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Immunology Flashcards

1
Q

What are the general ways to boost the immune system (4)

A

Vaccination
replacing missing components
Blocking immune checkpoints
Cytokine therapy

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2
Q

Briefly describe the adaptive immune response

A

The adaptive immune response consists of B and T cells, there is a wide repertoire of antigens receptors available from genetic recombination (SNPs, deletions etc).
There is a process of selection so that they are reactive enough but not autoreactive. Autoreactive antigens are deleted.
Upon detection of a specific antigen B cells undergo clonal expansion to produce effector (T cell-independent IgM secretion) cells and (germinal centre reaction to T cell-dependent )memory B cells -IgG, IgA and IgE. T cells will differentiate into effector cells to produce cytokines and cytotoxins

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3
Q

Which cells are antigen presenting cells?

A

Dendritic cells
Macrophages- Langerhans, Mesangial, Kupper cells, osteoclasts, microglia
B cells

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4
Q

Describe the formation and role of memory T cells

A

T cells are activated by antigen-presenting cells and undergo clonal (Cytokines are required for this usually from T helper cells - IL2. After expansion, many will apoptosis and some will survive as memory T cells - (Maintained by cytokines not antigen)
They have different surface proteins so can access non-lymphoid tissue (site of microbial entry).
More easily activated than naive cells

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5
Q

Explain the role of memory B cells

A

Survive a long time, rapid IgG response to antigen

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6
Q

Explain how the hemagglutinin is responsible for influenza infection and how the HA assay works

A

HA is responsible for the immune response against influenza and is one of the components of the flu vaccine.
In a red cells spot test- the red cells will clump together and form a red spot at the bottom. If HA is present the cells will bind to it and diffusely clump. If there is antigens to HA (eg vaccinated), this won’t happen and it will just look normal

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7
Q

Explain the role of the BCG and how the Mantoux test works

A

The BCG is a live attenuated vaccine, its purpose is to reduce the progression of TB rather than to stop primary infection.
The Mantoux test is injection of TB subdermal to check for an immune response (T4 response - T cell med)

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8
Q

What are the different types of vaccines (give examples)

A

Live attenuated (modified to limit pathogenesis)
-BCG, Polio (nasal), MMR, yellow fever, typhoid (oral), vaccinia
Inactivated and Component
-Inactivated:Flu, cholera, bubonic plague, Polio (salk- IM), Hep A, pertussis, Rabies
-Component: Hep B, HPV (capsid), Flu (neuraminidase and HA)
-Toxiods- inactivated toxins- diphtheria, tetanus

mRNA
-Sars-cov2
Dendritic - in dev for prostate cancer -tumour antigens as vaccines

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9
Q

What are the pros and cons of

a. live attenuated vaccines
b. inactive/ component
c. DNA vaccines
d. mRNA vaccines

A

a. + Mild symptomatic infection, broad immune response to lots of antigens (good strain coverage), long-lasting immunity, activates all phases of immune response
- Storage issues, Can revert to wild type pathogens, spread to contacts (ie they haven’t consented to be vaccinated) unsuitable for immunocompromised patients.
b. + safe for immunocompromised patients, easy storage, cheaper, no mutations
- less long-lasting and may need to be frequently updated, may need adjuvants, may be poorly immunogenic
c. +safe for immunocompromised patients, the potential for cancer vaccines
- expensive to store

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10
Q

Explain the role of conjugate vaccines and give examples

A

Conjugate vaccines.
Contain a polysaccharide + a protein carrier (the polysaccharide promotes a B cell response (transient), the protein carrier promotes T cell response.
-eg HiB, meningococcus, pneumococcus

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11
Q

What is the most common adjuvant and what are its proposed mechanisms of action

A

Aluminium salt - as it’s very safe and effective

  • slow down antigen release= continual stim
  • inflam reaction
  • Activates Gr1 , IL4 and eosinophils -prime B cells
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12
Q

Name two experimental adjuvants

A

ISCOMS- immune-stimulating complexes - cage structure of saponins, cholesterol, phospholipids protein mixed with antigen
CpG- Cytosine + guanine separate by phosphate - these motifs bind to PRR (TLR-9) -> immune response

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13
Q

What are the indications for B cell replacement?

