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Clinical pathology > Theme 2- week 2 > Flashcards

Theme 2- week 2 Flashcards

1
Q

What are the main physiological functions of the immune system?

A

Recognise pathogens

Mount an immune response which requires- cell- cell communication

Clear the pathogen

Self-regulation

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2
Q

What is the innate immunity? Is it general or antigen specific? How fast is it? Does it remember antigens?

A

Innate immunity

General, not antigen specific but can recognise broad classes e.g. bacteria

Rapid speed of onset

Does not alter on repeated exposure

No memory

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3
Q

What is the adaptive immunity? Is it general or antigen specific? How fast is it? Does it remember antigens?

A

Adaptive immunity

antigen specific

Slower response, but more potent

Subsequent exposure- more effective response

memory

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4
Q

What are the responses of the immune system?

A
  • nnate
  • Barrier and chemical mechanisms
  • Pathogen recognition
  • Cellular
  • Phagocytes Natural killer cells
  • complement
  • Adaptive
  • Humoral (antibodies and B cells)
  • Cellular
  • B and T cells
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5
Q

Definiton of immunodeficency?

A

Clinical situations where the immune system is not effective enough to protect the body against infection

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6
Q

What is primary immunodeficency?

A

Primary- Inherent defect within the immune system- usually genetic

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7
Q

What is secondary immunodeficency?

A

Secondary- Immune system affected due to external causes

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8
Q

What are secondary causes of immunodeficency?

A

Breakdown in physical barriers: Cystic Fibrosis- compromised mucosal barrier which leads to recurrent infection

Protein loss

Burns, protein loosing enteropathy, malnutrition

Malignancy

Especially lymphoproliferative disease (disorder of lymph glands, spleen or bone marrow), myeloma (blood cancer from plasma cells in bone marrow)

Drugs

Steroids, DMARDS (disease modified antirheumatic drugs), Rituximab, anti-convultants (stops rapid firing of neurons during seizures), myelosuppressive (drug used before a bone marrow transplant to get rid of any cancer immune cells within the marrow)

Infection

HIV, TB

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9
Q

What do phagocytes do?

A

Neutrophils (short lived, migrate into tissues when needed, found in blood), macrophages (found in tissue and longer lived)

Eat bacteria, fungi à and then destroy them

Once bacterium ingested by phagocyte, endocytosed, phagosome binds with lysosome to form a phagolysosome, bacteria then destroyed and debris is exocytosed.

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10
Q

What are pathogen recognition receptors?

A

Pathogen recognition receptors (PRRs)- recognise conserved pathogen associated molecular patterns (PAMPs)- various types like TLRs, NLRs

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11
Q

What is in example of a PAMP?

A

Lipopolysaccharide is an example of a PAMP- present on bacteria

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12
Q

What do phagocytes use to detect pathogens?

A

Phagocytes use PRRs to detect pathogens

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13
Q

What are Toll like receptors?

A

Toll like receptors are a type of PRR

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14
Q

Examples of toll-like receptors and what they recognise?

A

Toll like receptors are a type of PRR

TLR4 – recognises lipopolysaccharide

TLR5- recognises Flagellin

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15
Q

What happens when TLR’s recognise?

A

Cascade of events involving various molecules intracellularly then production of inflammatory cytokines.

MyD88 and IRAK4 are involved in this cascade

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16
Q

Boy age 12 months :History of recurrent pneumococcal pneumonia

Investigations:

Normal levels of immunoglobulins, normal numbers of lymphocytes and neutrophils

CRP only marginally elevated during the infection- goes up in bacterial infection as stimulates liver to produce CRP

Clinical presentation:

  • Recurrent bacterial infection, especially streptococcus and staphylococcus
  • Pneumonia, meningitis, arthritis
  • Poor inflammatory response
  • Susceptibility to infection decreases with age

Treatment? What is the diagnosis?

A
  • Rx: prophylactic antibiotics, iv immunoglobulin if severe
  • MyD88 presents in a similar manner

Case 1 : IRAK4 deficiency

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17
Q

What can disorders of phagolysosomes lead to?

A

Phagolysosome- disorders of this can lead to a primary immunodeficiency

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18
Q

How do disorders of phagolysosomes lead to primary immunodeficency?

