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YEAR 5: Immunopathology AS > Immuno: Immune modulating therapies 1 > Flashcards

Immuno: Immune modulating therapies 1 Flashcards

1
Q

List some approahces to boosting the immune system.

A
  • Vaccination
  • Replacement of missing components (e.g. replacing immune cells)
  • Blocking immune checkpoints
  • Cytokine therapy
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2
Q

Describe the variety of antigen receptors found in the adaptive immune system.

A
  • Contains a wide variety of antigen receptors
  • Not entirely genetically encoded as genes are rearranged and recombined
  • This has the potential to generate autoreactive cells but these are removed
  • The adaptive immune system has exquisite specificity
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3
Q

What happens when cells of the adaptive immune system engage with an antigen that it recognises?

A

Undergoes massive clonal expansion

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4
Q

What are the two ways in which B cells can undergo clonal expansion once activated?

A
  • They can differentiate into T-cell independent IgM memory and plasma cells
  • They can undergo a germinal centre reaction (with help from T helper cells) and become IgG/A/E memory and plasma cells
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5
Q

What happens after a T cell meets an antigen matching their receptor?

A

clonal expansion- T cells proliferate into effector cells: cytokine secreting / cytotoxic

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6
Q

Which type of T cell undergoes a more pronounced proliferation following activation?

A

CD8 > CD4

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7
Q

List three types of antigen-presenting cell.

A
  • Dendritic cells
  • Macrophages
  • B lymphocytes
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8
Q

What are some important characteristics of memory T cells?

A
  • Longevity - memory T cells persist for a long time in the absence of antigen due to low level proliferation in response to cytokines
  • Different pattern of cell surface proteins involved in chemotaxis cell adhesion - allows memory cells to rapidly access non-lymphoid tissues
  • Rapid, robust response to subsequenct antigen exposure (lower threshold for activation of naïve T cells)

NOTE: memory B cells have similar characteristics and are able to produce rapid and robust responses

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9
Q

What is Th cell role in the germinal centre?

A

CD49 and CD40 help B cells in germinal centre development

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10
Q

What are the aims of vaccines?

A
  • Generate protective, long-lasting immunity
  • No adverse reactions
  • Single shot
  • Easy storage
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11
Q

Which cell surface receptor is used in the influenza vaccine?

A

Haemagglutinin (HA) - this is a receptor-binding and membrane fusion glycoprotein

CD8+ T cells protect against flu AFTER infection

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12
Q

Describe how haemagglutinin inhibition assays work.

A
  • If you put normal red blood cells in a petri dish, they will clump at the bottom forming a red spot
  • If you add influenza virus, the HA makes red cells stick together and causes a diffuse coloration across the well
  • If you add the serum of someone who has a lot of antibodies against HA, it will inhibit the haemagglutination effects of HA so the red cells remain as a discrete red spot
  • The higher the dilution of serum at which the red cells remain as a little dot, the more antibodies are present in the serum

NOTE: sialic acid receptors on RBCs bind to HA leading to haemagglutination

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13
Q

How long does protection from the influenza vaccine last?

A

Starts 7 days after the vaccine and protection lasts for 6 months.

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14
Q

What agent is used in the BCG vaccine?

A

Attenuated strain of Mycobacterium bovis.

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15
Q

Describe the protection that is achieved by using the BCG.

A
  • Some protection against primary infection
  • Mainly protects against progression to active TB

NOTE: T cell response is important in protection

NOTE: protection lasts for 10-15 years

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16
Q

What is the Mantoux test?

A
  • A small amount of liquid tuberculin (PPD) is injected intradermally
  • The area of injection is examined 48-72 hours after the injection
  • A reaction would appear as a wheel around the injection site (this is suggestive of latent TB, active TB or previous BCG)

Type IV reaction

PPD: purified protein derivative

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17
Q

What is a live attenuated virus vaccine? List some examples.

A

The organism is alive but modified to limit its pathogenesis.

Examples: MMR, BCG, yellow fever, polio (Sabin), oral typhoid, Zostavax, influenza nasal spray 2-17yrs

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18
Q

List some advantages and disadvantages of live attenuated virus vaccines.

A
  • Advantages: establishes infections, raised broad immune response against multiple antigens, activates all phases of the immune system, often confer life-long immunity after one dose
  • Disadvantages: storage problems, possible reversion to virulence, spread to contacts, cannot be used in immunocompromised patients
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19
Q

Previous risk of polio vaccine

A

vaccine associated paralytic poliomyelitis

20
Q

List some examples of the following types of vaccine:

  1. Toxoids
  2. Component/Subunit
  3. Inactivated
A
  1. Toxoids
    • Diphtheria
    • Tetanus
  2. Component/Subunit
    • Hep B (HBsAg)
    • HPV (capsid)
    • Influenza (recombinant quadrivalent)
  3. Inactivated
    • influenza (quadrivalent)
    • cholera
    • bubonic plague
    • polio (salk)
    • hep A
    • pertussis
    • rabies
21
Q

What are the advantages and disadvantages of inactivated/component vaccines?

A
  • Advantages - no mutation or reversion, can be used in immunodeficient patients, easier storage, lower cost
  • Disadvantages - often do not follow normal route of infection, poor immunogenicity, may need multiple injections, may require conjugates/adjuvants
22
Q

Describe how conjugate vaccines work.

A
  • Polysaccharide and protein carrier
  • Polysaccharide induces a T-cell independent B cell response (transient)
  • Addition of the protein carrier promoted T cell immunity which enhances B cell/antibody responses
23
Q

List some examples of conjugate vaccines.

A
  • Haemophilus influenzae type B
  • Meningococcus
  • Pneumococcus
24
Q

Describe how adjuvants work.