A

Primary antibody deficiencies
- X linked agammaglobinaemia
-X linked hyper IgM syndrome
Common variable immune deficiency

Secondary deficiencies
- haematological deficiency - CLL, Multiple myeloma
After BM transplant

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14
Q

What are some clinical examples of specific immunoglobulin replacement?

A

Hep B IgG
VZV IgG
Tetany IgG
Rabies IgG

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15
Q

What are the different types of adoptive T cell transfer?

A

Virus-specific
Tumour infiltrating (TIL)
T cell receptor (TCR)
Chimeric antigen receptor (CAR)

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16
Q

Explain the role of virus-specific T cell transfer in EBV

A

Used to prevent B cell lymphoproliferative disease in the immunosuppressed.
Blood sample from pt or donor.
-Isolate mononucleocytes
-Stim with EBV peptides
-Expansion of EBV specific T cells which can be reinfused into the patient

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17
Q

What are the differences between TCR and CAR T cell therapy

A

Both have T cells from pt removed and inserted vector (Viral or non-viral)
TCR - is just a specific T cell receptor eg against a tumour antigen
CAR T - is a recombinant receptor with T and B cell surface proteins so can activate both TCR (CD28 and CD23)and CD19

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18
Q

Explain the role of adjuvants and their MOA (Plus examples)

A

Increase immune response without altering vaccine specificity.
Mimic PAMOs action on TLR and PRRs
aluminium salts (humans), Lipids (monophosphoryl lipid A), oils (Freund’s adjuvant -animals), ISCOMS, CpG DNA

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19
Q

Explain TIL T cell therapy

A

Remove tumour from the patient
Stim T cells from the tumour with cytokines (IL-2) in the presence of tumour cells.
T cell undergo clonal expansion
reinsert into the patient - infiltrating lymphocytes

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20
Q

Where is CAR- T cell therapy being utilised

A

NH lymphoma and ALL

less effective in solid tumours

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21
Q

What is the mechanism of Ipilimumab?

A

Binds to CTLA4 (a TCR that recognises CD80 and CD86 APCs and transducers and inhibitory signal) thus preventing this inhibition and enhancing T cell response

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22
Q

What is the mechanism of Pembrolizumab and Nivolumab

A

Antibodies that bind the PD-ligand 1 and in turn upregulates T cell action.
PD-1 (prevents death) is present on APCs and tumour cells - its role is to inhibit T cells.

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23
Q

Give examples of cytokine therapies and their uses

A

INF -a: hairy cell leukaemia, CML, MM
INF-2a: Bechet’s disease
INF-y: Chronic granulomatous disease
IL-2: Renal cell cancer

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24
Q

What are the uses and complications of Ipilimumab (CTLA4 inhib T signalling) and Pembrolizumab and Nivolumab (PD-1 inhibs)?

A

Ipilimumab: used in Multiple myeloma
Pembrolizumab and Nivolumab: Multiple myeloma and advanced renal cancer
Complication- autoimmunity (RA, Thyroid, diabetes)

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25
Q

What are the different methods for suppressing the immune system?

A 
Steroids
Cytotoxic drugs
Plasmapheresis
Inhibiting cell signalling
Agents targeting cell surface antigens
Agents targeting cytokines
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26
Q

What is the action of corticosteroids on prostaglandins

A

Corticosteroids inhibit phospholipase A2 ( which is required for the conversion of Arachidonic acid to prostaglandins and leukotriens by COX

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27
Q

What is the action of corticosteroids on phagocytes

A

v phagocytosis,
v proteolytic enzyme release.
v phagocytes in inflamed tissue:
v chemoattractants, v expression of adhesion molecules on endothelium

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28
Q

What is the action of corticosteroids on lymphocytes

A

Lymphopenia (sequestered in lymphoid tissue CD4>CD8> b)
x cytokine expression
v Ab synth
^ apoptosis

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29
Q

What are the SEs of steroids

A

Metabolic- Diabetes, moo face, central adiposity, buffalo fat pat, dyslipidemia, osteoporosis, adrenal suppression, hirsutism, acne
Other- cataracts, glaucoma, peptic ulcers, pancreatitis, avascular necrosis, immunosuppression

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30
Q

What are cytotoxic drugs and give examples

A

Cyclophosphamide
Mycophenolate mofetil
azathioprine

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31
Q

What are the general side effects of cytotoxic drugs?