A

NADPH complex in phagolysosome- formed of several proteins including gp91phox (coded by the X chromosome)- releases an electron, binds to oxygens leading to a superoxide then produces hypochlorous acid (bleach that kills the bacteria/fungi)

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19
Q

6 years old boy

History of recurrent skin abscesses, 1 x previous pneumonia

Presented to hospital with a liver abscesses

Mothers brother-similar but milder symptoms

Investigations:

Normal immunoglobulins, lymphocytes and neutrophil count

Diagnosis?

A

Case 2: Chronic granulomatous disease

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20
Q

What causes chronic granulamatous disease?

A

Disease from an abnormality of gp91phox- encoded by the X chromosome- affects males and females carriers- collections of granulomas- collections of macrophages which go to the site of infection and can try engulf the bacteria but cannot destroy it

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21
Q

Symptoms of chronic granulamtous disease? What organisms cause it?

A

Recurrent abscesses: lung, liver, bone, skin, gut

Unusual organisms e.g. Staphylococcus, Klebsiella, Serretia, Aspergillus, Fungi

Rx: haemopoeitic stem cell transplant, antibiotics

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22
Q

What is the test for chronic granulamtous disease? What does it measure?

A

Tests rely on REDUCTION (gain of electron)

Neutrophil Function Test

Measure Dihydrorhodamine reduction using flow cytometry- molecule that you can measure if it released or not- can manipulate that- stimulate DHR- measure number of neutrophils reduced before and after stimulating the neutrophils

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23
Q

What colour should healthy neutrophils go after dye added in test?

A

Nitro blue tetrazolium dye reduction- healthy neutrophils should go purple

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24
Q

What are complements?

A

Non immunoglobulin proteins

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25
Q

What do complements do?

A

Cell lysis (kill invading bacterium)

Control of inflammation

Stimulate phagocytosis

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26
Q

What is the complement pathway?

A

Complement pathway- classical pathway, triggered by antigen antibody complexes. Alternative pathway- on polysaccharides on the surface of microbes, MBL pathway which is similar to the classical pathway.

All 3 culminate in the formation of the membrane attack complex which lyses bacterial cell surfaces.

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27
Q

What do membrane attack complexes do?

A

Membrane attack complex punches holes in the membrane and that causes cells to lyse. This leads to defects in complement that make you prone to infection.

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28
Q

What should complement do?

A

Complement should lyse foreign cells if the foreign cells are covered in antibody

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29
Q

Complement should lyse foreign cells if the foreign cells are covered in antibody. What will this do?

A

Will trigger the classical complement cascade

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30
Q

What does C2, C4 deficency cause?

A

C2,C4 deficiency

SLE- no clearing of cellular debris after an injury infection and leads autoimmunity, infections, myositis (inflammation and degeneration of muscle tissue)

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31
Q

What does C5-9 deficency cause?

A

C5-C9 (form membrane attack complex)Presents with repeated episodes of BACTERIAL meningitis

Particularly Neisseria meningitis

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32
Q

What does the antigen bind to in adaptive immunity? What does the thing it binds to present it to?

A

Antigen that binds to a B cell on the B cell receptor, present to MHC class 2 molecule which presents it to T helper cell.

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33
Q

What do T helper cells produce?

A

T helper cells (CD4): Produce cytokines that effect B cells and the recruitment of other immune cells. B cells differentiate to memory B cells and plasma cells which will produce antibodies

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34
Q

What are the types of T helper cells?

A

Various types T helper 1, T helper 2, T helper 9, T helper 17

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35
Q

What are the function of antibodies?

A

Abs- neutralises viruses or toxins, putting bacteria together, dissolving or precipitating antigen molecules. They activate complement and removing sinopulmonary bacterial infections

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36
Q

Male patient

Presented before the age of 5

3 hospital admissions from pneumonia

Recurrent chest infections in between

Sinusitis

Mothers brother passed away aged 35 from bronchiectasis- scarring of the lungs

Bloods:

No B cells, normal T cells – use flow cytometry to detect- measures individual cells

No IgG, IgA, IgM

CT: bronchial thickening, evidence of recent pneumonia

Diagnosis?

A

Primary Antibody deficiency

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37
Q

Types of primary antibodu deficency?

A

X linked agammaglobulinaemia (no Ab)- Suspicion confirmed with genetics

Defect in Bruton’s Tryrosine kinase (BTK):

  • Needed for B cell signalling and B cell maturation
  • B cell maturation not completed in the bone marrow
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38
Q

What is BTK deficency mechanism?

