: mast cells

A
  • Important in parastic infections and allergic reactions
  • Activate type 1 hypersensitivity: IgE crosslinking -> degranulation -> histamine release
  • Fixed at tissues at mucosal surfaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Innate cells: natural killer cells

A
  • In blood and tissues
  • Express CD16+
  • Antibody-dependent cellular cytotoxicity
  • Recognise self and non-self by the presence of MHC-I on cell surfaces
  • Activation -> degranulation -> perforin -> perforates viral infected cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Non-cellular components of innate immunity

A

Physical and chemical barriers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Receptors on innate cells

A
  • Toll like receptors (TLRs) and nod like receptors that are pattern recognition receptors for pamps and damps
  • Respond to PAMPs and DAMPs (One major category of inflammatory stimulation, is the family of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). These patterns are found on bacterial cell walls, DNA etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which toll like receptors are intracellular?

A

3, 7, 8, 9
(rest are extracellular out of 10)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are antigen presenting cells?

A
  • The interface between innate and adaptive immunity
  • All present exogenous antigens in the presence of MHCII (major histocompatibility complex)
  • Best cells for this are dendritic cells
  • (macrophages and B-cells also do this)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Dendritic cell function?

A
  • Present foreign antigens to T helper cells
  • Stimulates further T helper proliferation
  • Stimulates B cell production -> antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is formed when a dendritic cell and T helper cell communicate?

A

Immune synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

3 conditions that must be met for antigen presenting cells to function

A

Receptor binding
- Co-stimulation (other molecules bind after primary receptor binding)
- Cytokine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Adaptive cells: T cells

A
  • Mature in the thymus
  • Thymic tolerance selects best T cells
  • T cell never encountering antigen (not matured in thymus yet) = naïve T cell
24
Q

Process of thymic tolerance

A
  • Positive selection - T cells tested to see if they recognise major histocompatability complexes 1 and 2 (selected FOR)
  • Negative selection - T cells tested to see if they produce an immunological response against MHCs (selected AGAINST)
  • Allocation
25
Q

Allocation in thymic tolerance

A
  • If interact with MHC1 -> CD8+ cells (cytotoxic, kill)
  • If interact with MHC2 -> CD4+ cells (helper, increase immunity response by activating cells)
26
Q

Adaptive cells: B cells

A
  • Maturation and production in the bone marrow
  • Any B cells with autoimmunity apoptose
27
Q

Activation of B cells

A
  • APC and interactions between MHC-II activates T helper 2 cells
  • T helper 2 cell releases IL4 (B cell proliferation) and IL5 (B cell differentiation into plasma cell -> immunoglobulins)
  • IGs act against specific pathogen present
  • Somatic hypermutation and class switching mutate IGs to target different variants
28
Q

What do IL4 and IL5 (interleukins (cytokines)) promote class switching to?

A

IL4 - IgA
IL5 - IgE

Class switching is the process whereby an activated B cell changes its antibody production from IgM to either IgA, IgG, or IgE depending on the functional requirements.

29
Q

IgG

A
  • Most abundant in blood
  • Highly specific
  • Key in secondary response
  • 4 subtypes
  • Can cross the placenta
30
Q

IgA

A
  • Most abundant in total body
  • Found on mucosal linings, colostrum and breast milk (a dimer)
31
Q

IgM

A
  • First Ig released in adaptive response
  • B cell mediated
  • A pentamer
32
Q

IgE

A
  • Least abundant in body
  • Activates mast cell + basophil degranulation in type 1 hypersensitivity (anaphylaxis)
33
Q

IgD

A

Unknown function, irrelevant. IgD is involved in the activation of B cells.

34
Q

Major histocompatability complex

A
  • Also known as human leukocyte antigen (HLA)
  • On chromosome 6
  • Interact with T cells
  • Confer susceptibility to inherited autoimmune diseases
35
Q

Type 1 hypersensitivity

A
  • Anaphylactic
  • Antigen reacts with IgE bound to mast cells
  • Vasodilation, increased permeability, bronchoconstriction, facial flush, puritis, swollen tongue and face
  • eg: atopy: asthma, eczema, hay fever
36
Q

Type 2 hypersensitivity

A
  • Antibody-antigen complex formation
    👴🏻
    Goodpasture’s
    Rheumatic fever
    AHA
    Myasthenia gravis
    Pernicious anaemia
    Anti-TSH (Graves’)
37
Q

Type 3 hypersensitivity

A
  • Antibody-antigen complex deposition
    💃🏻
    Haemolytic uraemic syndrome and hypersensitivity pneumonitis
    IgA nephropathy
    Post-strep glomerulonephritis
    SLE
    Rheumatoidarthritis
38
Q

Type 4 hypersensitivity

A

Type 4 hypersensitivity
- Delayed
- T-cell mediated and activated by antigen presenting cells

GBS
MS
🐱
Contact dermatitis + coeliac
Allopurinol drug reaction
Tuberculin skin test and T1DM

39
Q

Assessing vitals in anaphylaxis

A

A - airways - hoarse voice, stridor
B - breathing - SpO2 < 94%
C - circulation - are they pale, cold, clammy? low BP
D - disability - confused, comatose, movemet
E - exposure

40
Q

What is immune tolerance?