A

Bone marrow suppression - pancytopenia
loss of hair, sterility (M>F)
Infection risk - eg HSV and Pneumocystis jiroveci

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32
Q

What’s the MOA of cyclophosphamides

A

Alkylating agent of guanine -> DNA damage -> x cell replication.
(B>T>all high turnover cells)

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33
Q

What the indications for

a. cyclophosphamide
b. Mycophenolate mofetil
c. Azathioprine

A

a. major organ AI dissease eg SLE, GPA and anti-cancer
b. organ transplant (alt to azo), AI disease and vasculitis (alt to cylo)
c. Chron’s

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34
Q

What’s the MOA of mycophenolate mofetil?

A

Purine anti-metabolite-> prevents synthesis of guanosine -> prevents DNA replication (T>B cells)

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35
Q

What genetic varient should you check for before starting azathioprine

A

TPMT - thiopurine methyltransferase polymorphisms as they are unable to metabolism azathioprine 1:300.
susceptible to bm suppresion

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36
Q

Describe the process of plasmapheresis

A

The aim is to remove pathogenic antibodies from patient plasma.
Patient blood is passed through cells separator. Cellular constituents are reinfused. Plasma is treated to remove AB or plasma exchange - given albumin, re given to the patient

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37
Q

What are the indications of plasmapheresis

A

Severe AI disease.
- good pastures (anti-GMB)
-Severe acute MG (ANti-AChR)
Severe vascular rejection (HLA issues)`

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38
Q

Whats the MOA of Azothioprine

A

purine anti-metabolite/ analogue-> met to 6-mercaptopurine-> interferes with DNA synthesis (T>B)

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39
Q

What are the side effects specific to

a. cyclophosphamide
b. azathioprine

A

a. haemorrhagic cystitis - toxic metabolite acrolein excreted via urine
c. hepatotoxicity (uncommon)

40
Q

What are the different types of cell signalling inhibitors

A

calcineurin inhibitors
JAK inhibitors
PDE4 inhibitors

41
Q

What’s the MOA of calcineurin inhibitors (give examples)

A

Ciclosporin and tocrolimus

prevent T cell signalling -> v IL2 -> v T cell proliferation and activation

42
Q

Describe the side effect profile of calcineurin inhibitors

A

Nephrotoxic, ^BP, neurotoxic.
Ciclosporins less diabetes-inducing that tacrolimus
Ciclosporins cause dysmorphic features

43
Q

What’s the MOA of JAK inhibitors

A

JAK1 and 3 inhibitors prevent downstream activating of inflammation

44
Q

WHats the MOA of PDE4 inhibitors and their indications

A

Apremilast - psoriatic arthritis (future maybe copd and RA)

Phosphodiesterase 4 inhibitor-> x ^ cAMP-> v cytokine synthesis via PKA

45
Q

Give examples of agents directed at cell surface antigens (names and targets

A

Basiliximab CD25 -IL2a chain
Abatacept -CTLA4-Ig infusion protein (CD28)
Rituximab -anti CD20
Vedolizumab - a4b7 integrin
Tocilizumab, Sarlimumab -IL6R
Thymocyte globulin (non-specific T cell, CD2,3,4,8)

46
Q

What’s the MOA of thymocyte globulin

A

lymphocyte depletion, modulation of T activation and migration

47
Q

What is the clinical use of basiliximab

A

Pre and post allograft as it inhibits T cell proliferation

48
Q

What’s the MOA of Abatacept?

A

A receptor made from the fusion of CTLA4 and IgG Fc region. That binds to CD80 and 86 (preventing physiological engagement with CD28 and CTLA4 - normally are ^ and v respectively) -> v T cell activation

49
Q

What is the roll of NK cells?