A

BTK is a downstream molecule of the B cell receptor which is an Ab stuck on the B cell, patient had no functioning BTK so has the disease- BTK encoded on the X chromosome- this leads to B cells in bone marrow where B cells are expressed, can’t mature passed this thus blockade at this stage. Females are carriers and males are affected.

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39
Q

What are other B cell defects?

A

CVID- common variable immune deficiency

IgA deficiency- most common antigen deficency

X linked hyper IgM syndrome

transient hypogammaglobulinaemia of infancy- when child born has IgG from mother not produced by themselves- can be a lag which leads to this disease

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40
Q

What do defects in B cells mean? What do you treat them with?

A

loss of antibody secretion

Usually leads to recurrent bacterial infection with pyogenic organisms

Treat with antibiotics then i.v IgG for life

Most are very serious

Some less serious e.g IgA deficiency

1 in 5-700

Some completely well

Higher risk of autoimmune diseases e.g. coeliac

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41
Q

50 year old female

History of rheumatoid arthritis- severe

No infections most of adult life, but two year history of recurrent bacterial chest infections- 5 courses of antibiotics over the winter period

PMH: asthma

Drug Hx: currently on methotrexate and infliximab, previously rounds on Rituximab. Has also had gold, sulfasalazine in the past

Ix: slightly low B and T cells, low IgG and IgA

Diagnosis?

A

Secondary antibody deficiency due to drugs

Comparatively common

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42
Q

What is the mechanism for rituximab on B cells?

A

Rituximab is on B cells- targets CD20 and eliminates them from the immune system, they will repopulate unlike in primary immunodeficiencies leads to a lower level of antibodies.

Rituximab, methotrexate, azathioprine, ciclosporin, prednisolone, cyclophosphamide affect the immune system.

HIV kills CD4 cells which causes secondary immunodeficency.

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43
Q

Antibody deficiency Treatment

A

Antibiotics

Immunoglobulin G replacement- given blood serum samples with IgG

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44
Q

What does chicken pox show as?

A

Mild disease

Typical vesicles

Severe herpes zoster infection

Fulminant disease

Haemorrhagic lesions

Child may have an immunodeficency

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45
Q

Female baby age 3months

Severe herpes zoster infection- what causes chicken pox

Hospitalised with extensive oro-pharyngeal candida

Parents first cousins- can be caused by consaguinity

Sibling died at age of 4 months with sepsis

What investigations? What diagnosis?

A

Investigations:

Normal levels of IgG, no IgA and reduced IgM

Lymphocyte markers show absent/reduced T and NK cells but present B cells

Severe Combined Immunodeficiency (SCID)

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46
Q

How to diagnose SCID?

A

Diagnosis

No T cells +
suggestive history

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47
Q

Treatment for SCID?

A

Paediatric emergency

Antibiotics, antivirals, antifungals

Asepsis

Haemopoietic stem cell transplant (only cure)

?screen

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48
Q

What are the causes of SCID?

A

Defect/absence of critical T cell molecule- TCR (T cell receptor), common gamma chain

Loss of communication- MHCII deficiency

Metabolic- Adenosine deaminase deficiency- leads to environment when B and C cells can’t survive in the blood

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49
Q

PRR (pathogen receptor recognition)- problem with IRAK4 what happens?

A

IRAK4à recurrent pneumonia, poor inflammatory response

50
Q

Disorder of the function of phagocytes What happens?

A

Disorder of the function of phagocytes- digest bacteria but cannot destroy ità CGD (chronic granuloma disease)

51
Q

Complement deficency probelm?

A

Complement- bacterial meningitis

52
Q

What are primary antibody immunodeficencies caused by?

A

Antibodies- recurrent sinopulmonary infection- primary- innate inherited defect- X linked agammaglobulinaemia

53
Q

What are secondary antibody immunodeficencies caused by?

A

secondary if we use more drugs

54
Q

What is T cell deficency caused by?

A

T cells- SCID

55
Q

Immunomodulation-definition

A

The act of manipulating the immune system using immunomodulatory drugs to achieve a desired immune response

56
Q

A therapeutic effect of immunomodulation may lead to what?

A

A therapeutic effect of immunomodulation may lead to immunopotentiation, immunosuppression, or induction of immunological tolerance

57
Q

Biologic- Immunomodulators Definition

A

Medicinal products produced using molecular biology techniques including recombinant DNA technology

58
Q

Main classes of biologic immunomodulators?

