Immunology Flashcards

1
Q

What are the main 5 causes of secondary immune deficiency?

A

Physiological immune deficiency

Infection

Treatment interventions

Malignancy

Behavioural and nutritional disorders

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2
Q

Physiological causes of immune deficiency?

A

Extremes of life - aging, prematurity

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3
Q

Infectious causes of immune deficiency?

A

HIV, measles

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4
Q

Treatment intervention causes of immune deficiency?

A

Immunosuppressive therapy

Anti-cancer agents

Corticosteroids

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5
Q

Malignant causes of immune deficiency?

A

Cancer of the immune system - lymphoma, leukaemia, myeloma.

Metastatic tumour

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6
Q

Biochemical and nutritional disorder causes of immune deficiency?

A

Malnutrition

Renal insufficiency/dialysis

T1DM and T2DM

Specific mineral deficiencies e.g. iron, zinc

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7
Q

What is a granuloma?

A

An organised collection of activated macrophages and lymphocytes

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8
Q

Underlying process for the formation of a granuloma?

A

Non-specific inflammatory response triggered by diverse antigenic agents or by inert foreign materials

Results in activation of T lymphocytes and macrophages

Failure of removal of the stimulus results in persistent production of activated cytokines

End result is organised collection of persistently activated cells

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9
Q

What are the various conditions that could cause granulomas to be present in the lungs?

A

Sarcoidosis
Mycobacterial disease, e.g. Tuberculosis, leprosy
Leprosy (some forms)
Berylliosis, silicosis and other dust diseases
Chronic stage of hypersensitivity pneumonitis
Foreign bodies

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10
Q

Examples of antibody mediated autoimmune diseases?

A

Idiopathic thrombocytopaenia

Autoimmune haemolytic anaemia

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11
Q

Features of common variable immune deficiency?

A

Low IgG, IgA and IgM (causes mostly unknown)

Recurrent bacterial infections, esp. respiratory

Often associated with autoimmune disease

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12
Q

What is hypogammaglobinaemia?

A

A disorder caused by low serum immunoglobulin or antibody levels.

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13
Q

What are primary causes of recurrent bacterial infections and hypogammaglobulinaemia?

A

Antibody deficiency

Common variable immune deficiency

Specific antibody deficiency

Other conditions, rare in adults, f.i.:

Bruton’s agammaglobunemia (no B-cells)

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14
Q

What are secondary of recurrent bacterial infections and hypogammaglobulinaemia?

A
  • Protein loss
    Protein losing enteropathy
    Nephrotic syndrome
  • Failure of protein synthesis
    Lymphoproliferative disease
    - Chronic lymphocytic leukaemia
    - Myeloma
    - Non Hodgkins Lymphoma
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15
Q

What is the complement?

A

a system of plasma proteins that interacts with pathogens to mark them for destruction by phagocytes.

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16
Q

What are the 2 main groups of white blood cells?

A

Granulocytes

Agranulocytes

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17
Q

What are granulocytes?

A

Granulocytes: White blood cells with granules in their cytoplasm. Includes neutrophils, eosinophils, and basophils.

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18
Q

What are agranulocytes?

A

White blood cells without granules. Includes lymphocytes and monocytes.

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19
Q

Examples of granulocytes?

A

Neutrophils: Phagocytic cells that engulf and destroy pathogens.

Eosinophils: Involved in allergic responses and defense against parasites.

Basophils: Release histamine and other inflammatory mediators.

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20
Q

Examples of agranulocytes?

A

Lymphocytes: Key cells of the adaptive immune system.

  • B Cells: Produce antibodies to neutralize pathogens.
  • T Cells: Regulate immune responses and directly kill infected cells.
  • Natural Killer (NK) Cells: Attack infected or abnormal cells.

Monocytes: Precursors to macrophages and dendritic cells.
- Macrophages: Phagocytic cells that engulf pathogens and debris.
- Dendritic Cells: Antigen-presenting cells that initiate adaptive immune responses.

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21
Q

What are natural killer cells?

A

Natural killer (NK) cells are a type of lymphocyte that plays a crucial role in the innate immune response.

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22
Q

Functions of NK cells?