A

Lymphocytes that express inhibitory receptors for HLA1 to prevent self immune response and cytotoxic to altered self eg malignancy and virus infected cells

50
Q

Describe the compliment cascade

A

Classic pathway - activated by Ab-AG complexes >AB conformational change to bind to C1,C2,C4

Manose-binding lectin C2 and C4- MBL binds to bacterial carbohydrate

Alternative - direct binding of C3 to bacterial cell wall. (quicker)

common pathway C3
formation MAC (via C5-9) > perforation on bacteria
51
Q

Describe the role of dendritic cells

A

Immature cell = pathogen recognition and uptake

Mature = APC, present to T cells via MHC II

52
Q

Explain T cell maturation

A

BM> thymus-receptor recombination
low reactivity = not selcted
moderate= tolerant
reactive = negative selction

53
Q

What is the role of
T helper
T follicular and Treg
T killer

A

T helper CD4+, HLAII- recognise extracellular proteins and stimulate B and CD8

T follicular = help in germinal centre > B cell differentiation IgG and IgA

Treg- CD25 - negative immune modulation

T killer CD8 HLA-I - direct cytotoxic secrete IFNg and TNFa

54
Q

Describe B cell maturation

A

BM > germinal centres in lymphoid tissue is CD4 dependent. Isotope switching IgM-> g, E or A
+ negative selection of self reactive

55
Q

Describe the action of cytokines

A

Small protwin messenger that recruit and activate of WBC

can act autocrine and paracrine

56
Q

Give examples of secondary immunodeficiencies (4 types)

A

Infective - HIV, measles, mycobacterium
Malignancy - myeloma, leukaemia and lymphoma
Biochemic- malnutrition, zinc and iron deficiency, renal impairment
Drugs - corticosteroids, calcineurin inhibitors, JAKi, antiepileptic, biologics, DMARDS cytotoxics

57
Q

What clinical features suggest immunodeficiency

A 
Recurrent infections - 2 major or 1major and 1 minor in one year
Abnormal pathogen
Abnormal location
Unresponsive to Tx
chronic infections
Early structural damage

Primary - young age at presentation, FH of infant death, FTT

58
Q

Describe the test for chronic granulomatous disease

A

Persistent ^Neutrohpils and macrophage but persistent Antigen
Stim neutrophils and then:
Nitroblue tetrazolium (NBT) Yellow to blue with hydrogen peroxide
DihydroRhodamine - flow cytometry> fluroscence with hydrogen peroxide

59
Q

What are the 3 mechanisms of phagocytic immunodeficiecny

A

Abnormal development - eg Kostmann syndrome, Cyclical neutropenia and reticular dysgenesis (SCID)

Abnormal activation/migration- leukocyte adhesion v

Abnormal killing mechanism- chronic granulomatous disease, IL12/ INFg deficiency

60
Q

Which immunodeficiencies are due to v compliment

A

CH50=Classic pathway
AP50=Alternative pathway

SLE (can be chicken or egg) - vC3, vC4, vCH50
(so can have normal C3, but vC4 so can’t progress> lots of nuclear debri> SLE) or ^consumption due to SLE

C1q deficiency vCH50 -alternative
Properidin v =AP50
C7/9 v = v CH50 and vAP50

61
Q

What are the investigations for immunodeficiency?

A 
FISH
FBC - lymphocyte breakdown
Immunoglobulins - breakdown
Serum compliment - C3 and C4 -CH50=Classic pathway
AP50=Alternative pathway
HIV

Consider u&Es, Ca+, PTH and ALP, specific IgG to vaccinations, 3rd line - anti-cytokine and anti-compliment

62
Q

How can you differentiate between reticular dysgenesis, Kostmann syndrome and cyclical neutropenia?

A

Reticular dysgenesis- vT, vNK, normal but not functional B > vIg
Kostamnn syndrome - congenital neutropenia
Cyclical - neutropenia every4-6 weeks

63
Q

What is the treatment for polymorph deficiency (general)

A

Prophylaxis -
abx- Seprin antifungal- Itraconazole
INFg for chronic granulomatous disease
HPST dependent on severity

64
Q

What infections are associated with NK deficiency?

A

Viral - HSV, VZV, CMV, EBV, papilloma virus

65
Q

What infections are associate with B cell deficiency (or v functionality)?