A

Main classes

  • Substances that are (nearly) identical to the body’s own key signaling proteins
  • Monoclonal antibodies
  • Fusion proteins
59
Q

What are TNF molecules?

A

These all target TNF molecules which is an inflammatory cytokine which are used for various inflammatory conditions.

60
Q

What does it mean fully humanised? Example of something that is?

A

Adalimumab which is monoclonal antibody which is fully humanised (from non-humans species to make more similar to humans).

61
Q

What is chimeric? What is an example of chimeric?

A

Chimeric- problem with this is that it contains murine (relating to rodent) components which can be immunogenic and can cause an immune response against them.

Prior to having fully humanised monoclonal antibody which was targeting TNF was Infliximab- made of part human IgG molecule and part mouse which is attached for particular antibody.

62
Q

What is etanercept?

A

Etanercept where can create a fusion protein where combine Fc portion of antibody with TNF receptor 2 which is found on surface cell which contain TNF with high affinity.

63
Q

What is cerolizumab?

A

Certolizumab- uses a small proportion of antibody attached to a small arm of antibody attached to the regulated tail which allows it to become more stable in circulation- can target and neutralise TNF but this molecule unlike monoclonal antibodies doesn’t have potentially other side effects.

64
Q

What is immunopotentiation

A

Enhancement of the immune response by increasing the speed and extent of its development and by prolonging its duration.

65
Q

How can immunopotentation occur?

A

Immunisation:

  • Active
  • Passive

Replacement therapies

Immune stimulants

66
Q

Definiton of immunisation passive?

A

Definition

transfer of specific, high-titre antibody from donor to recipient. Provides immediate but transient protection

67
Q

Immunisation-passive problems?

A

Risk of transmission of viruses

Serum sickness- type 3 hypersensitive response

68
Q

Immunisation-passive types?

A
  • Convalescent plasma
  • Pooled specific human immunoglobulin- form a pool from humans to give to patient
  • Animal sera (antitoxins an antivenins)- inject into animals and they generate antibodies which can be used later on to neutralise- used in snake bites
69
Q

Immunisation-passive uses?

A

COVID19, Hep B prophylaxis and treatment

Botulism, VZV (pregnancy), diphtheria, snake bites

70
Q

Immunisation-active Definition

A

To stimulate the development of a protective immune response and immunological memory

71
Q

Immunisation-active Immunogenic material?

A
  • Weakened forms of pathogens
  • Killed inactivated pathogens
  • Purified materials (proteins, DNA, RNA)- recombinant vaccines
  • Adjuvants- stimulates the immune response
72
Q

Immunisation-active problems?

A
  • Allergy to any vaccine component
  • Limited usefulness in immunocompromised
  • Delay in achieving protection
73
Q

What are examples of replacement therapies and immune stimulation?

A
  • Pooled human immunoglobulin (IV or SC)- Used in Rx of antibody deficiency states
  • G-CSF/GM-CSF- small peptides to stimulate bone marrow- Act on bone marrow to increase production of mature neutrophils
  • γ-interferon- Can be useful in treatment of certain intracellular infections (atypical mycobacteria), also used in chronic granulomatous disease and IL-12 deficiency
74
Q

Examples of immunosuppression?

A
  • Corticosteroids
  • Cytotoxic/ agents
  • Anti-proliferative/activation agents
  • DMARD’s- Disease-modifying antirheumatic drugs
  • Biological-DMARD’s
75
Q

What can corticosteroids do to the body?

A
  • Decreased neutrophil margination
  • Reduced production of inflammatory cytokines
  • Inhibition phospholipase A2 (reduced arachidonic acid metabolites production)
  • Lymphopenia- lower than normal lymphocytes
  • Decreased T cells proliferation
  • Reduced immunoglobulins production
76
Q

What are the side effects of corticosteroids?

A

Carbohydrate and lipid metabolism

  • Diabetes
  • Hyperlipidaemia

Reduced protein synthesis

  • Poor wound healing

Osteoporosis

Glaucoma and cataracts

Psychiatric complications

77
Q

Corticosteroids-uses

A
  • Autoimmune diseases -CTD (connective tissue diseases), vasculitis, RA
  • Inflammatory diseases- Crohn’s, sarcoid, GCA (giant cell arteritis- swelling of BV)/polymyalgia rheumatica
  • Malignancies- Lymphoma
  • Allograft (organ from one person to another) rejection- transplantation
78
Q

Drugs targetting lymphocytes- What do antimetabolites do? Examples?