A

Innate immune response

Cytotoxic Activity

Recognition of Target Cells

Indirect Antigen Presentation

Regulation of Immune Responses

Role in Viral Defense

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23
Q

What is cytotoxic activity in NK cells?

A

NK cells have the ability to directly kill infected or cancerous cells by releasing cytotoxic molecules such as perforin and granzymes.

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24
Q

What is MHC in NK cells?

A

MHC (Major Histocompatibility Complex) complexes play a crucial role in the function of natural killer (NK) cells.

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25
Q

How does MHC affect the role of NK cells?

A

MHC complexes, specifically MHC class I molecules, play a role in regulating the activity of NK cells by providing inhibitory signals through inhibitory receptors.

Loss or downregulation of MHC-I expression on infected or abnormal cells can lead to NK cell activation and targeted destruction of these cells.

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26
Q

What are cytokines?

A

Cytokines are small proteins that act as messengers between cells in the immune system.

27
Q

Function of cytokines?

A

They regulate immune responses by promoting communication and coordination among immune cells.

28
Q

What are examples of cytokines?

A

Cytokines can be pro-inflammatory, promoting inflammation and immune activation, or anti-inflammatory, dampening immune responses and promoting resolution of inflammation.

Examples of cytokines include tumor necrosis factor-alpha (TNF-α), interleukins (IL), interferons (IFN), and chemokines.

29
Q

What are TNF inhibitors?

A

Medications that block the action of tumor necrosis factor-alpha (TNF-α), a pro-inflammatory cytokine.

TNF-α plays a key role in the immune response by promoting inflammation and activating immune cells.

By blocking TNF-α, TNF inhibitors reduce inflammation and modulate immune responses, making them effective in treating various autoimmune and inflammatory conditions.

30
Q

Conditions treated by TNF inhibitors?

A

rheumatoid arthritis, psoriasis, psoriatic arthritis, ankylosing spondylitis, Crohn’s disease, and ulcerative colitis.

31
Q

Common examples of TNF inhibitors?

A

adalimumab, infliximab, etanercept, certolizumab, and golimumab.

32
Q

Features of Adalimumab?

A

Molecular target: Anti-TNF

Main action: Anti-inflammatory

Used in: Many rheumatic and inflammatory diseases

33
Q

Features of Pembrolizumab?

A

Molecular target: Anti-PD1

Main action: Activates T-cells

Used in: Cancer

34
Q

Features of Secukinumab?

A

Molecular target: Anti – Interleukin 17

Main action: Blocks ONE inflammation pathway

Used in: Psoriasis, arthritis, (MS)

35
Q

Types of transplant rejection?

A

Hyperacute rejection

Acute cellular rejection

Acute vascular rejection

Chronic allograft failure

36
Q

Hyperacute transplant rejection features?

A

Time: min to hrs

Pathology: thrombosis and necrosis. Type 2 hypersensitivity.

Mechanism: preformed antibody and complement fixation.

37
Q

Acute cellular transplant rejection features?

A

Time: 5-30 days

Pathology: Cellular infiltration. Type 4 hypersensitivity.

Mechanism: CD4 and CD8 T cells

Treatment: immunosuppression

38
Q

Acute vascular transplant rejection features?

A

Time: 5-30 days

Pathology: Vasculitis. Type 2 hypersensitivity.

Mechanism: De novo antibody and complement fixation.

Treatment: immunosuppression +++ (high amounts)

39
Q

Chronic allograft failure features?

A

Time: > 30 days

Pathology: Fibrosis, scarring

Mechanism: Immune and non-immune mechanisms

Treatment: minimise drug toxicity, hypertension and hyperlipidaemia.

40
Q

What do vaccinations do?

A

Produces memory in both B and T cells (B and T lymphocytes).

41
Q

How are memory B cells generated?

A

Long-lived Memory B cells are generated during primary immune responses that can survive for many years even after the antigen has been eliminated

42
Q

When do memory B cells re-activate?

A

Memory B cells rapidly re-activate in response to a second encounter with that specific antigen

Clonal expansion, differentiation into plasma cells, antibody production

43
Q

What does the vaccination do to T cells?