A
  • Increases the immune response without altering its specificity
  • They mimic the action of PAMPs on TLR and other PRRs
25
Q

List some examples of adjuvants.

A
  • Aluminium salts (MOST COMMON)
  • Lipids (monophosphoryl lipid A)
  • Oils (freund’s adjuvant animals)

NOTE: the mechanism of action of aluminium salts is not fully understood but it may allow antigens to be released slowly over time, may induce a mild inflammatory reaction or may activate Gr1 + IL4 + eosinophils

26
Q

mRNA vaccines how were they developed?

A

Covid had spike proteins which bind to ACE2
1. infect E.coli with DNA for spike protein
2. excise DNA and transcribe it to mRNA
3. combine with lipids to produce vaccine
4. mRNA expressed on cell surface when injected, generating T cell and B cell response

27
Q

How were the adenoviral vector vaccines developed?

A
  1. DNA of relevant protein inserted into viral vector to produce vaccine
  2. Infect cells in vivo
  3. transcription/ translation to produce protein
  4. Stimulated immune response
28
Q

Examples of adenoviral vector vaccines

A

Astrazeneca
Sputnik Covid vaccine vector: adenovirus type 26 and 5

29
Q

List some example of experimental vaccine adjuvants.

A
  • ISCOMs - immune-stimulating complexes (enhances cell-mediated immunity)
  • CpG - cytosine-phosphate-guanosine motif that can bind via PRR to induce an immune response
  • DNA vaccines - plasmid containing a gene of choice (e.g. from a pathogen) is inserted into a muscle cell which will then express the antigen. This stimulates T cells responses (WARNING: this can lead to autoimmunity)
30
Q

What are dendritic cell vaccines?

A
  • Used against tumours
  • You collect some dendritic cells from the patient and load them with the antigen from the tumour to try and boost the immune response against tumour antigens
31
Q

What are the main indications for haematopoietic stem cell transplantation?

can be donor or autologous

A
  • Life-threatening immunodeficiency (SCID)
  • leukocyte adhesion deficiency
  • Haematological malignancy
32
Q

What is human normal immunoglobulin?

A
  • Immunoglobulin prepared from thousands of pooled donors
  • Contains pre-formed IgG
  • Administered IV or SC
33
Q

List some indications for IVIG

A
  • Primary antibody defect
    • X-linked agammaglobulinaemia
    • X-linked hyper IgM syndrome
    • Common variable immunodeficiency
  • Secondary antibody defect
    • CLL
    • Multiple myeloma
    • After bone marrow transplantation
34
Q

When might specific immunoglobulin be given?

A

Passive immunity as post-exposure prophylaxis (e.g. Hep B, tetanus, rabies, VZIG)

35
Q

List four types of T cell adaptive cell transfer.

A
  • Virus-specific T cells
  • Tumour infiltrating T cells (TIL)
  • T cell receptor T cells (TCR)
  • Chimeric antigen receptor T cells (CAR T Cell Therapy)
36
Q

Using an example, describe how virus-specific T cells are used.

A
  • Used for EBV in patients who are immunosuppressed to prevent the development of lymphoproliferative disease
  • Blood is taken from the patient or from a donor
  • Peripheral blood mononuclear cells are isolated and stimulated in vitro with EBV peptides
  • This creates and expansion of EBV-specific T cells which are then reinfused into the patient

NOTE: tumour infiltration T cell therapy follows the same principle but uses tumour antigens

37
Q

Describe how TCR and CAR T cell therapy works.

A
  • T cells are taken from the patient and vectors are used to insert gene fragents that encode receptors
  • In TCR therapy, the gene will encode a specific TCR (e.g. against tumour antigen)
  • In CAR therapy, the receptors are chimeric (containing both B and T cell components)
38
Q

Describe a use of CAR T cell therapy.

A
  • Used to target CD19 (present on B cells)
  • Receptors on the CAR cell have an immunoglobulin variable domain and is joined to a TCR
  • This means that it recognises CD19 through an immunoglobulin domain but signals through the TCR pathway

NOTE: this is used in ALL and NHL

39
Q

What is ipilimumab and how does it work?

A
  • CTLA4 and CD28 are both expressed by T cells and they recognise antigens (CD80 and CD86) on APCs
  • Signalling through CD28 results in a stimulatory response
  • Signalling through CTLA4 results in an inhibitory response
  • Ipilimumab is a monoclonal antibody that blocks CTLA4 thereby removing this inhibitory response
  • It is used in advance melanoma
40
Q

Explain the use of antibodies against PD-1 in treating cancer.

A
  • PD-1 and PD-2 ligands are present on APCs and interact via PD-1 receptors on T cells to cause an inhibitory response
  • They can also be expressed by some tumour cells
  • Pembrolizumab and nivolumab are antibodies that are specific to PD-1, thereby blocking this effect
  • This is also used in advanced melanoma
41
Q

pembrolizumab and nivolumab uses

A

metastatic renal cell carcinoma
advanced melanoma

42
Q

complications of antibodies against PD-1

A

activation of t cells can lead to autoimmune complications (thyroid/ gut)

43
Q

List some examples of the therapeutic use of recombinant cytokines.

A
  • Interferon alpha - used as an adjunct in the treatment of Hep B, Hep C, Kaposi sarcoma, CML and multiple myeloma
  • Interferon beta - Behcet’s disease, relapsing MS
  • Interferon gamma - chronic granulomatous disease
44
Q

What can IL-2 be used for

A

Stimulate T cell response in renal cell carcinoma

45
Q

Interferon alpha use

A

direct antiviral effect in Hep B and Hep c

46
Q

IFN-gamma use

A

chronic granulomatous disease

YEAR 5: Immunopathology AS (12 decks)

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