A

Antimetabolites- prevent T cell proliferation

Azathioprine (AZA)

Mycophenolate mofetil (MMF)

79
Q

Drugs targeting lymphocytes- what do calcineurin inhibitors do? Examples?

A

Calcineurin inhibitors – inhibit early stages of T cell activation

Ciclosporin A (CyA)

Tacrolimus (FK506)

80
Q

Drugs targeting lymphocytes- MTOR inhibitors- what do they do? Examples?

A

M-TOR inhibitors- inhibit further stages of T cell activation

Sirolimus

81
Q

Drugs targeting lymphocytes- IL-2 receptor mABs- what do they do?

A

IL-2 receptor mABs- block signalling of IL-2 receptor

Basiliximab

Daclizumab

82
Q

What is CyA? What does it do?

A

Calcineurin inhibitors

Binds to intracellular protein cyclophilin

83
Q

What is tacrolimus? What does it do?

A

Calcineurin inhibitors

Binds to intracellular protein FKBP-12

84
Q

What is mode of action calcineurin inhibitors?

A

Mode of action

Prevents activation of NFAT (nuclear factor of activate T cells)

Factors which stimulate cytokines (i.e IL-2 and INFγ) gene transcription

85
Q

What are T cell effects of calcineurin inhibitors?

A

T cell effects

Reversible inhibition of T-cell activation, proliferation and clonal expansion- can control immunosuppression

86
Q

What is sirolimus? What does it do?

A

Sirolimus (rapamycin)

Macrolide antibiotic

Also binds to FKBP12 but different effects

Inhibits mammalian target of rapamycin (mTOR)

87
Q

What is the mode of action of sirolimus?

A

Mode of action

Inhibits response to IL-2

88
Q

T cell effects of sirolimus?

A

T cell effects

Cell cycle arrest at G1-S phase

89
Q

Calcineurin/mTOR-side-effects

A
  • Hypertension
  • Hirsutism- women grow facial hair and on chest and back
  • Nephrotoxicity
  • Hepatotoxicity
  • Lymphomas
  • Opportunistic infections
  • Neurotoxicity
  • Multiple drug interactions (induce P450)
90
Q

Clinical use of drugs targetting lymphocytes?

A

Transplantation- Allograft rejection

Autoimmune diseases

91
Q

What do antimetabolites do?

A

Inhibit nucleotide (purine) synthesis

92
Q

What is azathioprine and what does it do?

A

Antimetabolites

Azathioprine

Guanine anti-metabolite

Rapidly converted into 6-mercaptopurine

93
Q

What is mycophenolate? What does it do?

A

Antimetabolites

Mycophenolate mofetil (MMF)- Prevents production of guanosine triphosphate

94
Q

What are the T and B cell effects of antimetabolites?

A

T and B cells effects

Impaired DNA production

Prevents early stages of activated cells proliferation

95
Q

What doanti metabolites and cytotoxic drugs like methotrexate (MTX) and cyclophosphamide do?

A

Methotrexate (MTX)- Folate antagonists

Cyclophosphamide- Cross-link DNA

96
Q

What are the advantages of antimetabolites?

A

Advantages of these are that the T cells that are activated are the ones that are rapidly dividing and in autoimmune conditions, the T cells that are rapidly dividing are against self-antigens of against transplant organs- when use the antimetabolite the cells that are potentially affected more are the cells that are rapidly dividing thus the autoreactive T cells are the ones being targeted preferentially by antimetabolite drugs

97
Q

Cytotoxic drugs-side-effects

A

ALL

  • Bone marrow suppression- as divides to form RBCs and neutrophils etc
  • Gastric upset- as cells dividing rapidly to provide protection to acid environment
  • Hepatitis
  • Susceptibility to infections
98
Q

Cytotoxic drugs-side-effects- Cylophosphamide

A

Cystitis

99
Q

Cytotoxic drugs-side-effects- MTX

A

Pneumonitis- inflammation of lung tissue

100
Q

Cytotoxic drugs-clinical uses

AZA/MMF

A

Autoimmune diseases (SLE, vasculitis, IBD)

Allograft rejection

101
Q

Cytotoxic drugs-clinical uses- MTX

A

MTX

RA, PsA (psoriatic arthritis, Polymyositis, vasculitis

GvHD in BMT

102
Q

Cytotoxic drugs-clinical uses- Cyclophosphamide

A

Cyclophosphamide

Vasculitis (Wagner’s, CSS)

SLE

103
Q

Biologics-examples

A
  • Anti-cytokines (TNF, IL-6 and IL-1)
  • Anti-B cell therapies
  • Anti-T cell activation
  • Anti-adhesion molecules
  • Complement inhibitors
  • Check point inhibitors
104
Q

Anti-cytokines mAB’s- Anti-TNF uses?