A
  • Physiological
  • Central - thymic tolerance
  • Peripheral - If T/B faulty cell evade central tolerance, they’re dealt with in secondary lymphoid organs
41
Q

What is autoimmunity?

A
  • Pathological response vs self
  • Faulty immune tolerance
  • Molecularmimickery
42
Q

Organ specific autoimmunity

A
  • Type 1 Diabetes M - endocrine pancrease b cells
  • MS - oligodendrocytes of CNS
  • Pernicious anaemia - parietal cells of stomach
  • Myesthemia gravis - causes muscle weakness
43
Q

Non-organ specific autoimmunity

A
  • Affects DNA, eg: SLE
  • Affects cell antigens
    • RBCs -> autoimmune haemolytic anaemia
    • Platelets - > immune thrombocytopenic purpura
  • Rheumatoid arthritis
44
Q

Immunodeficiency can be…

A

Inherited (defects in T cells), eg: IgA deficiency (north Europe), SCID (death within 2 years)
- Acquired, eg: HIV

45
Q

Patterns of immunodeficiency

A
  • Decrease in T helper cells in HIV, PCP pneumonia
  • B cell deficiency
  • Complement deficiency (SLE)
  • Hyposplenism - lack of/decreased function of the spleen ->
46
Q

What are the Pfizer and Biotech Moderna COVID-19 vaccines made from?

A

mRNA

47
Q

What are vaccinations?

A

A form of active immunity

48
Q

Forms of vaccines

A
  • Live attenuated (genetically modified) organism, eg: MMR, BCG, Polio
  • DNA Antigens
  • Subunit/toxoid vaccines, eg: tetanus, diphteria, cholera
  • Recombinant vector, eg: Hep B
  • Whole inactivated pathogen, eg: influenza
49
Q

Active immunity natural vs artificial

A

Natural - Body encounters pathogen + produces memory cell after infection
Artificial - Vaccine mimics encountering pathogen + stimulates Ig production

50
Q

Passive immunity natural vs artificial

A

Natural - Maternal Igs passed onto feeding baby in breast milk/colostrum
Artificial - Antivenom, injection of Ig from another organism

51
Q

Advantages and disadvantages of live attentuated pathogens

A

Advantages:
- Full natural immune response
- Prolonged protection
- Often only single immunisation
Disadvantages:
- Immunocompromised patients may become infected
- Can have outbreak in places with poor sanitation

52
Q

Advantages and disadvantages of whole inactivated pathogens

A

Advantages:
- No risk of infection
- Storage less critical
- Good immune response
Disadvantages:
- Just activates humoral response (not T cells)
- Not full transient infection
- Boosters required

53
Q

Advantages and disadvantages of subunit/toxoid vaccines

A

Advantages:
- Safe (only parts of pathogen are used)
- No risk of infection
- Easier to store and preserve
Disadvantages:
- Less powerful immune response
- Repeated vaccinations and edjuvants
- Consider genetic heterogeneity of population and choice of antigen

54
Q

Advantages and disadvantages of DNA antigen vaccine

A

Advantages:
- Safe, even in immunocompromised patients
- No complex storage or transport
- Simple drug delivery
Disadvantages:
- Mild response during boosting
- No transient infection

55
Q

Advantages and disadvantages of recombinant vector vaccines

A

Advantages:
- Ideal stimulus to immune system
- Immunological memory
- Flexible
Disadvantages:
- Can cause illness in compromised individuals
- Immune response can regate effectiveness
- Requires refridgeration for transport

56
Q

What are the only polysaccharide vaccines?

A
  • Pneumococcal disease
  • Meningococcal disease
  • Samonella typhi
57
Q

Which vaccines are administered as live attentuated in the UK?

A
  • BCG
  • MMR
58
Q

Classical PAMPs

A

Pathogen-associated molecular pattern molecules
- Flagellin
- Lipopolysaccharide
- Peptidoglycan
- Liparabinomannan of mycobacteria

59
Q

What immunoglobulins are involved in inactivated vaccines?

A

IgM followed by IgG

60
Q

TLRs and their targets?

A

TLR2: Gram positive bacteria and mycobacteria (inc fungi)
TLR4: Gram negative bacteria and lipopolysaccharides
TLR5: Bacteria and flagellin
TLR7: Single-strand RNA
TLR9: Non-methylated DNA