A

Bacterial - staph, strep
Toxins - diphtheria, tetanus
previously vaccinated - Pneumococcal, Hib, MMR

66
Q

What infections are associated with T cell deficiency?

A

Fungal, viral, intracellular bacteria (mTB, salmonella) Viral associated malignancy

67
Q

What are the causes of T cell deficiency (stages of development + examples)

A

Failure of precursors - SCID reticular dysgenesis
Failure of thymic development - DiGeorge syndrome
Failure of HLA expression - Bare lymphocyte syndrome (BLS) T1 and T2
Failure of signalling/cytokines- IFNv and vIL12r > abnormal TB

68
Q

Describe the presentation of DiGeorge syndrome 22q11.2 deletion

A

Abnormal development of pharyngeal pouch
Face- high forehead, cleft palate, low set folded ears
Throat- vCa2+ as no PTH, oesophageal atresia
Chest- vT cells due to vthymus (mild immunodeficiency as B cells normal), congenital cardiac abnormalities

69
Q

Describe the aetiology of Bare lymphocyte syndrome

A 
Failure of HLA class TII -> vT CD4+ > v B cell isotype switching > ^IgM and no G, A or E
TI > vCD8
70
Q

What are the leukopenias associated with SCID

a. reticular dysgenesis
b. X linked
c. Adenosine deaminase deficiency

A

a. reticular dysgenesis - vT, vNK, vB
b. vT, vNk, -B
c. vT, vNK, immature B

71
Q

What are the different stages of B cell maturation that can leads to B cell deficiency (+ examples)

A 
Failure of precursors -SCID
Failure of B cell maturation - Bruton's Xlinked agammaglobulinaemia
Failure of T costimulation - Hyper IgM
Failure of IgG CVID
Failure of IgA - severe IgA deficiency
72
Q

What causes hyper IgM

A

no CD40 on T helper cell . no B cell isotype switching . build up of IgM with no G,A or E

73
Q

What is the treatment for B cell deficiency

A 
Aggressive prophylaxis (vaccines have no role other than IgA deficiency)
Replacement of IgG - donor life long
74
Q

What is the treatment for T cell deficiency?

A 
Aggressive prophylaxis
HPST- SCIDS, BLS2
Replace enzymes - PEG-ADA (ADA scid)
Gene therapy
Thymic transplant - Digeorge
75
Q

What are the monogenic auto-INFLAMatory diseases (and must)

A

Familial Mediterranean syndrome
TRAPs (TNF associated periodic syndrome)
Muckle wells hyper IgD (HIDS)

76
Q

What is the presentation of familial mediterranean syndrome

A 
periodic fever (rest is heterogeneous), rash, abdo pain(peritonitic), pericarditis> chest pain, arthritis and sersitis.
^amyloid in kidneys, liver and spleen> nephrotic syndrome
77
Q

What is the treatment of familial mediterranean syndrome?

A

Colchine (as its anti mitotic > v neutrophil recruitment and activation)
IL-1 blockers (anakinra or canukinumab)
TNFa blocker - Entercept

78
Q

What are the polygenic autoINFLAMatory conditions?

A

IBD - Crohn’s and UC
Vascular - GCA, Takasayau’s arteritis
OA

79
Q

What is the pathological process associated with Crohn’s and therefore its treatment

A

Proinflammory state > ^cyto/chemokines > WBC recruitment> ^ proteases and free radicles> crypt inflammation> damage ulceration and granulomas.
(p-ANCA+ve)

Steroids, anti-proliferatives and NSAIDs
-Azathioprine
Targeted biological - anti-TNF and IL12/23

80
Q

What factors affect the development of polygenic autoINFLAMatory conditions? (6)

A 
Genetics
epigenetics
environmental
microbiome
local inflma - smoking
miRNA
81
Q

What is the difference between auto-inflammaory, mixed and auto-immune conditions?

A

Autoinflammatory involves dysfunction of the innate immune system including neutrophils, macrophages causes inappropriate tissue damage.

Autoimmune has dysfunction of the adaptive immune response

Mixed has degrees of both (no auto antibodies as this > autoimmune)

82
Q

WHat are the polygenic mixed auto conditions?