A

Vaccination simulates rare naive T cells

Induces a strong T-cell response in 14–21 days

44
Q

What can occur with T cells after the vaccination is administered?

A

Some become effector T cells, which:

  • Mostly die by apoptosis in the absence of persisting antigen
  • Smaller number become memory T cells and are maintained at low frequency
45
Q

What are the 5 main vaccine types?

A

Inactivated

Live attenuated

RNA vaccines

DNA vaccines

Virus – like particles

Each of these have their own strengths and limitations.

46
Q

Advantages of inactivated vaccines?

A

Can be made quickly (prevent epidemics)

Elicit good antibody responses

Easy to store; No refrigeration required

Usually safe

47
Q

Disadvantages of inactivated vaccines?

A

Overall not very potent

many killed organisms don’t stimulate good immune response because they don’t replicate or disseminate

Doesn’t stimulate clonal expansion of B and T cells, thereby requiring multiple injections

Antibody titres diminish over time, requiring booster-shots

48
Q

What are the two main groups of inactivated vaccines?

A

Whole cell vaccines i.e. whole organism used

Fractional vaccines - Only part of the organism used in the vaccine

49
Q

Examples of whole cell inactivated vaccines?

A

Polio (Salk, inactivated)
Hepatitis A
Rabies
Cholera
Plague
Pertussis (now superceded)

50
Q

Examples of fractional inactivated vaccines?

A

Subunit vaccines
- Hepatitis B
- Influenza
- Acellular pertussis
- HPV
- Anthrax

Toxoid
- Diphtheria
- Tetanus

Pure polysaccharide vaccines
- Haemophilus influenza type B

51
Q

What is vaccinated against with the UK’s “5in1” vaccination?

A

Polio

Pertussis

Diphtheria

Tetanus

Haemophilus influenza type B

52
Q

Advantages of live attenuated vaccines?

A

All relevant effector mechanisms elicited (antibody, AND activated T cells)

Localised, strong response

Usually only one single dose required

53
Q

Disadvantages of live attenuated vaccines?

A

Safety

May revert to virulence (eg vaccine associated poliomyelitis)

May cause infection in immune-compromised host

Fragile – must be stored and handled carefully i.e. depends on cold chain

54
Q

Viral examples of live attenuated vaccines?

A

Measles
Mumps
Rubella
Chickenpox
Yellow fever
Rotavirus
Smallpox (vaccinia)
Polio (Sabin, “sugar lump”)

55
Q

Bacterial examples of live attenuated vaccines?

A

BCG
oral typhoid

56
Q

What does the MMR jab vaccinate against?

A

Measles

Mumps

Rubella

57
Q

What are DNA/RNA vaccines?

A

DNA or RNA which directs the assembly of the antigenic protein inside the host cell

Can be given as “naked” DNA/RNA or packaged into a virus which then infects the host cells, instructing the cells to assemble the antigenic protein

58
Q

Advantages of DNA/RNA vaccines?

A

Can be very potent

Easier to make than protein vaccines

One production platform adaptable to other vaccines

Can be applied to target mutated proteins found in cancer (so-called “neo antigens”)

59
Q

Disadvantages of DNA/RNA vaccines?

A

May require complex cold-chain

So far no long-term experience

60
Q

Examples of DNA/RNA vaccines?

A

Against Covid 19:
- Johnson&Johnson vaccine (adenovirus)
- Oxford vaccine (adenovirus)
- Moderna vaccine (RNA)
- Biontech vaccine (RNA)

61
Q

What are virus like particles (VLP) vaccinations?

A

Empty shells (“capsids”) made from viruses that look like the real virus but have no DNA/RNA

62
Q

Advantages of VLP vaccines?

A

Non-infectious

Very potent, usually only one single dose required

Activates both T- and B-cell responses

63
Q

Disadvantages of VLP vaccines?

A

Complex manufacture

Fragile – must be stored and handled carefully i.e. depends on cold chain

64
Q

Examples of VLP vaccines?

A

Against Papillomavirus associated cancer:
Cervarix
Gardasil
Gardasil-9

Against Hepatitis B:
Engerix