A

Anti-TNF

First biologics to be successfully used in therapy of RA (multiple different agents now licensed)

Used in a number of other inflammatory conditions (Crohn’s, psoriasis, ankylosing spondylitis)

Caution: increase risk of TB

105
Q

Anti-cytokines mAB’s (monoclonal antibodies)- Anti-IL-6 (Tocilizumab) use?

A

Blocks IL-6 receptor

Used in therapy of RA and AOSD (adult-onset Still’s disease- type of arthritis)

May cause problems with control of serum lipids

106
Q

Anti-cytokines mAB’s (monoclonal antibodies)- Anti-IL-1 use?

A

Used in treatment of AOSD and autoinflammatory syndromes

107
Q

Rituximab what is it?

A

Chimeric mAb (part mouse part human) against CD20- B cell surface

108
Q

Rituximab uses?

A
  • Many uses:
  • Lymphomas, leukaemias
  • Transplant rejection
  • Autoimmune disorders- targets specific proportion of B cells- only binds to the population that is within the circulation- doesn’t affect the cells that are dividing within the bone marrow- advantages is if you are targeting the cells in circulation you are hoping to wipe out all of the auto-immune diseases and not destroying the early B cells in the bone marrow. Allowing long lived plasma cells to produce Ab to provide protection against various infections.
109
Q

Example of adoptive immunotherapy?

A

Bone marrow transplant (BMT)

Stem cell transplant (SCT)

110
Q

Adoptive immunotherapy uses?

A
  • Immunodeficiencies (SCID)- replace immune system with donor one
  • Lymphomas and leukaemias
  • Inherited metabolic disorders (osteopetrosis)
  • Autoimmune diseases
111
Q

What are check point inhibitor uses?

A

These drugs used for treatment in malignancies

112
Q

WHat happens in normal T cell activation?

A

In normal T cell activation there is APC which can stimulate the immune cells by interaction with T cell receptor and providing co-stimulatory signals but tumours have evolved ways to interfere with activation of T cells so they can block this important signal which is necessary for T cell activation.

113
Q

How do tumours interfere with T cell activation?

A
  • Tumour cells can express certain molecules such as PDL-1 which inhibits activation of T cells. There are monoclonal antibodies which interfere with these processes. CTLA-4 supress the molecule on T cells preventing T cell activation
  • By providing anti-CTLA4 antibodies into the system you restart T cell activation and allow immune system to be rebooted
  • Anti-PDL1 monoclonal antibody which blocks the molecule PDL1 which is produced by tumours which reduces T cell activation
114
Q

What are examples of immunomodulators?

A
  • Immune suppressants
  • Allergen specific immunotherapy
  • Anti-IgE monoclonal therapy
  • Anti-IL-5 monoclonal treatment
115
Q

When is allergen specific immunotherapy needed?

A

Indications:

  • Allergic rhinoconjutivitis not controlled on maximum medical therapy
  • Anaphylaxis to insect venoms
116
Q

What is the mechanism for allergen specific immunotherapy?

A

Mechanisms:

Switching of immune response from Th2 (allergic) to Th1 (non-allergic)

Development of T reg cells and tolerance

117
Q

Routes for allergen specific immunotherapy?

A

Routes:

SC or sublingual for aero-allergens

118
Q

Side effecrs of allergen specific immunotherapy?

A

Side-effects:

Localised and systemic allergic reactions

119
Q

What is omalizumab used for?

A

Omalizumab

  • mAb (monoclonal Ab) against IgE
  • Used in Rx (to take) of asthma
  • NICE approved for chronic urticaria and angioedema
  • May cause severe systemic anaphylaxis
120
Q

What does mepolizumab do? What does it prevent?

A
  • mAb against IL-5- cytokine that activates eosinophils and causes recruitment and activation
  • Prevents eosinophil recruitment and activation
  • NICE approved for asthma
  • No clinical efficacy in hypereosinophilic syndrome
121
Q
A

Clinical pathology (8 decks)

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