A

ankylosis spondylitis (axial spondylitis)
Bechet’s disease
Psoriatic arthritis

83
Q

What is the genetic component of ankylosisng spondylitis (and its presentation)

A

HLA B27 association 90% heritability

SI enthesitis, pain, stiffness and large joint arthritis

84
Q

What are the gel and coombs hypersensitivity reactions?

A

T1- anaphylaxis - IgE,
T2- cytoxic AB against cellular Ag
T3- immune complex (to soluble Ag)
T4- Tcell mediated delayed onset reaction

85
Q

What are the monogenic autoIMMUNE diseases (split by causative category)?

A

abnormal Treg - IPEX immune dysregulation polyendocrinopathy enteropathy
abnormal WBC apop - AI lymphoproliferative syndrome
general abnormal tolerance - APECED, APS-1, primary endocrine gland dysfunction (Addison’s, hypothyroid, hyperparathyroidism, vitiligo, enteropathy)

86
Q

What polymorphism can lead to autoIMMUNE conditions?
eg loss of tolerance
auto reactive T and B cells
auto ABs

A

AutoABs
PTPN22 (Ra, SLE T1DM)
CTLA4- SLE and thyroid
costimulatory molecules eg CD40L-CD40, CD80-CD86,

87
Q

What are the mutisystem autoIMMUNE conditions?

spilt by AB

A

ANCA - vasculitis - Wegner’s
ANA- SLE, systemic sclerosis (diffuse and limited), Sjogren’s syndrome, dermato/polymyositis
anti-CCP - RA

88
Q

What are the different types of vasculitis?

A

Large - GCA, Takaysaku arteritis, polymyalgia rheumatica

medium - Kawasaki, poly arteritis nodosa

small - Wegner’s( granulomatosis with polyangiitis) Churgstrauss (eosinophilic granulomatosis with polyangiitis), microscopic polyangiitis

Small immune complex - Anti-GBM (Goodpasture’s), IgA, cryogloninaemia

89
Q

What is the pathology of RA?

A

Anti-CCP antidodies (or anti-RF)
^citrillinated load > braking of tolerance
RFs= Smoking> ^ citrullination of proteins, PAD enzyme must, gingivitis (porphyromonas expresses PAD)

90
Q

Describe the investigations for SLE (and post-diagnosis ix)?

A

ANA - anti-ds DNA
full AI screen - Ro, La, Sm, U1PNP, SCL70 topoisomerase, centromere
Compliment
ESR^, CRP -

post- antiphospholipid syndrome - anti-cardiolipin, lupus anti-coagulant

91
Q

Describe the pathology associated with SLE

A

Abnormal clearance of apoptosed cells -> ^ nuclear debris and loss of tolerance

Abnormal cellular activation > ^cyto/chemo and costims

B cell hyperactivity> AutoABs

T3 hypersensitivity AB-AG deposition> C3 and C4 in kidney, skin and joints

92
Q

Describe the presentation of systemic sclerosis

A 
Limited - CREST - 
calcinosis
Raynaud's
Oesophagal dysmotility
Sclerodactyly
Telangiectasia
Pulmonary HTN

Diffuse- skin involvement above forearms, GI- small bowel blind loop and SIBO, ILD, scleroderma kidney >AKI

93
Q

What is the difference between dermatomyositis and polymyositis

A

dermatomyositis has a rash CD4 and B cell.

Polymyositis has no cutaneous involvement just CD8 in muscles

94
Q

What diseases are associated with pANCA and cANCA

A

PANCA

  • vaculitides micro, churgg strauss
  • uc and CD
  • psc
  • not main but sle, ra, Sjogren

cANCA - wegners (granulomatos)
(And CF)

95
Q

What are the organ-specific auto IMMUNE conditions and their associated auto AB?

A 
T1DM - pancreas anti- islet cells
pernicious anaemia - anti-IF or parietal cells
Hashimoto's- anti TSH
Grave's - anti-TSHR
Good pastures - anti-BM
MG- anti-AchR
AI-hep - ANA, SMA, Anti-LKM, pANCA
PBC- ANA pANCA, AMA
Pemphigus Vulgaris - anti-epidermal caherin

Pathology (6 decks)

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